Skip to content

Phase 1/2 Study of the Highly-selective RET Inhibitor, Pralsetinib (BLU-667), in Participants With Thyroid Cancer, Non-Small Cell Lung Cancer, and Other Advanced Solid Tumors

A Phase 1/2 Study of the Highly-selective RET Inhibitor, BLU-667, in Patients With Thyroid Cancer, Non-Small Cell Lung Cancer (NSCLC) and Other Advanced Solid Tumors

Status
Completed
Phases
Phase 1Phase 2
Study type
Interventional
Source
ClinicalTrials.gov
Registry ID
NCT03037385
Acronym
ARROW
Enrollment
590
Registered
2017-01-31
Start date
2017-03-17
Completion date
2024-03-21
Last updated
2025-05-31

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Adenocarcinoma, Adenocarcinoma, Papillary, Bronchial Neoplasms, Carcinoma, Carcinoma, Bronchogenic, Carcinoma, Neuroendocrine, Carcinoma, Non-Small-Cell Lung, Colonic Diseases, Colonic Neoplasms, Colorectal Neoplasms, Digestive System Disease, Digestive System Neoplasm, Endocrine Gland Neoplasm, Endocrine System Diseases, Gastrointestinal Disease, Gastrointestinal Neoplasms, Head and Neck Neoplasms, Intestinal Disease, Intestinal Neoplasms, Lung Diseases, Lung Neoplasm, Medullary Thyroid Cancer, Neoplasms, Neoplasms by Histologic Type, Neoplasms by Site, Neoplasms, Germ Cell and Embryonal, Neoplasms, Glandular and Epithelial, Neoplasms, Nerve Tissue, Neuroectodermal Tumors, Neuroendocrine Tumors, Respiratory Tract Disease, Respiratory Tract Neoplasms, RET-altered Colon Cancer, RET-altered Non Small Cell Lung Cancer, RET-altered Papillary Thyroid Cancer, RET-altered Solid Tumors, Thoracic Neoplasms, Thyroid Cancer, Papillary, Thyroid Diseases, Thyroid Neoplasm

Keywords

RET Lung, RET Thyroid, RET fusion, RET alteration, RET mutation, RET positive, RET inhibitor, RET altered, RET rearrangement, RET NSCLC, RET medullary thyroid cancer, RET-rearranged NSCLC, RET-rearranged thyroid, M918T, TRIM33-RET, RET fusion lung cancer, RET fusion thyroid cancer, lung cancer mutation, BLU 667, RET tyrosine kinase, RET gene mutation, RET kinase, RET MTC, advanced lung cancer, advanced non small cell lung cancer, metastatic lung cancer, KIF5B-RET, CCDC6-RET, NCOA4-RET, advance solid tumor, V804L, V804M, thyroid cancer RET inhibitor, lung cancer RET inhibitor, RET PTC, rearranged during transfection, RET-PTC1, RET-PTC, RET-PTC3, RET-PTC4, PRKAR1A-RET, RET-PTC2, GOLGA5-RET, RET-PTC5, ERC1-RET, KTN1-RET, RET-PTC8, HOOK3-RET, PCM1-RET, TRIM24-RET, RET-PTC6, TRIM27-RET, RET-PTC7, AKAP13-RET, FKBP15-RET, SPECC1L-RET, TBL1XR1-RET, BCR-RET, FGRF1OP-RET, RFG8-RET

Brief summary

This is a Phase 1/2, open-label, first-in-human (FIH) study designed to evaluate the safety, tolerability, pharmacokinetics (PK), pharmacodynamics (PD), and preliminary antineoplastic activity of pralsetinib (BLU-667) administered orally in participants with medullary thyroid cancer (MTC), RET-altered NSCLC and other RET-altered solid tumors.

Detailed description

The study consists of 2 parts, a dose-escalation part (Phase 1) and an expansion part (Phase 2). Both parts will enroll participants with advanced non-resectable NSCLC, advanced non-resectable thyroid cancer and other advanced solid tumors that have progressed following standard systemic therapy, have not adequately responded to standard systemic therapy, or the participants must be intolerant to or the Investigator has determined that treatment with standard therapy is not appropriate, or there must be no accepted standard therapy for their disease.

Interventions

pralsetinib (BLU-667) is a potent and selective inhibitor of the RET mutations, fusions, and predicted resistant mutants

Sponsors

Hoffmann-La Roche
Lead SponsorINDUSTRY

Study design

Allocation
NON_RANDOMIZED
Intervention model
PARALLEL
Primary purpose
TREATMENT
Masking
NONE

Intervention model description

Phase 1 (Complete): * Advanced MTC, NSCLC or other solid tumor * 30-600mg (PO QD or BID) Phase 2 (400mg QD): * Group 1: RET fusion NSCLC previously treated with a platinum chemotherapy * Group 2: RET fusion NSCLC not previously treated for metastatic disease * Group 3: MTC previously treated with cabozantinib and/or vandetanib * Group 4: MTC not previously treated with cabozantinib or vandetanib * Group 5: Other solid tumors with a RET fusion not eligible for any of the other groups and previously treated with SOC or have no acceptable SOC for their tumor type as determined by the investigator * Group 6: Any solid tumor with a RET alteration (fusion or mutation) previously treated with a selective RET Inhibitor * Group 7: Other solid tumors with a RET mutation previously treated with SOC * Group 8: RET fusion NSCLC previously treated with a platinum chemotherapy (China only) * Group 9: MTC not previously treated with systemic therapy for advanced or metastatic disease (China only)

Eligibility

Sex/Gender
ALL
Age
18 Years to No maximum
Healthy volunteers
No

Inclusion criteria

Key Inclusion Criteria: * Diagnosis during dose escalation (Phase 1) - Pathologically documented, definitively diagnosed non-resectable advanced solid tumor. * All participants treated at doses \> 120 mg per day must have MTC, or a RET-altered solid tumor per local assessment of tumor tissue and/or blood. * Diagnosis during dose expansion (Phase 2) - All participants (with the exception of participants with MTC enrolled in Groups 3, 4, and 9) must have an oncogenic RET-rearrangement/fusion or mutation (excluding synonymous, frameshift, and nonsense mutations) solid tumor, as determined by local or central testing of tumor or circulating tumor nucleic acid in blood; as detailed below. * Group 1 - participants must have pathologically documented, definitively diagnosed locally advanced or metastatic NSCLC with a RET fusion previously treated with a platinum-based chemotherapy. * Group 2 - participants must have pathologically documented, definitively diagnosed locally advanced or metastatic NSCLC with a RET fusion not previously treated with a platinum-based chemotherapy, including those who have not had any systemic therapy. Prior platinum chemotherapy in the neoadjuvant and adjuvant setting is permitted if the last dose of platinum was 4 months or more before the first dose of study drug. * Group 3 - participants must have pathologically documented, definitively diagnosed advanced MTC that had progressed within 14 months prior to the Screening Visit and was previously treated with cabozantinib and/or vandetanib. * Group 4 - participants must have pathologically documented, definitively diagnosed advanced MTC that had progressed within 14 months prior to the Screening Visit and was not previously treated with cabozantinib and/or vandetanib. * Group 5 - participants must have a pathologically documented, definitively diagnosed advanced solid tumor with an oncogenic RET fusion, have previously received standard of care (SOC) appropriate for their tumor type (unless there is no accepted standard therapy for the tumor type or the Investigator has determined that treatment with standard therapy is not appropriate), and must not have been eligible for any of the other groups. * Group 6 - participants must have a pathologically documented, definitively diagnosed advanced solid tumor with an oncogenic RET fusion or mutation that was previously treated with a selective tyrosine kinase inhibitor (TKI) that inhibits RET * Group 7 - participants must have a pathologically documented, definitively diagnosed advanced solid tumor with an oncogenic RET mutation previously treated with SOC appropriate for the tumor type and not eligible for any of the other groups * Group 8 - participants must have pathologically documented, definitively diagnosed locally advanced or metastatic NSCLC with a RET fusion that was previously treated with a platinum based chemotherapy (China only). * Group 9 - participants must have pathologically documented, definitively diagnosed advanced MTC that had progressed within 14 months prior to the Screening Visit, and was not previously treated with systemic therapy (except prior cytotoxic chemotherapy is allowed) for advanced or metastatic disease (China only). * Participants must have non-resectable disease. * Dose expansion (Phase 2): Participants in all groups (except Group 7) must have measurable disease per RECIST v1.1 (or RANO, criteria if appropriate for tumor type). * Participants agrees to provide tumor tissue (archived, if available or a fresh biopsy) for RET status confirmation and is willing to consider an on-treatment tumor biopsy, if considered safe and medically feasible by the treating Investigator. For Phase 2, Group 6, participants are required to undergo a pretreatment biopsy to define baseline RET status in tumor tissue. * Participants has Eastern Cooperative Oncology Group (ECOG) performance status (PS) of 0-1. Key

Exclusion criteria

* Participant's cancer has a known primary driver alteration other than RET. For example, NSCLC with a targetable mutation in EGFR, ALK, ROS1 or BRAF; colorectal with an oncogenic KRAS, NRAS, or BRAF mutation. * Participants had any of the following within 14 days prior to the first dose of study drug: 1. Platelet count \< 75 × 10\^9/L. 2. Absolute neutrophil count \< 1.0 × 10\^9/L. 3. Hemoglobin \< 9.0 g/dL (red blood cell transfusion and erythropoietin may be used to reach at least 9.0 g/dL, but must have been administered at least 2 weeks prior to the first dose of study drug. 4. Aspartate aminotransferase (AST) or alanine aminotransferase (ALT) \> 3 × the upper limit of normal (ULN) if no hepatic metastases are present; \> 5 × ULN if hepatic metastases are present. 5. Total bilirubin \> 1.5 × ULN; \> 3 × ULN with direct bilirubin \> 1.5 × ULN in presence of Gilbert's disease. 6. Estimated (Cockcroft-Gault formula) or measured creatinine clearance \< 40 mL/min. 7. Total serum phosphorus \> 5.5 mg/dL * QT interval corrected using Fridericia's formula (QTcF) \> 470 msec or history of prolonged QT syndrome or Torsades de pointes, or familial history of prolonged QT syndrome. * Clinically significant, uncontrolled, cardiovascular disease. * Central nervous system (CNS) metastases or a primary CNS tumor that is associated with progressive neurological symptoms. * Clinically symptomatic interstitial lung disease or interstitial pneumonitis including radiation pneumonitis * Participants in Groups 1-5 and 7 (Phase 2) previously treated with a selective RET inhibitor * Participant had a major surgical procedure within 14 days of the first dose of study drug * Participant had a history of another primary malignancy that had been diagnosed or required therapy within the a year prior to the study * Pregnant or breastfeeding female participants

Design outcomes

Primary

MeasureTime frameDescription
Phase 1 : Maximum Tolerated Dose (MTD) and Recommended Phase 2 Dose (RP2D) of PralsetinibUp to approximately 30.8 monthsMTD was defined as the highest tolerated dose of pralsetinib without causing dose limiting toxicities (DLTs). DLT was defined as any Grade ≥3 adverse event (AE) occurring during Cycle 1 during Phase 1 (dose escalation) that is not clearly caused by something other than pralsetinib. RP2D was defined as the highest dose with acceptable toxicity as determined from dose-escalation phase.
Phase 1 and Phase 2: Number of Participants With AEs and Serious AEs (SAEs)From Cycle 1 Day 1 up to 30 days after the final dose of study drug (up to approximately 6.7 years)An AE was any untoward medical occurrence associated with the use of a drug in humans, whether or not considered drug related. An AE can be any unfavorable and unintended sign (e.g., an abnormal laboratory finding), symptom, or disease temporally associated with the use of a drug, without any judgment about causality. A SAE is any significant hazard, contraindication, side effect that is fatal or life-threatening, requires hospitalization or prolongation of existing hospitalization, results in persistent or significant disability/incapacity, is a congenital anomaly or birth defect, is medically significant or requires intervention to prevent one or other of the outcomes listed above.
Phase 2: Overall Response Rate (ORR)Up to approximately 79.8 monthsORR was defined as the percentage of participants with a confirmed complete response (CR) or partial response (PR) for at least two assessments with at least 28 days apart and no disease progression (PD) in between. Per Response Evaluation Criteria in Solid Tumors, Version 1.1 (RECIST v1.1), CR was defined as the disappearance of all target lesions or any pathological lymph nodes (whether target or non-target) having a reduction in the short axis to \<10 millimeters (mm). PR was defined as at least a 30% decrease in the sum of diameters (SOD) of all target lesions, taking as reference the baseline SOD, in the absence of CR. PD was defined as at least a 20% increase in SOD of target lesions, taking as reference the smallest SOD on study (including baseline). ORR and its two-sided 95% CI, based on the exact binomial distribution (Clopper-Pearson), were presented.

Secondary

MeasureTime frameDescription
Phase 1 and Phase 2: ORR in RET-fusion Positive TC Participants With Specific RET Gene StatusUp to approximately 79.8 monthsOncogenic RET activation has been implicated as a driver in both MTC and differentiated TC (DTC). These rearrangements typically produce chimeric transcripts that encode a fusion protein consisting of the RET kinase domain coupled to a protein with a dimerization domain (e.g., KIF5B, CCDC6, NCOA4). RET genotypes were determined by local testing and/or central analysis of ctDNA. ORR was assessed in participants having specific RET rearrangements. ORR was defined as the percentage of participants with a confirmed CR or PR for at least 2 assessments with at least 28 days apart and no PD in between. CR, PR, and PD were defined per RECIST as outlined in the description for OM 3.
Phase 1 and Phase 2: Clinical Benefit Rate (CBR) in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusUp to approximately 79.8 monthsOncogenic RET rearrangements have been identified in 1%-2% of NSCLC. These rearrangements typically produce chimeric transcripts that encode a fusion protein consisting of the RET kinase domain coupled to a protein with a dimerization domain (e.g., KIF5B, CCDC6, NCOA4). RET genotypes were determined by local testing and/or central analysis of ctDNA. CBR was assessed in participants having specific RET rearrangements. CBR was defined as the percentage of participants with a confirmed CR or PR, or stable disease (SD) which has been lasting at least 16 weeks (i.e. 4 cycles if 28 days are in one cycle) from the first dose date. CR and PR were defined per RECIST as outlined in the description for OM 3. SD was defined as neither sufficient shrinkage to qualify for CR or PR nor sufficient increase to qualify for PD. PD was defined as at least a 20% increase in SOD of target lesions, taking as reference the smallest SOD on study (including baseline).
Phase 1 and Phase 2: CBR in RET-mutation MTC Participants With Specific RET Gene StatusUp to approximately 79.8 monthsOncogenic RET activation has been implicated as a driver in MTC. These rearrangements typically produce chimeric transcripts that encode a fusion protein consisting of the RET kinase domain coupled to a protein with a dimerization domain (e.g., M918T, cysteine rich domain, V804X). RET genotypes were determined by local testing and/or central analysis of ctDNA. CBR was assessed in participants having specific RET rearrangements. CBR was defined as the percentage of participants with a confirmed CR or PR, or SD which has been lasting at least 16 weeks (i.e. 4 cycles if 28 days are in one cycle) from the first dose date. CR and PR were defined per RECIST as outlined in the description for OM 3. SD was defined as neither sufficient shrinkage to qualify for CR or PR nor sufficient increase to qualify for PD. PD was defined as at least a 20% increase in SOD of target lesions, taking as reference the smallest SOD on study (including baseline).
Phase 1 and Phase 2: CBR in RET-fusion Positive TC Participants With Specific RET Gene StatusUp to approximately 79.8 monthsOncogenic RET activation has been implicated as a driver in both MTC and DTC. These rearrangements typically produce chimeric transcripts that encode a fusion protein consisting of the RET kinase domain coupled to a protein with a dimerization domain (e.g., KIF5B, CCDC6, NCOA4). RET genotypes were determined by local testing and/or central analysis of ctDNA. CBR was assessed in participants having specific RET rearrangements. CBR was defined as the percentage of participants with a confirmed CR or PR or SD which has been lasting at least 16 weeks (i.e. 4 cycles if 28 days are in one cycle) from the first dose date. CR and PR were defined per RECIST as outlined in the description for OM 3. SD was defined as neither sufficient shrinkage to qualify for CR or PR nor sufficient increase to qualify for PD. PD was defined as at least a 20% increase in SOD of target lesions, taking as reference the smallest SOD on study (including baseline).
Phase 1 and Phase 2: Disease Control Rate (DCR) in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusUp to approximately 79.8 monthsOncogenic RET rearrangements have been identified in 1%-2% of NSCLC. These rearrangements typically produce chimeric transcripts that encode a fusion protein consisting of the RET kinase domain coupled to a protein with a dimerization domain (e.g., KIF5B, CCDC6, NCOA4). RET genotypes were determined by local testing and/or central analysis of ctDNA. DCR was assessed in participants having specific RET rearrangements. DCR was defined as the percentage of participants with a confirmed CR/PR, or SD. CR and PR were defined per RECIST as outlined in the description for OM 3. SD was defined as neither sufficient shrinkage to qualify for CR or PR nor sufficient increase to qualify for PD. PD was defined as at least a 20% increase in SOD of target lesions, taking as reference the smallest SOD on study (including baseline).
Phase 1 and Phase 2: DCR in RET-mutation MTC Participants With Specific RET Gene StatusUp to approximately 79.8 monthsOncogenic RET activation has been implicated as a driver in MTC. These rearrangements typically produce chimeric transcripts that encode a fusion protein consisting of the RET kinase domain coupled to a protein with a dimerization domain (e.g., M918T, cysteine rich domain, V804X). RET genotypes were determined by local testing and/or central analysis of ctDNA. DCR was assessed in participants having specific RET rearrangements. DCR was defined as the percentage of participants with a confirmed CR/PR, or SD. CR and PR were defined per RECIST as outlined in the description for OM 3. SD was defined as neither sufficient shrinkage to qualify for CR or PR nor sufficient increase to qualify for PD. PD was defined as at least a 20% increase in SOD of target lesions, taking as reference the smallest SOD on study (including baseline).
Phase 1 and Phase 2: DCR in RET-fusion Positive TC Participants With Specific RET Gene StatusUp to approximately 79.8 monthsOncogenic RET activation has been implicated as a driver in both MTC and DTC. These rearrangements typically produce chimeric transcripts that encode a fusion protein consisting of the RET kinase domain coupled to a protein with a dimerization domain (e.g., KIF5B, CCDC6, NCOA4). RET genotypes were determined by local testing and/or central analysis of ctDNA. DCR was assessed in participants having specific RET rearrangements. DCR was defined as the percentage of participants with a confirmed CR/PR, or SD. CR and PR were defined per RECIST as outlined in the description for OM 3. SD was defined as neither sufficient shrinkage to qualify for CR or PR nor sufficient increase to qualify for PD. PD was defined as at least a 20% increase in SOD of target lesions, taking as reference the smallest SOD on study (including baseline).
Phase 1 and Phase 2: Duration of Response (DOR) in RET-mutation NSCLC Participants With Specific RET Gene StatusUp to approximately 79.8 monthsOncogenic RET rearrangements have been identified in 1%-2% of NSCLC. These rearrangements typically produce chimeric transcripts that encode a fusion protein consisting of the RET kinase domain coupled to a protein with a dimerization domain (e.g., KIF5), CCDC6, NCOA4). RET genotypes were determined by local testing &/or central analysis of circulating tumor deoxyribonucleic acid (ctDNA). DOR was assessed in participants having specific RET rearrangements. DOR=time from first documented CR/PR to date of first documented PD or death due to any cause, whichever occurs first. Per RECIST, CR=disappearance of all target lesions or any pathological lymph nodes (target or non-target) having a reduction in the short axis to \<10 mm. PR=at least a 30% decrease in SOD of all target lesions, taking as reference the baseline SOD, in absence of CR. PD=as at least a 20% increase in SOD of target lesions, taking as reference smallest SOD on study. DOR was analyzed using the Kaplan-Meier (KM) method.
Phase 1 and Phase 2: DOR in RET-mutation MTC Participants With Specific RET Gene StatusUp to approximately 79.8 monthsOncogenic RET activation has been implicated as a driver in MTC. These rearrangements typically produce chimeric transcripts that encode a fusion protein consisting of the RET kinase domain coupled to a protein with a dimerization domain (e.g., M918T, cysteine rich domain, V804X). RET genotypes were determined by local testing and/or central analysis of ctDNA. DOR was assessed in participants having specific RET rearrangements. DOR=time from first documented CR/PR to date of first documented PD or death due to any cause, whichever occurs first. Per RECIST, CR= disappearance of all target lesions or any pathological lymph nodes (target or non-target) having a reduction in the short axis to \<10 mm. PR=at least a 30% decrease in the SOD of all target lesions, taking as reference the baseline SOD, in absence of CR. PD=as at least a 20% increase in SOD of target lesions, taking as reference smallest SOD on study (including baseline). DOR was analyzed using the Kaplan-Meier (KM) method.
Phase 1 and Phase 2: DOR in RET-fusion Positive TC Participants With Specific RET Gene StatusUp to approximately 79.8 monthsOncogenic RET activation has been implicated as a driver in MTC. These rearrangements typically produce chimeric transcripts that encode a fusion protein consisting of the RET kinase domain coupled to a protein with a dimerization domain (e.g., KIF5B, CCDC6, NCOA4). RET genotypes were determined by local testing and/or central analysis of ctDNA. DOR was assessed in participants having specific RET rearrangements. DOR=time from first documented CR/PR to date of first documented PD or death due to any cause, whichever occurs first. Per RECIST, CR= disappearance of all target lesions or any pathological lymph nodes (target or non-target) having a reduction in the short axis to \<10 mm. PR=at least a 30% decrease in the SOD of all target lesions, taking as reference the baseline SOD, in absence of CR. PD=as at least a 20% increase in SOD of target lesions, taking as reference smallest SOD on study (including baseline). DOR was analyzed using the KM method.
Phase 2: DORUp to approximately 79.8 monthsDOR was defined as the time from first documented response (CR/PR) to the date of first documented PD or death due to any cause, whichever occurs first. CR was defined as the disappearance of all target lesions or any pathological lymph nodes (whether target or non-target) having a reduction in the short axis to \<10 mm. PR was defined as at least a 30% decrease in the SOD of all target lesions, taking as reference the baseline SOD, in the absence of CR. PD was defined as at least a 20% increase in SOD of target lesions, taking as reference the smallest SOD on study (including baseline). DOR was analyzed using the KM methods.
Phase 2: CBRUp to approximately 79.8 monthsCBR was defined as the percentage of participants with CR or PR, or SD which has been lasting at least 16 weeks (i.e. 4 cycles if 28 days are in one cycle) from the first dose date. CR was defined as the disappearance of all target lesions or any pathological lymph nodes (whether target or non-target) having a reduction in the short axis to \<10 mm. PR was defined as at least a 30% decrease in the SOD of all target lesions, taking as reference the baseline SOD, in the absence of CR. SD was defined as neither sufficient shrinkage to qualify for CR or PR nor sufficient increase to qualify for PD. PD was defined as at least a 20% increase in SOD of target lesions, taking as reference the smallest SOD on study (including baseline). CBR and its two-sided 95% CI, which is based on the exact binomial distribution (Clopper-Pearson), were presented.
Phase 2: DCRUp to approximately 79.8 monthsDCR was defined as the percentage of participants with a confirmed CR/PR, or SD, per RECIST v1.1. CR was defined as the disappearance of all target lesions or any pathological lymph nodes (whether target or non-target) having a reduction in the short axis to \<10 mm. PR was defined as at least a 30% decrease in the SOD of all target lesions, taking as reference the baseline SOD, in the absence of CR. SD was defined as neither sufficient shrinkage to qualify for CR or PR nor sufficient increase to qualify for PD. PD was defined as at least a 20% increase in SOD of target lesions, taking as reference the smallest SOD on study (including baseline). DCR and its two-sided 95% CI, which is based on the exact binomial distribution (Clopper-Pearson), were presented.
Phase 2: Progression-free Survival (PFS)Up to approximately 7 yearsPFS was defined as the time from the first dose of pralsetinib to the date of first documented PD or death due to any cause, whichever occurred first. PD was defined as at least a 20% increase in SOD of target lesions, taking as reference the smallest SOD on study (including baseline). PFS was analyzed using KM methods.
Phase 2: Overall Survival (OS)Up to approximately 7 yearsOS was defined as the time from the first dose of pralsetinib to the date of death due to any causes.
Phase 2: Intracranial ORR in RET-fusion Positive NSCLC Central Nervous System (CNS) Metastases ParticipantsUp to approximately 79.8 monthsORR=percentage of participants with CR or PR for at least 2 assessments with at least 28 days apart & no PD in between. CR=disappearance of all target CNS/brain lesion, including lesions in brain stem &/or cerebellum identified at baseline & disappearance of all non-target CNS/brain lesion at baseline & no identification of new CNS/brain lesion. PR =at least a 30% decrease in the SOD of any CNS/brain lesion, identified as RECIST 1.1 target lesions at baseline & if in the absence of unequivocal progression of any non-target CNS/brain lesion at baseline, or the identification of new CNS/brain lesion. PD=either at least 20% increase in the SOD of target CNS/brain lesion, taking as reference the smallest sum on study. In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of at least 5mm or unequivocal progression of any CNS/brain lesion identified as RECIST 1.1 nontarget lesions at baseline, or the identification of new CNS/brain lesion.
Phase 1: Time to Maximum Plasma Concentration (Tmax)Predose on 0.5, 1, 2, 4, 6, 8 and 24 hours postdose on Days 1 and 15 of Cycle 1 (1 cycle = 28 days)Number of participants in each arm of this OM is based on the actual treatment received. 1 participant originally assigned to the 200/100 mg arm received the 100/100 mg treatment and hence, was counted under the 100/100 mg arm for this OM.
Phase 2: Intracranial DOR in RET-fusion Positive NSCLC CNS Metastases ParticipantsUp to approximately 79.8 monthsDOR=time from first documented CR/PR to the date of first documented PD/death due to any cause, whichever occurs first. CR=disappearance of all target CNS/brain lesion, including lesions in brain stem &/ cerebellum identified at baseline & disappearance of all non-target CNS/brain lesion at baseline & no identification of new CNS/brain lesion. PR=at least a 30% decrease in SOD of any CNS/brain lesion, identified as RECIST 1.1 target lesions at baseline & if in absence of unequivocal progression of any non-target CNS/brain lesion at baseline, or identification of new CNS/brain lesion. PD=either at least 20% increase in SOD of target CNS/brain lesion, taking as reference smallest sum on study. Unequivocal progression of any CNS/brain lesion nontarget lesions at baseline, or identification of new CNS/brain lesion. DOR was analyzed using the KM methods.
Phase 2: Intracranial CBR in RET-fusion Positive NSCLC CNS Metastases ParticipantsUp to approximately 79.8 monthsCBR=percentage of participants with CR/PR/SD which has been lasting at least 16 weeks (i.e. 4 cycles if 28 days are in 1 cycle) from first dose date. CR=disappearance of all target CNS/brain lesion, including lesions in brain stem &/ cerebellum identified at baseline&disappearance of all non-target CNS/brain lesion at baseline & no identification of new CNS/brain lesion. PR=at least a 30% decrease in SOD of any CNS/brain lesion, identified as target lesions at baseline & if in absence of unequivocal progression of any non-target CNS/brain lesion at baseline, or identification of new CNS/brain lesion. SD=neither sufficient shrinkage for PR nor sufficient increase for PD for target/non-target CNS/brain lesion, taking as reference smallest SOD while on study. PD=either at least 20% increase in SOD of target CNS/brain lesion, taking as reference smallest sum on study. Unequivocal progression of any CNS/brain lesion nontarget lesions at baseline, or identification of new CNS/brain lesion.
Phase 2: Intracranial DCR in RET-fusion Positive NSCLC CNS Metastases ParticipantsUp to approximately 79.8 monthsDCR=percentage of participants with a confirmed CR/PR, or SD. CR=disappearance of all target CNS/brain lesion, including lesions in brain stem &/or cerebellum identified at baseline & disappearance of all non-target CNS/brain lesion at baseline & no identification of new CNS/brain lesion. PR =at least a 30% decrease in the SOD of any CNS/brain lesion, identified as RECIST 1.1 target lesions at baseline & if in the absence of unequivocal progression of any non-target CNS/brain lesion at baseline, or the identification of new CNS/brain lesion. SD=neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD for target/non-target CNS/brain lesion, taking as reference the smallest SOD while on study. PD=either at least 20% increase in SOD of target CNS/brain lesion, taking as reference smallest sum on study. Unequivocal progression of any CNS/brain lesion nontarget lesions at baseline, or identification of new CNS/brain lesion.
Phase 1: Maximum Plasma Concentration (Cmax)Predose on 0.5, 1, 2, 4, 6, 8 and 24 hours postdose on Days 1 and 15 of Cycle 1 (1 cycle = 28 days)Number of participants in each arm of this OM is based on the actual treatment received. 1 participant originally assigned to the 200/100 mg arm received the 100/100 mg treatment and hence, was counted under the 100/100 mg arm for this OM.
Phase 1: Time of Last Quantifiable Plasma Drug Concentration (Tlast)Predose on 0.5, 1, 2, 4, 6, 8 and 24 hours postdose on Days 1 and 15 of Cycle 1 (1 cycle = 28 days)The maximum values for Tlast slightly exceed 24 hours because the analysis used the actual time, i.e., the duration between dosing and actual sample collection, rather than the nominal sampling time of 24 hours specified in the protocol. The timeframe has been given as per nominal sampling timepoints pre-specified in the protocol. Number of participants in each arm of this OM is based on the actual treatment received. 1 participant originally assigned to the 200/100 mg arm received the 100/100 mg treatment and hence, was counted under the 100/100 mg arm for this OM.
Phase 1: Area Under the Plasma Concentration Versus Time Curve From Time 0 to 24 Hours Postdose (AUC0-24)24 hours postdose on Day 1 of Cycle 1 (1 cycle = 28 days)Number of participants in each arm of this OM is based on the actual treatment received. 1 participant originally assigned to the 200/100 mg arm received the 100/100 mg treatment and hence, was counted under the 100/100 mg arm for this OM.
Phase 1: Plasma Drug Concentration at 24 Hours Postdose (C24hr)24 hours postdose on Days 1 and 15 of Cycle 1 (1 cycle = 28 days)Number of participants in each arm of this OM is based on the actual treatment received. 1 participant originally assigned to the 200/100 mg arm received the 100/100 mg treatment and hence, was counted under the 100/100 mg arm for this OM.
Phase 1: Apparent Volume of Distribution (Vz/F)Predose on 0.5, 1, 2, 4, 6, 8 and 24 hours postdose on Days 1 and 15 of Cycle 1 (1 cycle = 28 days)Number of participants in each arm of this OM is based on the actual treatment received. 1 participant originally assigned to the 200/100 mg arm received the 100/100 mg treatment and hence, was counted under the 100/100 mg arm for this OM.
Phase 1: Terminal Elimination Half-Life (t½)Predose on 0.5, 1, 2, 4, 6, 8 and 24 hours postdose on Days 1 and 15 of Cycle 1 (1 cycle = 28 days)The maximum values for t1/2 slightly exceed 24 hours because the analysis used the actual time, i.e., the duration between dosing and actual sample collection, rather than the nominal sampling time of 24 hours specified in the protocol. The timeframe has been given as per nominal sampling timepoints pre-specified in the protocol. Number of participants in each arm of this OM is based on the actual treatment received. 1 participant originally assigned to the 200/100 mg arm received the 100/100 mg treatment and hence, was counted under the 100/100 mg arm for this OM.
Phase 1: Apparent Oral Clearance (CL/F)Predose on 0.5, 1, 2, 4, 6, 8 and 24 hours postdose on Days 1 and 15 of Cycle 1 (1 cycle = 28 days)Number of participants in each arm of this OM is based on the actual treatment received. 1 participant originally assigned to the 200/100 mg arm received the 100/100 mg treatment and hence, was counted under the 100/100 mg arm for this OM.
Phase 1: Accumulation Ratio for Cmax (RCmax)24 hours postdose on Day 15 of Cycle 1 (1 cycle = 28 days)Number of participants in each arm of this OM is based on the actual treatment received. 1 participant originally assigned to the 200/100 mg arm received the 100/100 mg treatment and hence, was counted under the 100/100 mg arm for this OM.
Phase 1: Accumulation Ratio for AUC (RAUC)24 hours postdose on Day 15 of Cycle 1 (1 cycle = 28 days)Number of participants in each arm of this OM is based on the actual treatment received. 1 participant originally assigned to the 200/100 mg arm received the 100/100 mg treatment and hence, was counted under the 100/100 mg arm for this OM.
Phase 2: CmaxPredose on 0.5, 1, 2, 4, 6, 8 and 24 hours postdose on Days 1 and 15 of Cycle 1 (1 cycle = 28 days)
Phase 2: TmaxPredose on 0.5, 1, 2, 4, 6, 8 and 24 hours postdose on Days 1 and 15 of Cycle 1 (1 cycle = 28 days)
Phase 2: TlastPredose on 0.5, 1, 2, 4, 6, 8 and 24 hours postdose on Days 1 and 15 of Cycle 1 (1 cycle = 28 days)The maximum values for Tlast slightly exceed 24 hours because the analysis used the actual time, i.e., the duration between dosing and actual sample collection, rather than the nominal sampling time of 24 hours specified in the protocol. The timeframe has been given as per nominal sampling timepoints pre-specified in the protocol.
Phase 2: AUC0-2424 hours postdose on Days 1 and 15 of Cycle 1 (1 cycle = 28 days)
Phase 2: C24hr24 hours postdose on Days 1 and 15 of Cycle 1 (1 cycle = 28 days)
Phase 2: t½Predose on 0.5, 1, 2, 4, 6, 8 and 24 hours postdose on Days 1 and 15 of Cycle 1 (1 cycle = 28 days)The maximum values for t1/2 slightly exceed 24 hours because the analysis used the actual time, i.e., the duration between dosing and actual sample collection, rather than the nominal sampling time of 24 hours specified in the protocol. The timeframe has been given as per nominal sampling timepoints pre-specified in the protocol.
Phase 1: ORRUp to approximately 28 monthsORR was defined as the percentage of participants with a confirmed CR or PR for at least two assessments with at least 28 days apart and no PD in between. Per RECIST v1.1, CR was defined as the disappearance of all target lesions or any pathological lymph nodes (whether target or non-target) having a reduction in the short axis to \<10 mm. PR was defined as at least a 30% decrease in the SOD of all target lesions, taking as reference the baseline SOD, in the absence of CR. PD was defined as at least a 20% increase in SOD of target lesions, taking as reference the smallest SOD on study (including baseline). ORR and its two-sided 95% CI, based on the exact binomial distribution (Clopper-Pearson), was presented.
Phase 1: Percent Change From Baseline in Dual Specificity Phosphatase 6 (DUSP6)Baseline, Week 4The dose dependent change in a mitogen-activated protein kinases (MAPK) pathway expression signature was analyzed for all available samples of MTC and NSCLC participants. Participants with archived sample (used as baseline) and on treatment Cycle 2 Day 1 (1 cycle = 28 days) tumor tissues with greater than 20% tumor cells are included in the analysis. The changes in tumor biomarker DUSP6 levels was explored.
Phase 1: Percent Change From Baseline in Sprout Receptor Tyrosine Kinase Signaling Antagonist 4 (SPRY4)Baseline, Week 4The dose dependent change in a MAPK pathway expression signature was analyzed for all available samples of MTC and NSCLC participants. Participants with archived sample (used as baseline) and on treatment Cycle 2 Day 1 (1 cycle = 28 days) tumor tissues with greater than 20% tumor cells are included in the analysis. The changes in tumor biomarker SPRY4 levels was explored.
Phase 2: CL/FPredose on 0.5, 1, 2, 4, 6, 8 and 24 hours postdose on Days 1 and 15 of Cycle 1 (1 cycle = 28 days)
Phase 1 and Phase 2: ORR in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusUp to approximately 79.8 monthsOncogenic RET rearrangements have been identified in 1%-2% of NSCLC. These rearrangements typically produce chimeric transcripts that encode a fusion protein consisting of the RET kinase domain coupled to a protein with a dimerization domain (e.g., Kinesin family member 5B (KIF5B), coiled-coil domain containing 6 (CCDC6), nuclear receptor coactivator 4 (NCOA4)). RET genotypes were determined by local testing and/or central analysis of circulating tumor deoxyribonucleic acid (ctDNA). ORR was assessed in participants having specific RET rearrangements. ORR was defined as the percentage of participants with a confirmed CR or PR for at least 2 assessments with at least 28 days apart and no PD in between. CR, PR, and PD were defined per RECIST as outlined in the description for OM 3.
Phase 1 and Phase 2: ORR in RET-mutation MTC Participants With Specific RET Gene StatusUp to approximately 79.8 monthsOncogenic RET activation has been implicated as a driver in MTC. These rearrangements typically produce chimeric transcripts that encode a fusion protein consisting of the RET kinase domain coupled to a protein with a dimerization domain (e.g., M918T, cysteine rich domain, V804X). RET genotypes were determined by local testing and/or central analysis of ctDNA. ORR was assessed in participants having specific RET rearrangements. ORR was defined as the percentage of participants with a confirmed CR or PR for at least 2 assessments with at least 28 days apart and no PD in between. CR, PR, and PD were defined per RECIST as outlined in the description for OM 3.

Countries

Belgium, China, France, Germany, Hong Kong, Italy, Netherlands, Singapore, South Korea, Spain, Taiwan, United Kingdom, United States

Participant flow

Recruitment details

A total of 590 participants with rearranged during transfection (RET) fusion-positive non-small cell lung cancer (NSCLC), RET mutation-positive medullary thyroid cancer (also known as RET-mutant MTC), RET fusion-positive thyroid cancer (TC) and other advanced solid tumors took part in the study at 74 investigative sites across 13 countries from 17 March 2017 to 21 March 2024. The study was divided into two parts: Phase 1 (Dose Escalation) and Phase 2 (Dose Expansion).

Pre-assignment details

For Phase I, The number of participants in each arm within the participant flow reflects the arms they were originally assigned to, whereas numbers reported in the pharmacokinetics outcome measure (OM) represent the number based on actual treatment received by the participants. 1 participant assigned to the 200/100 mg arm received the 100/100 mg treatment. Hence, was counted under the 100/100 mg arm in the PK-evaluable population.

Participants by arm

ArmCount
Phase I: Pralsetinib 30 mg
Participants received pralsetinib 30 milligrams (mg) orally, QD until discontinuation due to toxicity, disease progression, or other reasons.
2
Phase I: Pralsetinib 60 mg
Participants received pralsetinib 60 mg orally, QD until discontinuation due to toxicity, disease progression, or other reasons.
6
Phase I: Pralsetinib 100 mg
Participants received pralsetinib 100 mg orally, QD until discontinuation due to toxicity, disease progression, or other reasons.
5
Phase I: Pralsetinib 200 mg
Participants received pralsetinib 200 mg orally, QD until discontinuation due to toxicity, disease progression, or other reasons.
13
Phase I: Pralsetinib 300 mg
Participants received pralsetinib 300 mg, orally, QD until discontinuation due to toxicity, disease progression, or other reasons.
11
Phase I: Pralsetinib 400 mg
Participants received pralsetinib 400 mg orally, QD until discontinuation due to toxicity, disease progression, or other reasons.
12
Phase I: Pralsetinib 600 mg
Participants received pralsetinib 600 mg orally, QD until discontinuation due to toxicity, disease progression, or other reasons.
4
Phase I: Pralsetinib 100/100 mg
Participants received pralsetinib 100 mg, orally, twice a day (BID) until discontinuation due to toxicity, disease progression, or other reasons.
5
Phase I: Pralsetinib 200/100 mg
Participants received pralsetinib 200 mg in the morning and then 100 mg in the evening orally until discontinuation due to toxicity, disease progression, or other reasons.
4
Phase II: Pralsetinib 400 mg
Participants with advanced NSCLC, advanced non-resectable TC and other advanced non-resectable solid tumors with various rearranged during transfection (RET)-alterations were enrolled in this arm to receive pralsetinib, 400 mg, QD until discontinuation due to toxicity, disease progression, or other reasons.
528
Total590

Withdrawals & dropouts

PeriodReasonFG000FG001FG002FG003FG004FG005FG006FG007FG008FG009
Overall StudyAdverse Event0010000006
Overall StudyDeath142252143240
Overall StudyInitiation of Another Therapy1000000102
Overall StudyLost to Follow-up00000100016
Overall StudyPhysician Decision0000000001
Overall StudyProgressive Disease01152010030
Overall StudyReason Not Specified010436201181
Overall StudyWithdrawal by Subject00121300052

Baseline characteristics

CharacteristicPhase I: Pralsetinib 30 mgPhase I: Pralsetinib 60 mgPhase I: Pralsetinib 100 mgPhase I: Pralsetinib 200 mgPhase I: Pralsetinib 300 mgPhase I: Pralsetinib 400 mgPhase I: Pralsetinib 600 mgPhase I: Pralsetinib 100/100 mgPhase I: Pralsetinib 200/100 mgPhase II: Pralsetinib 400 mgTotal
Age, Continuous54.5 years
STANDARD_DEVIATION 9.2
49.5 years
STANDARD_DEVIATION 18
51.2 years
STANDARD_DEVIATION 13.2
53.8 years
STANDARD_DEVIATION 13.6
60.6 years
STANDARD_DEVIATION 11
49.2 years
STANDARD_DEVIATION 17.8
59.5 years
STANDARD_DEVIATION 9.1
63.0 years
STANDARD_DEVIATION 11.09
61.8 years
STANDARD_DEVIATION 18.25
57.7 years
STANDARD_DEVIATION 12.6
57.5 years
STANDARD_DEVIATION 12.8
Ethnicity (NIH/OMB)
Hispanic or Latino
2 Participants2 Participants1 Participants1 Participants0 Participants3 Participants0 Participants0 Participants0 Participants19 Participants28 Participants
Ethnicity (NIH/OMB)
Not Hispanic or Latino
0 Participants4 Participants4 Participants12 Participants11 Participants9 Participants4 Participants3 Participants4 Participants465 Participants516 Participants
Ethnicity (NIH/OMB)
Unknown or Not Reported
0 Participants0 Participants0 Participants0 Participants0 Participants0 Participants0 Participants2 Participants0 Participants44 Participants46 Participants
Race/Ethnicity, Customized
Asian
0 Participants1 Participants2 Participants0 Participants0 Participants2 Participants0 Participants1 Participants0 Participants203 Participants209 Participants
Race/Ethnicity, Customized
Black or African American
0 Participants0 Participants0 Participants1 Participants0 Participants1 Participants0 Participants0 Participants0 Participants4 Participants6 Participants
Race/Ethnicity, Customized
Native Hawaiian or Other Pacific Islander
0 Participants0 Participants0 Participants0 Participants0 Participants0 Participants0 Participants0 Participants0 Participants2 Participants2 Participants
Race/Ethnicity, Customized
Other
0 Participants0 Participants0 Participants0 Participants0 Participants0 Participants0 Participants0 Participants0 Participants3 Participants3 Participants
Race/Ethnicity, Customized
Unknown or Not Reported
2 Participants2 Participants1 Participants1 Participants0 Participants0 Participants0 Participants1 Participants0 Participants32 Participants39 Participants
Race/Ethnicity, Customized
White
0 Participants3 Participants2 Participants11 Participants11 Participants9 Participants4 Participants3 Participants4 Participants284 Participants331 Participants
Sex: Female, Male
Female
1 Participants3 Participants4 Participants5 Participants4 Participants3 Participants3 Participants1 Participants2 Participants257 Participants283 Participants
Sex: Female, Male
Male
1 Participants3 Participants1 Participants8 Participants7 Participants9 Participants1 Participants4 Participants2 Participants271 Participants307 Participants

Adverse events

Event typeEG000
affected / at risk
EG001
affected / at risk
EG002
affected / at risk
EG003
affected / at risk
deaths
Total, all-cause mortality
15 / 37245 / 5407 / 9268 / 590
other
Total, other adverse events
36 / 37536 / 5409 / 9585 / 590
serious
Total, serious adverse events
26 / 37381 / 5407 / 9416 / 590

Outcome results

Primary

Phase 1 and Phase 2: Number of Participants With AEs and Serious AEs (SAEs)

An AE was any untoward medical occurrence associated with the use of a drug in humans, whether or not considered drug related. An AE can be any unfavorable and unintended sign (e.g., an abnormal laboratory finding), symptom, or disease temporally associated with the use of a drug, without any judgment about causality. A SAE is any significant hazard, contraindication, side effect that is fatal or life-threatening, requires hospitalization or prolongation of existing hospitalization, results in persistent or significant disability/incapacity, is a congenital anomaly or birth defect, is medically significant or requires intervention to prevent one or other of the outcomes listed above.

Time frame: From Cycle 1 Day 1 up to 30 days after the final dose of study drug (up to approximately 6.7 years)

Population: Safety Population included all participants who have received at least 1 dose of the study drug regardless of starting dose levels. As pre-specified in the SAP, safety data was to be analyzed and reported as per the pre-planned grouped dose level II (SAP section 3.6.5.2). Hence, per dose safety data is not presented for this study.

ArmMeasureGroupValue (NUMBER)
Phase 1: All Participants QDPhase 1 and Phase 2: Number of Participants With AEs and Serious AEs (SAEs)AEs37 percentage of participants
Phase 1: All Participants QDPhase 1 and Phase 2: Number of Participants With AEs and Serious AEs (SAEs)SAEs26 percentage of participants
Pralsetinib 400 mg QDPhase 1 and Phase 2: Number of Participants With AEs and Serious AEs (SAEs)SAEs381 percentage of participants
Pralsetinib 400 mg QDPhase 1 and Phase 2: Number of Participants With AEs and Serious AEs (SAEs)AEs540 percentage of participants
Pralsetinib BID Dosing SchedulePhase 1 and Phase 2: Number of Participants With AEs and Serious AEs (SAEs)AEs9 percentage of participants
Pralsetinib BID Dosing SchedulePhase 1 and Phase 2: Number of Participants With AEs and Serious AEs (SAEs)SAEs7 percentage of participants
Pralsetinib All DosesPhase 1 and Phase 2: Number of Participants With AEs and Serious AEs (SAEs)AEs590 percentage of participants
Pralsetinib All DosesPhase 1 and Phase 2: Number of Participants With AEs and Serious AEs (SAEs)SAEs416 percentage of participants
Primary

Phase 1 : Maximum Tolerated Dose (MTD) and Recommended Phase 2 Dose (RP2D) of Pralsetinib

MTD was defined as the highest tolerated dose of pralsetinib without causing dose limiting toxicities (DLTs). DLT was defined as any Grade ≥3 adverse event (AE) occurring during Cycle 1 during Phase 1 (dose escalation) that is not clearly caused by something other than pralsetinib. RP2D was defined as the highest dose with acceptable toxicity as determined from dose-escalation phase.

Time frame: Up to approximately 30.8 months

Population: Dose-determining population included all participants in the dose-escalation part who have received ≥75% (21 days) of the study drug and completed safety evaluations through Cycle 1 Day 28 or experienced a DLT.

ArmMeasureGroupValue (NUMBER)
Phase 1: All Participants QDPhase 1 : Maximum Tolerated Dose (MTD) and Recommended Phase 2 Dose (RP2D) of PralsetinibMTD400 mg
Phase 1: All Participants QDPhase 1 : Maximum Tolerated Dose (MTD) and Recommended Phase 2 Dose (RP2D) of PralsetinibRP2D400 mg
Primary

Phase 2: Overall Response Rate (ORR)

ORR was defined as the percentage of participants with a confirmed complete response (CR) or partial response (PR) for at least two assessments with at least 28 days apart and no disease progression (PD) in between. Per Response Evaluation Criteria in Solid Tumors, Version 1.1 (RECIST v1.1), CR was defined as the disappearance of all target lesions or any pathological lymph nodes (whether target or non-target) having a reduction in the short axis to \<10 millimeters (mm). PR was defined as at least a 30% decrease in the sum of diameters (SOD) of all target lesions, taking as reference the baseline SOD, in the absence of CR. PD was defined as at least a 20% increase in SOD of target lesions, taking as reference the smallest SOD on study (including baseline). ORR and its two-sided 95% CI, based on the exact binomial distribution (Clopper-Pearson), were presented.

Time frame: Up to approximately 79.8 months

Population: RET-altered measurable disease population included participants in the efficacy population who had measurable (target) disease per RECIST v1.1 at baseline according to blinded central review (BICR) and sufficient evidence of a RET alteration. As prespecified in the SAP, Phase 1 participants treated at 400 mg QD are also included in Phase 2 efficacy analysis.

ArmMeasureValue (NUMBER)
Phase 1: All Participants QDPhase 2: Overall Response Rate (ORR)63.1 percentage of participants
Pralsetinib 400 mg QDPhase 2: Overall Response Rate (ORR)73.9 percentage of participants
Pralsetinib BID Dosing SchedulePhase 2: Overall Response Rate (ORR)78.3 percentage of participants
Pralsetinib All DosesPhase 2: Overall Response Rate (ORR)56.7 percentage of participants
RET-mutation MTC With No Prior Cabozantinib or Vandetanib TreatmentPhase 2: Overall Response Rate (ORR)77.8 percentage of participants
RET-fusion Positive TCPhase 2: Overall Response Rate (ORR)85.2 percentage of participants
RET-fusion Positive Solid Tumors Other Than NSCLC and TCPhase 2: Overall Response Rate (ORR)46.4 percentage of participants
RET-altered Solid Tumors Previously Treated With RET InhibitorPhase 2: Overall Response Rate (ORR)19.0 percentage of participants
RET-mutation Positive Tumors Other Than MTCPhase 2: Overall Response Rate (ORR)7.7 percentage of participants
Secondary

Phase 1: Accumulation Ratio for AUC (RAUC)

Number of participants in each arm of this OM is based on the actual treatment received. 1 participant originally assigned to the 200/100 mg arm received the 100/100 mg treatment and hence, was counted under the 100/100 mg arm for this OM.

Time frame: 24 hours postdose on Day 15 of Cycle 1 (1 cycle = 28 days)

Population: PK evaluable population included all participants who received at least one dose of pralsetinib and from whom at least one post dose PK sample was collected. Overall number analyzed is the number of participants with data available for analysis.

ArmMeasureValue (GEOMETRIC_MEAN)Dispersion
Phase 1: All Participants QDPhase 1: Accumulation Ratio for AUC (RAUC)1.43 ratio
Pralsetinib 400 mg QDPhase 1: Accumulation Ratio for AUC (RAUC)1.47 ratioGeometric Coefficient of Variation 11.1
Pralsetinib BID Dosing SchedulePhase 1: Accumulation Ratio for AUC (RAUC)3.22 ratio
Pralsetinib All DosesPhase 1: Accumulation Ratio for AUC (RAUC)1.31 ratioGeometric Coefficient of Variation 147
RET-mutation MTC With No Prior Cabozantinib or Vandetanib TreatmentPhase 1: Accumulation Ratio for AUC (RAUC)2.33 ratioGeometric Coefficient of Variation 11.4
RET-fusion Positive TCPhase 1: Accumulation Ratio for AUC (RAUC)2.75 ratioGeometric Coefficient of Variation 70.9
RET-fusion Positive Solid Tumors Other Than NSCLC and TCPhase 1: Accumulation Ratio for AUC (RAUC)2.48 ratio
RET-altered Solid Tumors Previously Treated With RET InhibitorPhase 1: Accumulation Ratio for AUC (RAUC)4.28 ratio
RET-mutation Positive Tumors Other Than MTCPhase 1: Accumulation Ratio for AUC (RAUC)1.21 ratio
Secondary

Phase 1: Accumulation Ratio for Cmax (RCmax)

Number of participants in each arm of this OM is based on the actual treatment received. 1 participant originally assigned to the 200/100 mg arm received the 100/100 mg treatment and hence, was counted under the 100/100 mg arm for this OM.

Time frame: 24 hours postdose on Day 15 of Cycle 1 (1 cycle = 28 days)

Population: PK evaluable population included all participants who received at least one dose of pralsetinib and from whom at least one post dose PK sample was collected. Overall number analyzed is the number of participants with data available for analysis.

ArmMeasureValue (GEOMETRIC_MEAN)Dispersion
Phase 1: All Participants QDPhase 1: Accumulation Ratio for Cmax (RCmax)1.04 ratio
Pralsetinib 400 mg QDPhase 1: Accumulation Ratio for Cmax (RCmax)1.25 ratioGeometric Coefficient of Variation 27.6
Pralsetinib BID Dosing SchedulePhase 1: Accumulation Ratio for Cmax (RCmax)3.20 ratioGeometric Coefficient of Variation 114
Pralsetinib All DosesPhase 1: Accumulation Ratio for Cmax (RCmax)1.17 ratioGeometric Coefficient of Variation 110
RET-mutation MTC With No Prior Cabozantinib or Vandetanib TreatmentPhase 1: Accumulation Ratio for Cmax (RCmax)1.87 ratioGeometric Coefficient of Variation 40.5
RET-fusion Positive TCPhase 1: Accumulation Ratio for Cmax (RCmax)1.62 ratioGeometric Coefficient of Variation 102
RET-fusion Positive Solid Tumors Other Than NSCLC and TCPhase 1: Accumulation Ratio for Cmax (RCmax)2.97 ratio
RET-altered Solid Tumors Previously Treated With RET InhibitorPhase 1: Accumulation Ratio for Cmax (RCmax)1.91 ratioGeometric Coefficient of Variation 40.7
RET-mutation Positive Tumors Other Than MTCPhase 1: Accumulation Ratio for Cmax (RCmax)1.41 ratio
Secondary

Phase 1 and Phase 2: CBR in RET-fusion Positive TC Participants With Specific RET Gene Status

Oncogenic RET activation has been implicated as a driver in both MTC and DTC. These rearrangements typically produce chimeric transcripts that encode a fusion protein consisting of the RET kinase domain coupled to a protein with a dimerization domain (e.g., KIF5B, CCDC6, NCOA4). RET genotypes were determined by local testing and/or central analysis of ctDNA. CBR was assessed in participants having specific RET rearrangements. CBR was defined as the percentage of participants with a confirmed CR or PR or SD which has been lasting at least 16 weeks (i.e. 4 cycles if 28 days are in one cycle) from the first dose date. CR and PR were defined per RECIST as outlined in the description for OM 3. SD was defined as neither sufficient shrinkage to qualify for CR or PR nor sufficient increase to qualify for PD. PD was defined as at least a 20% increase in SOD of target lesions, taking as reference the smallest SOD on study (including baseline).

Time frame: Up to approximately 79.8 months

Population: RET-altered measurable disease population included participants in the efficacy population who have measurable (target) disease per RECIST v1.1, at baseline according to BICR and sufficient evidence of a RET alteration. As prespecified in the SAP, Phase 1 participants treated at 400 mg QD are pooled with Phase 2 participants for efficacy analysis. Number analyzed is the number of participants with the specified mutation.

ArmMeasureGroupValue (NUMBER)
Phase 1: All Participants QDPhase 1 and Phase 2: CBR in RET-fusion Positive TC Participants With Specific RET Gene StatusCCDC682.4 percentage of participants
Phase 1: All Participants QDPhase 1 and Phase 2: CBR in RET-fusion Positive TC Participants With Specific RET Gene StatusNCOA4100 percentage of participants
Phase 1: All Participants QDPhase 1 and Phase 2: CBR in RET-fusion Positive TC Participants With Specific RET Gene StatusOther75.0 percentage of participants
UnknownPhase 1 and Phase 2: CBR in RET-fusion Positive TC Participants With Specific RET Gene StatusKIF5B percentage of participants
Secondary

Phase 1 and Phase 2: CBR in RET-mutation MTC Participants With Specific RET Gene Status

Oncogenic RET activation has been implicated as a driver in MTC. These rearrangements typically produce chimeric transcripts that encode a fusion protein consisting of the RET kinase domain coupled to a protein with a dimerization domain (e.g., M918T, cysteine rich domain, V804X). RET genotypes were determined by local testing and/or central analysis of ctDNA. CBR was assessed in participants having specific RET rearrangements. CBR was defined as the percentage of participants with a confirmed CR or PR, or SD which has been lasting at least 16 weeks (i.e. 4 cycles if 28 days are in one cycle) from the first dose date. CR and PR were defined per RECIST as outlined in the description for OM 3. SD was defined as neither sufficient shrinkage to qualify for CR or PR nor sufficient increase to qualify for PD. PD was defined as at least a 20% increase in SOD of target lesions, taking as reference the smallest SOD on study (including baseline).

Time frame: Up to approximately 79.8 months

Population: RET-altered measurable disease population included participants in the efficacy population who have measurable (target) disease per RECIST v1.1, at baseline according to BICR and sufficient evidence of a RET alteration. As prespecified in the SAP, Phase 1 participants treated at 400 mg QD are pooled with Phase 2 participants for efficacy analysis. Number analyzed is the number of participants with the specified mutation.

ArmMeasureGroupValue (NUMBER)
Phase 1: All Participants QDPhase 1 and Phase 2: CBR in RET-mutation MTC Participants With Specific RET Gene StatusM918T78.0 percentage of participants
Phase 1: All Participants QDPhase 1 and Phase 2: CBR in RET-mutation MTC Participants With Specific RET Gene StatusCysteine Rich Domain76.9 percentage of participants
Phase 1: All Participants QDPhase 1 and Phase 2: CBR in RET-mutation MTC Participants With Specific RET Gene StatusV804X100 percentage of participants
Phase 1: All Participants QDPhase 1 and Phase 2: CBR in RET-mutation MTC Participants With Specific RET Gene StatusOther100 percentage of participants
Pralsetinib 400 mg QDPhase 1 and Phase 2: CBR in RET-mutation MTC Participants With Specific RET Gene StatusOther100 percentage of participants
Pralsetinib 400 mg QDPhase 1 and Phase 2: CBR in RET-mutation MTC Participants With Specific RET Gene StatusM918T86.0 percentage of participants
Pralsetinib 400 mg QDPhase 1 and Phase 2: CBR in RET-mutation MTC Participants With Specific RET Gene StatusV804X100 percentage of participants
Pralsetinib 400 mg QDPhase 1 and Phase 2: CBR in RET-mutation MTC Participants With Specific RET Gene StatusCysteine Rich Domain96.0 percentage of participants
Secondary

Phase 1 and Phase 2: Clinical Benefit Rate (CBR) in RET-fusion Positive NSCLC Participants With Specific RET Gene Status

Oncogenic RET rearrangements have been identified in 1%-2% of NSCLC. These rearrangements typically produce chimeric transcripts that encode a fusion protein consisting of the RET kinase domain coupled to a protein with a dimerization domain (e.g., KIF5B, CCDC6, NCOA4). RET genotypes were determined by local testing and/or central analysis of ctDNA. CBR was assessed in participants having specific RET rearrangements. CBR was defined as the percentage of participants with a confirmed CR or PR, or stable disease (SD) which has been lasting at least 16 weeks (i.e. 4 cycles if 28 days are in one cycle) from the first dose date. CR and PR were defined per RECIST as outlined in the description for OM 3. SD was defined as neither sufficient shrinkage to qualify for CR or PR nor sufficient increase to qualify for PD. PD was defined as at least a 20% increase in SOD of target lesions, taking as reference the smallest SOD on study (including baseline).

Time frame: Up to approximately 79.8 months

Population: RET-altered measurable disease population included participants in the efficacy population who have measurable (target) disease per RECIST v1.1, at baseline according to BICR and sufficient evidence of a RET alteration. As prespecified in the SAP, Phase 1 participants treated at 400 mg QD are pooled with Phase 2 participants for efficacy analysis. Number analyzed is the number of participants with the specified mutation.

ArmMeasureGroupValue (NUMBER)
Phase 1: All Participants QDPhase 1 and Phase 2: Clinical Benefit Rate (CBR) in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusCCDC676.0 percentage of participants
Phase 1: All Participants QDPhase 1 and Phase 2: Clinical Benefit Rate (CBR) in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusKIF5B76.9 percentage of participants
Phase 1: All Participants QDPhase 1 and Phase 2: Clinical Benefit Rate (CBR) in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusOther53.8 percentage of participants
Phase 1: All Participants QDPhase 1 and Phase 2: Clinical Benefit Rate (CBR) in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusNCOA4100 percentage of participants
Pralsetinib 400 mg QDPhase 1 and Phase 2: Clinical Benefit Rate (CBR) in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusOther0 percentage of participants
Pralsetinib 400 mg QDPhase 1 and Phase 2: Clinical Benefit Rate (CBR) in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusCCDC675.0 percentage of participants
Pralsetinib 400 mg QDPhase 1 and Phase 2: Clinical Benefit Rate (CBR) in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusKIF5B88.2 percentage of participants
Pralsetinib BID Dosing SchedulePhase 1 and Phase 2: Clinical Benefit Rate (CBR) in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusOther63.6 percentage of participants
Pralsetinib BID Dosing SchedulePhase 1 and Phase 2: Clinical Benefit Rate (CBR) in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusKIF5B81.6 percentage of participants
Pralsetinib BID Dosing SchedulePhase 1 and Phase 2: Clinical Benefit Rate (CBR) in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusCCDC684.2 percentage of participants
Secondary

Phase 1 and Phase 2: DCR in RET-fusion Positive TC Participants With Specific RET Gene Status

Oncogenic RET activation has been implicated as a driver in both MTC and DTC. These rearrangements typically produce chimeric transcripts that encode a fusion protein consisting of the RET kinase domain coupled to a protein with a dimerization domain (e.g., KIF5B, CCDC6, NCOA4). RET genotypes were determined by local testing and/or central analysis of ctDNA. DCR was assessed in participants having specific RET rearrangements. DCR was defined as the percentage of participants with a confirmed CR/PR, or SD. CR and PR were defined per RECIST as outlined in the description for OM 3. SD was defined as neither sufficient shrinkage to qualify for CR or PR nor sufficient increase to qualify for PD. PD was defined as at least a 20% increase in SOD of target lesions, taking as reference the smallest SOD on study (including baseline).

Time frame: Up to approximately 79.8 months

Population: RET-altered measurable disease population included participants in the efficacy population who have measurable (target) disease per RECIST v1.1, at baseline according to BICR and sufficient evidence of a RET alteration. As prespecified in the SAP, Phase 1 participants treated at 400 mg QD are pooled with Phase 2 participants for efficacy analysis. Number analyzed is the number of participants with the specified mutation.

ArmMeasureGroupValue (NUMBER)
Phase 1: All Participants QDPhase 1 and Phase 2: DCR in RET-fusion Positive TC Participants With Specific RET Gene StatusCCDC694.1 percentage of participants
Phase 1: All Participants QDPhase 1 and Phase 2: DCR in RET-fusion Positive TC Participants With Specific RET Gene StatusNCOA4100 percentage of participants
Phase 1: All Participants QDPhase 1 and Phase 2: DCR in RET-fusion Positive TC Participants With Specific RET Gene StatusOther100 percentage of participants
UnknownPhase 1 and Phase 2: DCR in RET-fusion Positive TC Participants With Specific RET Gene StatusKIF5B percentage of participants
Secondary

Phase 1 and Phase 2: DCR in RET-mutation MTC Participants With Specific RET Gene Status

Oncogenic RET activation has been implicated as a driver in MTC. These rearrangements typically produce chimeric transcripts that encode a fusion protein consisting of the RET kinase domain coupled to a protein with a dimerization domain (e.g., M918T, cysteine rich domain, V804X). RET genotypes were determined by local testing and/or central analysis of ctDNA. DCR was assessed in participants having specific RET rearrangements. DCR was defined as the percentage of participants with a confirmed CR/PR, or SD. CR and PR were defined per RECIST as outlined in the description for OM 3. SD was defined as neither sufficient shrinkage to qualify for CR or PR nor sufficient increase to qualify for PD. PD was defined as at least a 20% increase in SOD of target lesions, taking as reference the smallest SOD on study (including baseline).

Time frame: Up to approximately 79.8 months

Population: RET-altered measurable disease population included participants in the efficacy population who have measurable (target) disease per RECIST v1.1, at baseline according to BICR and sufficient evidence of a RET alteration. As prespecified in the SAP, Phase 1 participants treated at 400 mg QD are pooled with Phase 2 participants for efficacy analysis. Number analyzed is the number of participants with the specified mutation.

ArmMeasureGroupValue (NUMBER)
Phase 1: All Participants QDPhase 1 and Phase 2: DCR in RET-mutation MTC Participants With Specific RET Gene StatusM918T95.1 percentage of participants
Phase 1: All Participants QDPhase 1 and Phase 2: DCR in RET-mutation MTC Participants With Specific RET Gene StatusCysteine Rich Domain92.3 percentage of participants
Phase 1: All Participants QDPhase 1 and Phase 2: DCR in RET-mutation MTC Participants With Specific RET Gene StatusV804X100 percentage of participants
Phase 1: All Participants QDPhase 1 and Phase 2: DCR in RET-mutation MTC Participants With Specific RET Gene StatusOther100 percentage of participants
Pralsetinib 400 mg QDPhase 1 and Phase 2: DCR in RET-mutation MTC Participants With Specific RET Gene StatusOther100 percentage of participants
Pralsetinib 400 mg QDPhase 1 and Phase 2: DCR in RET-mutation MTC Participants With Specific RET Gene StatusM918T90.7 percentage of participants
Pralsetinib 400 mg QDPhase 1 and Phase 2: DCR in RET-mutation MTC Participants With Specific RET Gene StatusV804X100 percentage of participants
Pralsetinib 400 mg QDPhase 1 and Phase 2: DCR in RET-mutation MTC Participants With Specific RET Gene StatusCysteine Rich Domain96.0 percentage of participants
Secondary

Phase 1 and Phase 2: Disease Control Rate (DCR) in RET-fusion Positive NSCLC Participants With Specific RET Gene Status

Oncogenic RET rearrangements have been identified in 1%-2% of NSCLC. These rearrangements typically produce chimeric transcripts that encode a fusion protein consisting of the RET kinase domain coupled to a protein with a dimerization domain (e.g., KIF5B, CCDC6, NCOA4). RET genotypes were determined by local testing and/or central analysis of ctDNA. DCR was assessed in participants having specific RET rearrangements. DCR was defined as the percentage of participants with a confirmed CR/PR, or SD. CR and PR were defined per RECIST as outlined in the description for OM 3. SD was defined as neither sufficient shrinkage to qualify for CR or PR nor sufficient increase to qualify for PD. PD was defined as at least a 20% increase in SOD of target lesions, taking as reference the smallest SOD on study (including baseline).

Time frame: Up to approximately 79.8 months

Population: RET-altered measurable disease population included participants in the efficacy population who have measurable (target) disease per RECIST v1.1, at baseline according to BICR and sufficient evidence of a RET alteration. As prespecified in the SAP, Phase 1 participants treated at 400 mg QD are pooled with Phase 2 participants for efficacy analysis. Number analyzed is the number of participants with the specified mutation.

ArmMeasureGroupValue (NUMBER)
Phase 1: All Participants QDPhase 1 and Phase 2: Disease Control Rate (DCR) in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusCCDC688.0 percentage of participants
Phase 1: All Participants QDPhase 1 and Phase 2: Disease Control Rate (DCR) in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusKIF5B93.4 percentage of participants
Phase 1: All Participants QDPhase 1 and Phase 2: Disease Control Rate (DCR) in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusOther84.6 percentage of participants
Phase 1: All Participants QDPhase 1 and Phase 2: Disease Control Rate (DCR) in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusNCOA4100 percentage of participants
Pralsetinib 400 mg QDPhase 1 and Phase 2: Disease Control Rate (DCR) in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusOther50.0 percentage of participants
Pralsetinib 400 mg QDPhase 1 and Phase 2: Disease Control Rate (DCR) in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusCCDC6100 percentage of participants
Pralsetinib 400 mg QDPhase 1 and Phase 2: Disease Control Rate (DCR) in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusKIF5B94.1 percentage of participants
Pralsetinib BID Dosing SchedulePhase 1 and Phase 2: Disease Control Rate (DCR) in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusOther100 percentage of participants
Pralsetinib BID Dosing SchedulePhase 1 and Phase 2: Disease Control Rate (DCR) in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusKIF5B88.2 percentage of participants
Pralsetinib BID Dosing SchedulePhase 1 and Phase 2: Disease Control Rate (DCR) in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusCCDC689.5 percentage of participants
Secondary

Phase 1 and Phase 2: DOR in RET-fusion Positive TC Participants With Specific RET Gene Status

Oncogenic RET activation has been implicated as a driver in MTC. These rearrangements typically produce chimeric transcripts that encode a fusion protein consisting of the RET kinase domain coupled to a protein with a dimerization domain (e.g., KIF5B, CCDC6, NCOA4). RET genotypes were determined by local testing and/or central analysis of ctDNA. DOR was assessed in participants having specific RET rearrangements. DOR=time from first documented CR/PR to date of first documented PD or death due to any cause, whichever occurs first. Per RECIST, CR= disappearance of all target lesions or any pathological lymph nodes (target or non-target) having a reduction in the short axis to \<10 mm. PR=at least a 30% decrease in the SOD of all target lesions, taking as reference the baseline SOD, in absence of CR. PD=as at least a 20% increase in SOD of target lesions, taking as reference smallest SOD on study (including baseline). DOR was analyzed using the KM method.

Time frame: Up to approximately 79.8 months

Population: RET-altered measurable disease population included participants in the efficacy population who have measurable (target) disease per RECIST v1.1, at baseline according to BICR \& sufficient evidence of a RET alteration. As prespecified in SAP, Phase 1 participants treated at 400 mg QD are pooled with Phase 2 participants for efficacy analysis. Participants who had a response of CR/PR were analyzed in this outcome measure. Number analyzed is the number of participants with the specified mutation.

ArmMeasureGroupValue (MEDIAN)
Phase 1: All Participants QDPhase 1 and Phase 2: DOR in RET-fusion Positive TC Participants With Specific RET Gene StatusCCDC6NA months
Phase 1: All Participants QDPhase 1 and Phase 2: DOR in RET-fusion Positive TC Participants With Specific RET Gene StatusNCOA415.2 months
Phase 1: All Participants QDPhase 1 and Phase 2: DOR in RET-fusion Positive TC Participants With Specific RET Gene StatusOtherNA months
Secondary

Phase 1 and Phase 2: DOR in RET-mutation MTC Participants With Specific RET Gene Status

Oncogenic RET activation has been implicated as a driver in MTC. These rearrangements typically produce chimeric transcripts that encode a fusion protein consisting of the RET kinase domain coupled to a protein with a dimerization domain (e.g., M918T, cysteine rich domain, V804X). RET genotypes were determined by local testing and/or central analysis of ctDNA. DOR was assessed in participants having specific RET rearrangements. DOR=time from first documented CR/PR to date of first documented PD or death due to any cause, whichever occurs first. Per RECIST, CR= disappearance of all target lesions or any pathological lymph nodes (target or non-target) having a reduction in the short axis to \<10 mm. PR=at least a 30% decrease in the SOD of all target lesions, taking as reference the baseline SOD, in absence of CR. PD=as at least a 20% increase in SOD of target lesions, taking as reference smallest SOD on study (including baseline). DOR was analyzed using the Kaplan-Meier (KM) method.

Time frame: Up to approximately 79.8 months

Population: RET-altered measurable disease population included participants in the efficacy population who have measurable (target) disease per RECIST v1.1, at baseline according to BICR \& sufficient evidence of a RET alteration. As prespecified in SAP, Phase 1 participants treated at 400 mg QD are pooled with Phase 2 participants for efficacy analysis. Participants who had a response of CR/PR were analyzed in this outcome measure. Number analyzed is the number of participants with the specified mutation.

ArmMeasureGroupValue (MEDIAN)
Phase 1: All Participants QDPhase 1 and Phase 2: DOR in RET-mutation MTC Participants With Specific RET Gene StatusV804X21.8 months
Phase 1: All Participants QDPhase 1 and Phase 2: DOR in RET-mutation MTC Participants With Specific RET Gene StatusOtherNA months
Phase 1: All Participants QDPhase 1 and Phase 2: DOR in RET-mutation MTC Participants With Specific RET Gene StatusCysteine Rich Domain29.5 months
Phase 1: All Participants QDPhase 1 and Phase 2: DOR in RET-mutation MTC Participants With Specific RET Gene StatusM918T18.4 months
Pralsetinib 400 mg QDPhase 1 and Phase 2: DOR in RET-mutation MTC Participants With Specific RET Gene StatusCysteine Rich Domain36.8 months
Pralsetinib 400 mg QDPhase 1 and Phase 2: DOR in RET-mutation MTC Participants With Specific RET Gene StatusM918T51.8 months
Pralsetinib 400 mg QDPhase 1 and Phase 2: DOR in RET-mutation MTC Participants With Specific RET Gene StatusOtherNA months
Secondary

Phase 1 and Phase 2: Duration of Response (DOR) in RET-mutation NSCLC Participants With Specific RET Gene Status

Oncogenic RET rearrangements have been identified in 1%-2% of NSCLC. These rearrangements typically produce chimeric transcripts that encode a fusion protein consisting of the RET kinase domain coupled to a protein with a dimerization domain (e.g., KIF5), CCDC6, NCOA4). RET genotypes were determined by local testing &/or central analysis of circulating tumor deoxyribonucleic acid (ctDNA). DOR was assessed in participants having specific RET rearrangements. DOR=time from first documented CR/PR to date of first documented PD or death due to any cause, whichever occurs first. Per RECIST, CR=disappearance of all target lesions or any pathological lymph nodes (target or non-target) having a reduction in the short axis to \<10 mm. PR=at least a 30% decrease in SOD of all target lesions, taking as reference the baseline SOD, in absence of CR. PD=as at least a 20% increase in SOD of target lesions, taking as reference smallest SOD on study. DOR was analyzed using the Kaplan-Meier (KM) method.

Time frame: Up to approximately 79.8 months

Population: RET-altered measurable disease population included participants in the efficacy population who have measurable (target) disease per RECIST v1.1, at baseline according to BICR \& sufficient evidence of a RET alteration. As prespecified in SAP, Phase 1 participants treated at 400 mg QD are pooled with Phase 2 participants for efficacy analysis. Participants who had a response of CR/PR were analyzed in this outcome measure. Number analyzed is the number of participants with the specified mutation.

ArmMeasureGroupValue (MEDIAN)
Phase 1: All Participants QDPhase 1 and Phase 2: Duration of Response (DOR) in RET-mutation NSCLC Participants With Specific RET Gene StatusKIF5B15.1 months
Phase 1: All Participants QDPhase 1 and Phase 2: Duration of Response (DOR) in RET-mutation NSCLC Participants With Specific RET Gene StatusNCOA412.9 months
Phase 1: All Participants QDPhase 1 and Phase 2: Duration of Response (DOR) in RET-mutation NSCLC Participants With Specific RET Gene StatusOther35.2 months
Phase 1: All Participants QDPhase 1 and Phase 2: Duration of Response (DOR) in RET-mutation NSCLC Participants With Specific RET Gene StatusCCDC646.7 months
Pralsetinib 400 mg QDPhase 1 and Phase 2: Duration of Response (DOR) in RET-mutation NSCLC Participants With Specific RET Gene StatusCCDC629.6 months
Pralsetinib 400 mg QDPhase 1 and Phase 2: Duration of Response (DOR) in RET-mutation NSCLC Participants With Specific RET Gene StatusKIF5B21.5 months
Pralsetinib BID Dosing SchedulePhase 1 and Phase 2: Duration of Response (DOR) in RET-mutation NSCLC Participants With Specific RET Gene StatusCCDC6NA months
Pralsetinib BID Dosing SchedulePhase 1 and Phase 2: Duration of Response (DOR) in RET-mutation NSCLC Participants With Specific RET Gene StatusKIF5B9.2 months
Pralsetinib BID Dosing SchedulePhase 1 and Phase 2: Duration of Response (DOR) in RET-mutation NSCLC Participants With Specific RET Gene StatusOther41.2 months
Secondary

Phase 1 and Phase 2: ORR in RET-fusion Positive NSCLC Participants With Specific RET Gene Status

Oncogenic RET rearrangements have been identified in 1%-2% of NSCLC. These rearrangements typically produce chimeric transcripts that encode a fusion protein consisting of the RET kinase domain coupled to a protein with a dimerization domain (e.g., Kinesin family member 5B (KIF5B), coiled-coil domain containing 6 (CCDC6), nuclear receptor coactivator 4 (NCOA4)). RET genotypes were determined by local testing and/or central analysis of circulating tumor deoxyribonucleic acid (ctDNA). ORR was assessed in participants having specific RET rearrangements. ORR was defined as the percentage of participants with a confirmed CR or PR for at least 2 assessments with at least 28 days apart and no PD in between. CR, PR, and PD were defined per RECIST as outlined in the description for OM 3.

Time frame: Up to approximately 79.8 months

Population: RET-altered measurable disease population included participants in the efficacy population who have measurable (target) disease per RECIST v1.1, at baseline according to BICR and sufficient evidence of a RET alteration. As prespecified in the SAP, Phase 1 participants treated at 400 mg QD are pooled with Phase 2 participants for efficacy analysis. Number analyzed is the number of participants with the specified mutation.

ArmMeasureGroupValue (NUMBER)
Phase 1: All Participants QDPhase 1 and Phase 2: ORR in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusCCDC668.0 percentage of participants
Phase 1: All Participants QDPhase 1 and Phase 2: ORR in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusKIF5B63.7 percentage of participants
Phase 1: All Participants QDPhase 1 and Phase 2: ORR in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusOther46.2 percentage of participants
Phase 1: All Participants QDPhase 1 and Phase 2: ORR in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusNCOA4100 percentage of participants
Pralsetinib 400 mg QDPhase 1 and Phase 2: ORR in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusOther0 percentage of participants
Pralsetinib 400 mg QDPhase 1 and Phase 2: ORR in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusCCDC675.0 percentage of participants
Pralsetinib 400 mg QDPhase 1 and Phase 2: ORR in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusKIF5B82.4 percentage of participants
Pralsetinib BID Dosing SchedulePhase 1 and Phase 2: ORR in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusOther63.6 percentage of participants
Pralsetinib BID Dosing SchedulePhase 1 and Phase 2: ORR in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusKIF5B78.9 percentage of participants
Pralsetinib BID Dosing SchedulePhase 1 and Phase 2: ORR in RET-fusion Positive NSCLC Participants With Specific RET Gene StatusCCDC684.2 percentage of participants
Secondary

Phase 1 and Phase 2: ORR in RET-fusion Positive TC Participants With Specific RET Gene Status

Oncogenic RET activation has been implicated as a driver in both MTC and differentiated TC (DTC). These rearrangements typically produce chimeric transcripts that encode a fusion protein consisting of the RET kinase domain coupled to a protein with a dimerization domain (e.g., KIF5B, CCDC6, NCOA4). RET genotypes were determined by local testing and/or central analysis of ctDNA. ORR was assessed in participants having specific RET rearrangements. ORR was defined as the percentage of participants with a confirmed CR or PR for at least 2 assessments with at least 28 days apart and no PD in between. CR, PR, and PD were defined per RECIST as outlined in the description for OM 3.

Time frame: Up to approximately 79.8 months

Population: RET-altered measurable disease population included participants in the efficacy population who have measurable (target) disease per RECIST v1.1, at baseline according to BICR and sufficient evidence of a RET alteration. As prespecified in the SAP, Phase 1 participants treated at 400 mg QD are pooled with Phase 2 participants for efficacy analysis. Number analyzed is the number of participants with the specified mutation.

ArmMeasureGroupValue (NUMBER)
Phase 1: All Participants QDPhase 1 and Phase 2: ORR in RET-fusion Positive TC Participants With Specific RET Gene StatusCCDC682.4 percentage of participants
Phase 1: All Participants QDPhase 1 and Phase 2: ORR in RET-fusion Positive TC Participants With Specific RET Gene StatusNCOA4100 percentage of participants
Phase 1: All Participants QDPhase 1 and Phase 2: ORR in RET-fusion Positive TC Participants With Specific RET Gene StatusOther75.0 percentage of participants
UnknownPhase 1 and Phase 2: ORR in RET-fusion Positive TC Participants With Specific RET Gene StatusKIF5B percentage of participants
Secondary

Phase 1 and Phase 2: ORR in RET-mutation MTC Participants With Specific RET Gene Status

Oncogenic RET activation has been implicated as a driver in MTC. These rearrangements typically produce chimeric transcripts that encode a fusion protein consisting of the RET kinase domain coupled to a protein with a dimerization domain (e.g., M918T, cysteine rich domain, V804X). RET genotypes were determined by local testing and/or central analysis of ctDNA. ORR was assessed in participants having specific RET rearrangements. ORR was defined as the percentage of participants with a confirmed CR or PR for at least 2 assessments with at least 28 days apart and no PD in between. CR, PR, and PD were defined per RECIST as outlined in the description for OM 3.

Time frame: Up to approximately 79.8 months

Population: RET-altered measurable disease population included participants in the efficacy population who have measurable (target) disease per RECIST v1.1, at baseline according to BICR and sufficient evidence of a RET alteration. As prespecified in the SAP, Phase 1 participants treated at 400 mg QD are pooled with Phase 2 participants for efficacy analysis. Number analyzed is the number of participants with the specified mutation.

ArmMeasureGroupValue (NUMBER)
Phase 1: All Participants QDPhase 1 and Phase 2: ORR in RET-mutation MTC Participants With Specific RET Gene StatusM918T53.7 percentage of participants
Phase 1: All Participants QDPhase 1 and Phase 2: ORR in RET-mutation MTC Participants With Specific RET Gene StatusCysteine Rich Domain46.2 percentage of participants
Phase 1: All Participants QDPhase 1 and Phase 2: ORR in RET-mutation MTC Participants With Specific RET Gene StatusV804X100 percentage of participants
Phase 1: All Participants QDPhase 1 and Phase 2: ORR in RET-mutation MTC Participants With Specific RET Gene StatusOther100 percentage of participants
Pralsetinib 400 mg QDPhase 1 and Phase 2: ORR in RET-mutation MTC Participants With Specific RET Gene StatusOther66.7 percentage of participants
Pralsetinib 400 mg QDPhase 1 and Phase 2: ORR in RET-mutation MTC Participants With Specific RET Gene StatusM918T74.4 percentage of participants
Pralsetinib 400 mg QDPhase 1 and Phase 2: ORR in RET-mutation MTC Participants With Specific RET Gene StatusV804X0 percentage of participants
Pralsetinib 400 mg QDPhase 1 and Phase 2: ORR in RET-mutation MTC Participants With Specific RET Gene StatusCysteine Rich Domain88.0 percentage of participants
Secondary

Phase 1: Apparent Oral Clearance (CL/F)

Number of participants in each arm of this OM is based on the actual treatment received. 1 participant originally assigned to the 200/100 mg arm received the 100/100 mg treatment and hence, was counted under the 100/100 mg arm for this OM.

Time frame: Predose on 0.5, 1, 2, 4, 6, 8 and 24 hours postdose on Days 1 and 15 of Cycle 1 (1 cycle = 28 days)

Population: PK evaluable population included all participants who received at least one dose of pralsetinib and from whom at least one post dose PK sample was collected. Overall number analyzed is the number of participants with data available for analysis. Number analyzed is the number of participants with data available for analysis at the specified timepoint.

ArmMeasureGroupValue (GEOMETRIC_MEAN)Dispersion
Phase 1: All Participants QDPhase 1: Apparent Oral Clearance (CL/F)Cycle 1 Day 14.26 liters per hour (L/hr)
Phase 1: All Participants QDPhase 1: Apparent Oral Clearance (CL/F)Cycle 1 Day 1514.0 liters per hour (L/hr)
Pralsetinib 400 mg QDPhase 1: Apparent Oral Clearance (CL/F)Cycle 1 Day 114.7 liters per hour (L/hr)Geometric Coefficient of Variation 42.3
Pralsetinib 400 mg QDPhase 1: Apparent Oral Clearance (CL/F)Cycle 1 Day 1511.3 liters per hour (L/hr)Geometric Coefficient of Variation 51.2
Pralsetinib BID Dosing SchedulePhase 1: Apparent Oral Clearance (CL/F)Cycle 1 Day 120.6 liters per hour (L/hr)Geometric Coefficient of Variation 48.1
Pralsetinib BID Dosing SchedulePhase 1: Apparent Oral Clearance (CL/F)Cycle 1 Day 1512.0 liters per hour (L/hr)Geometric Coefficient of Variation 38.9
Pralsetinib All DosesPhase 1: Apparent Oral Clearance (CL/F)Cycle 1 Day 127.3 liters per hour (L/hr)Geometric Coefficient of Variation 60.3
Pralsetinib All DosesPhase 1: Apparent Oral Clearance (CL/F)Cycle 1 Day 1531.4 liters per hour (L/hr)Geometric Coefficient of Variation 97.8
RET-mutation MTC With No Prior Cabozantinib or Vandetanib TreatmentPhase 1: Apparent Oral Clearance (CL/F)Cycle 1 Day 123.3 liters per hour (L/hr)Geometric Coefficient of Variation 40.2
RET-mutation MTC With No Prior Cabozantinib or Vandetanib TreatmentPhase 1: Apparent Oral Clearance (CL/F)Cycle 1 Day 1513.2 liters per hour (L/hr)Geometric Coefficient of Variation 33
RET-fusion Positive TCPhase 1: Apparent Oral Clearance (CL/F)Cycle 1 Day 115.2 liters per hour (L/hr)Geometric Coefficient of Variation 88.1
RET-fusion Positive TCPhase 1: Apparent Oral Clearance (CL/F)Cycle 1 Day 1511.1 liters per hour (L/hr)Geometric Coefficient of Variation 72.2
RET-fusion Positive Solid Tumors Other Than NSCLC and TCPhase 1: Apparent Oral Clearance (CL/F)Cycle 1 Day 111.6 liters per hour (L/hr)Geometric Coefficient of Variation 81.3
RET-fusion Positive Solid Tumors Other Than NSCLC and TCPhase 1: Apparent Oral Clearance (CL/F)Cycle 1 Day 158.57 liters per hour (L/hr)
Secondary

Phase 1: Apparent Volume of Distribution (Vz/F)

Number of participants in each arm of this OM is based on the actual treatment received. 1 participant originally assigned to the 200/100 mg arm received the 100/100 mg treatment and hence, was counted under the 100/100 mg arm for this OM.

Time frame: Predose on 0.5, 1, 2, 4, 6, 8 and 24 hours postdose on Days 1 and 15 of Cycle 1 (1 cycle = 28 days)

Population: PK evaluable population included all participants who received at least one dose of pralsetinib and from whom at least one post dose PK sample was collected. Overall number analyzed is the number of participants with data available for analysis. Number analyzed is the number of participants with data available for analysis at the specified timepoint.

ArmMeasureGroupValue (GEOMETRIC_MEAN)Dispersion
Phase 1: All Participants QDPhase 1: Apparent Volume of Distribution (Vz/F)Cycle 1 Day 196.1 liters
Phase 1: All Participants QDPhase 1: Apparent Volume of Distribution (Vz/F)Cycle 1 Day 15355 liters
Pralsetinib 400 mg QDPhase 1: Apparent Volume of Distribution (Vz/F)Cycle 1 Day 1230 litersGeometric Coefficient of Variation 37.1
Pralsetinib 400 mg QDPhase 1: Apparent Volume of Distribution (Vz/F)Cycle 1 Day 15171 litersGeometric Coefficient of Variation 176
Pralsetinib BID Dosing SchedulePhase 1: Apparent Volume of Distribution (Vz/F)Cycle 1 Day 1458 litersGeometric Coefficient of Variation 125
Pralsetinib BID Dosing SchedulePhase 1: Apparent Volume of Distribution (Vz/F)Cycle 1 Day 15232 litersGeometric Coefficient of Variation 43.7
Pralsetinib All DosesPhase 1: Apparent Volume of Distribution (Vz/F)Cycle 1 Day 1499 litersGeometric Coefficient of Variation 50.8
Pralsetinib All DosesPhase 1: Apparent Volume of Distribution (Vz/F)Cycle 1 Day 15622 litersGeometric Coefficient of Variation 67.3
RET-mutation MTC With No Prior Cabozantinib or Vandetanib TreatmentPhase 1: Apparent Volume of Distribution (Vz/F)Cycle 1 Day 1543 litersGeometric Coefficient of Variation 82.6
RET-mutation MTC With No Prior Cabozantinib or Vandetanib TreatmentPhase 1: Apparent Volume of Distribution (Vz/F)Cycle 1 Day 15367 litersGeometric Coefficient of Variation 86.6
RET-fusion Positive TCPhase 1: Apparent Volume of Distribution (Vz/F)Cycle 1 Day 1430 litersGeometric Coefficient of Variation 62.6
RET-fusion Positive TCPhase 1: Apparent Volume of Distribution (Vz/F)Cycle 1 Day 15418 litersGeometric Coefficient of Variation 19.9
RET-fusion Positive Solid Tumors Other Than NSCLC and TCPhase 1: Apparent Volume of Distribution (Vz/F)Cycle 1 Day 1350 litersGeometric Coefficient of Variation 115
RET-fusion Positive Solid Tumors Other Than NSCLC and TCPhase 1: Apparent Volume of Distribution (Vz/F)Cycle 1 Day 15181 liters
Secondary

Phase 1: Area Under the Plasma Concentration Versus Time Curve From Time 0 to 24 Hours Postdose (AUC0-24)

Number of participants in each arm of this OM is based on the actual treatment received. 1 participant originally assigned to the 200/100 mg arm received the 100/100 mg treatment and hence, was counted under the 100/100 mg arm for this OM.

Time frame: 24 hours postdose on Day 1 of Cycle 1 (1 cycle = 28 days)

Population: PK evaluable population included all participants who received at least one dose of pralsetinib and from whom at least one post dose PK sample was collected. Overall number analyzed is the number of participants with data available for analysis.

ArmMeasureValue (GEOMETRIC_MEAN)Dispersion
Phase 1: All Participants QDPhase 1: Area Under the Plasma Concentration Versus Time Curve From Time 0 to 24 Hours Postdose (AUC0-24)4450 hours*nanograms/milliliter (hours*ng/ml)
Pralsetinib 400 mg QDPhase 1: Area Under the Plasma Concentration Versus Time Curve From Time 0 to 24 Hours Postdose (AUC0-24)3620 hours*nanograms/milliliter (hours*ng/ml)Geometric Coefficient of Variation 50.8
Pralsetinib BID Dosing SchedulePhase 1: Area Under the Plasma Concentration Versus Time Curve From Time 0 to 24 Hours Postdose (AUC0-24)3010 hours*nanograms/milliliter (hours*ng/ml)Geometric Coefficient of Variation 84.8
Pralsetinib All DosesPhase 1: Area Under the Plasma Concentration Versus Time Curve From Time 0 to 24 Hours Postdose (AUC0-24)5260 hours*nanograms/milliliter (hours*ng/ml)Geometric Coefficient of Variation 46.2
RET-mutation MTC With No Prior Cabozantinib or Vandetanib TreatmentPhase 1: Area Under the Plasma Concentration Versus Time Curve From Time 0 to 24 Hours Postdose (AUC0-24)8470 hours*nanograms/milliliter (hours*ng/ml)Geometric Coefficient of Variation 54.5
RET-fusion Positive TCPhase 1: Area Under the Plasma Concentration Versus Time Curve From Time 0 to 24 Hours Postdose (AUC0-24)14700 hours*nanograms/milliliter (hours*ng/ml)Geometric Coefficient of Variation 60.3
RET-fusion Positive Solid Tumors Other Than NSCLC and TCPhase 1: Area Under the Plasma Concentration Versus Time Curve From Time 0 to 24 Hours Postdose (AUC0-24)27700 hours*nanograms/milliliter (hours*ng/ml)Geometric Coefficient of Variation 94.1
Secondary

Phase 1: Maximum Plasma Concentration (Cmax)

Number of participants in each arm of this OM is based on the actual treatment received. 1 participant originally assigned to the 200/100 mg arm received the 100/100 mg treatment and hence, was counted under the 100/100 mg arm for this OM.

Time frame: Predose on 0.5, 1, 2, 4, 6, 8 and 24 hours postdose on Days 1 and 15 of Cycle 1 (1 cycle = 28 days)

Population: Pharmacokinetic (PK)-evaluable population included all participants who received at least one dose of pralsetinib and from whom at least one post dose PK sample was collected. Number analyzed is the number of participants with data available for analysis at the specified timepoint.

ArmMeasureGroupValue (GEOMETRIC_MEAN)Dispersion
Phase 1: All Participants QDPhase 1: Maximum Plasma Concentration (Cmax)Cycle 1 Day 1346 nanograms per milliliters (ng/mL)
Phase 1: All Participants QDPhase 1: Maximum Plasma Concentration (Cmax)Cycle 1 Day 15130 nanograms per milliliters (ng/mL)
Pralsetinib 400 mg QDPhase 1: Maximum Plasma Concentration (Cmax)Cycle 1 Day 1335 nanograms per milliliters (ng/mL)Geometric Coefficient of Variation 52.8
Pralsetinib 400 mg QDPhase 1: Maximum Plasma Concentration (Cmax)Cycle 1 Day 15420 nanograms per milliliters (ng/mL)Geometric Coefficient of Variation 56.9
Pralsetinib BID Dosing SchedulePhase 1: Maximum Plasma Concentration (Cmax)Cycle 1 Day 1198 nanograms per milliliters (ng/mL)Geometric Coefficient of Variation 99.8
Pralsetinib BID Dosing SchedulePhase 1: Maximum Plasma Concentration (Cmax)Cycle 1 Day 15586 nanograms per milliliters (ng/mL)Geometric Coefficient of Variation 47.8
Pralsetinib All DosesPhase 1: Maximum Plasma Concentration (Cmax)Cycle 1 Day 1459 nanograms per milliliters (ng/mL)Geometric Coefficient of Variation 52.3
Pralsetinib All DosesPhase 1: Maximum Plasma Concentration (Cmax)Cycle 1 Day 15525 nanograms per milliliters (ng/mL)Geometric Coefficient of Variation 72.5
RET-mutation MTC With No Prior Cabozantinib or Vandetanib TreatmentPhase 1: Maximum Plasma Concentration (Cmax)Cycle 1 Day 1688 nanograms per milliliters (ng/mL)Geometric Coefficient of Variation 53.3
RET-mutation MTC With No Prior Cabozantinib or Vandetanib TreatmentPhase 1: Maximum Plasma Concentration (Cmax)Cycle 1 Day 151390 nanograms per milliliters (ng/mL)Geometric Coefficient of Variation 35.3
RET-fusion Positive TCPhase 1: Maximum Plasma Concentration (Cmax)Cycle 1 Day 151930 nanograms per milliliters (ng/mL)Geometric Coefficient of Variation 66.7
RET-fusion Positive TCPhase 1: Maximum Plasma Concentration (Cmax)Cycle 1 Day 11210 nanograms per milliliters (ng/mL)Geometric Coefficient of Variation 85.3
RET-fusion Positive Solid Tumors Other Than NSCLC and TCPhase 1: Maximum Plasma Concentration (Cmax)Cycle 1 Day 154330 nanograms per milliliters (ng/mL)
RET-fusion Positive Solid Tumors Other Than NSCLC and TCPhase 1: Maximum Plasma Concentration (Cmax)Cycle 1 Day 11820 nanograms per milliliters (ng/mL)Geometric Coefficient of Variation 63.8
RET-altered Solid Tumors Previously Treated With RET InhibitorPhase 1: Maximum Plasma Concentration (Cmax)Cycle 1 Day 1569 nanograms per milliliters (ng/mL)Geometric Coefficient of Variation 42
RET-altered Solid Tumors Previously Treated With RET InhibitorPhase 1: Maximum Plasma Concentration (Cmax)Cycle 1 Day 151080 nanograms per milliliters (ng/mL)Geometric Coefficient of Variation 43.8
RET-mutation Positive Tumors Other Than MTCPhase 1: Maximum Plasma Concentration (Cmax)Cycle 1 Day 1715 nanograms per milliliters (ng/mL)Geometric Coefficient of Variation 64.1
RET-mutation Positive Tumors Other Than MTCPhase 1: Maximum Plasma Concentration (Cmax)Cycle 1 Day 151780 nanograms per milliliters (ng/mL)
Secondary

Phase 1: ORR

ORR was defined as the percentage of participants with a confirmed CR or PR for at least two assessments with at least 28 days apart and no PD in between. Per RECIST v1.1, CR was defined as the disappearance of all target lesions or any pathological lymph nodes (whether target or non-target) having a reduction in the short axis to \<10 mm. PR was defined as at least a 30% decrease in the SOD of all target lesions, taking as reference the baseline SOD, in the absence of CR. PD was defined as at least a 20% increase in SOD of target lesions, taking as reference the smallest SOD on study (including baseline). ORR and its two-sided 95% CI, based on the exact binomial distribution (Clopper-Pearson), was presented.

Time frame: Up to approximately 28 months

Population: Efficacy population included all participants who have been exposed to at least one dose of the study drug on or prior to 11 July 2019.

ArmMeasureValue (NUMBER)
Phase 1: All Participants QDPhase 1: ORR0 percentage of participants
Pralsetinib 400 mg QDPhase 1: ORR50.0 percentage of participants
Pralsetinib BID Dosing SchedulePhase 1: ORR40.0 percentage of participants
Pralsetinib All DosesPhase 1: ORR38.5 percentage of participants
RET-mutation MTC With No Prior Cabozantinib or Vandetanib TreatmentPhase 1: ORR45.5 percentage of participants
RET-fusion Positive TCPhase 1: ORR41.7 percentage of participants
RET-fusion Positive Solid Tumors Other Than NSCLC and TCPhase 1: ORR25.0 percentage of participants
RET-altered Solid Tumors Previously Treated With RET InhibitorPhase 1: ORR80.0 percentage of participants
RET-mutation Positive Tumors Other Than MTCPhase 1: ORR75.0 percentage of participants
Secondary

Phase 1: Percent Change From Baseline in Dual Specificity Phosphatase 6 (DUSP6)

The dose dependent change in a mitogen-activated protein kinases (MAPK) pathway expression signature was analyzed for all available samples of MTC and NSCLC participants. Participants with archived sample (used as baseline) and on treatment Cycle 2 Day 1 (1 cycle = 28 days) tumor tissues with greater than 20% tumor cells are included in the analysis. The changes in tumor biomarker DUSP6 levels was explored.

Time frame: Baseline, Week 4

Population: Safety Population included all participants who have received at least 1 dose of the study drug regardless of starting dose levels.

ArmMeasureValue (MEAN)Dispersion
Phase 1: All Participants QDPhase 1: Percent Change From Baseline in Dual Specificity Phosphatase 6 (DUSP6)0 percent changeStandard Deviation 0
Pralsetinib 400 mg QDPhase 1: Percent Change From Baseline in Dual Specificity Phosphatase 6 (DUSP6)54.26 percent changeStandard Deviation 88.318
Pralsetinib BID Dosing SchedulePhase 1: Percent Change From Baseline in Dual Specificity Phosphatase 6 (DUSP6)0 percent changeStandard Deviation 0
Pralsetinib All DosesPhase 1: Percent Change From Baseline in Dual Specificity Phosphatase 6 (DUSP6)-20.27 percent changeStandard Deviation 42.971
RET-mutation MTC With No Prior Cabozantinib or Vandetanib TreatmentPhase 1: Percent Change From Baseline in Dual Specificity Phosphatase 6 (DUSP6)-74.87 percent changeStandard Deviation 15.707
RET-fusion Positive TCPhase 1: Percent Change From Baseline in Dual Specificity Phosphatase 6 (DUSP6)-13.32 percent changeStandard Deviation 82.394
RET-fusion Positive Solid Tumors Other Than NSCLC and TCPhase 1: Percent Change From Baseline in Dual Specificity Phosphatase 6 (DUSP6)0 percent changeStandard Deviation 0
RET-altered Solid Tumors Previously Treated With RET InhibitorPhase 1: Percent Change From Baseline in Dual Specificity Phosphatase 6 (DUSP6)-81.57 percent changeStandard Deviation 3.057
RET-mutation Positive Tumors Other Than MTCPhase 1: Percent Change From Baseline in Dual Specificity Phosphatase 6 (DUSP6)-61.96 percent changeStandard Deviation 39.141
Secondary

Phase 1: Percent Change From Baseline in Sprout Receptor Tyrosine Kinase Signaling Antagonist 4 (SPRY4)

The dose dependent change in a MAPK pathway expression signature was analyzed for all available samples of MTC and NSCLC participants. Participants with archived sample (used as baseline) and on treatment Cycle 2 Day 1 (1 cycle = 28 days) tumor tissues with greater than 20% tumor cells are included in the analysis. The changes in tumor biomarker SPRY4 levels was explored.

Time frame: Baseline, Week 4

Population: Safety Population included all participants who have received at least 1 dose of the study drug regardless of starting dose levels.

ArmMeasureValue (MEAN)Dispersion
Phase 1: All Participants QDPhase 1: Percent Change From Baseline in Sprout Receptor Tyrosine Kinase Signaling Antagonist 4 (SPRY4)0 percent changeStandard Deviation 0
Pralsetinib 400 mg QDPhase 1: Percent Change From Baseline in Sprout Receptor Tyrosine Kinase Signaling Antagonist 4 (SPRY4)210.16 percent changeStandard Deviation 309.468
Pralsetinib BID Dosing SchedulePhase 1: Percent Change From Baseline in Sprout Receptor Tyrosine Kinase Signaling Antagonist 4 (SPRY4)0 percent changeStandard Deviation 0
Pralsetinib All DosesPhase 1: Percent Change From Baseline in Sprout Receptor Tyrosine Kinase Signaling Antagonist 4 (SPRY4)-34.98 percent changeStandard Deviation 29.569
RET-mutation MTC With No Prior Cabozantinib or Vandetanib TreatmentPhase 1: Percent Change From Baseline in Sprout Receptor Tyrosine Kinase Signaling Antagonist 4 (SPRY4)-69.00 percent changeStandard Deviation 28.731
RET-fusion Positive TCPhase 1: Percent Change From Baseline in Sprout Receptor Tyrosine Kinase Signaling Antagonist 4 (SPRY4)-3.26 percent changeStandard Deviation 99.349
RET-fusion Positive Solid Tumors Other Than NSCLC and TCPhase 1: Percent Change From Baseline in Sprout Receptor Tyrosine Kinase Signaling Antagonist 4 (SPRY4)0 percent changeStandard Deviation 0
RET-altered Solid Tumors Previously Treated With RET InhibitorPhase 1: Percent Change From Baseline in Sprout Receptor Tyrosine Kinase Signaling Antagonist 4 (SPRY4)-75.65 percent changeStandard Deviation 10.944
RET-mutation Positive Tumors Other Than MTCPhase 1: Percent Change From Baseline in Sprout Receptor Tyrosine Kinase Signaling Antagonist 4 (SPRY4)124.93 percent changeStandard Deviation 311.21
Secondary

Phase 1: Plasma Drug Concentration at 24 Hours Postdose (C24hr)

Number of participants in each arm of this OM is based on the actual treatment received. 1 participant originally assigned to the 200/100 mg arm received the 100/100 mg treatment and hence, was counted under the 100/100 mg arm for this OM.

Time frame: 24 hours postdose on Days 1 and 15 of Cycle 1 (1 cycle = 28 days)

Population: PK evaluable population included all participants who received at least one dose of pralsetinib and from whom at least one post dose PK sample was collected. Overall number analyzed is the number of participants with data available for analysis. Number analyzed is the number of participants with data available for analysis at the specified timepoint.

ArmMeasureGroupValue (GEOMETRIC_MEAN)Dispersion
Phase 1: All Participants QDPhase 1: Plasma Drug Concentration at 24 Hours Postdose (C24hr)Cycle 1 Day 1110 ng/mL
Phase 1: All Participants QDPhase 1: Plasma Drug Concentration at 24 Hours Postdose (C24hr)Cycle 1 Day 1555.9 ng/mL
Pralsetinib 400 mg QDPhase 1: Plasma Drug Concentration at 24 Hours Postdose (C24hr)Cycle 1 Day 169.2 ng/mLGeometric Coefficient of Variation 81
Pralsetinib 400 mg QDPhase 1: Plasma Drug Concentration at 24 Hours Postdose (C24hr)Cycle 1 Day 1594.2 ng/mLGeometric Coefficient of Variation 123
Pralsetinib BID Dosing SchedulePhase 1: Plasma Drug Concentration at 24 Hours Postdose (C24hr)Cycle 1 Day 15175 ng/mLGeometric Coefficient of Variation 31.3
Pralsetinib BID Dosing SchedulePhase 1: Plasma Drug Concentration at 24 Hours Postdose (C24hr)Cycle 1 Day 165.8 ng/mLGeometric Coefficient of Variation 59.6
Pralsetinib All DosesPhase 1: Plasma Drug Concentration at 24 Hours Postdose (C24hr)Cycle 1 Day 1104 ng/mLGeometric Coefficient of Variation 76.6
Pralsetinib All DosesPhase 1: Plasma Drug Concentration at 24 Hours Postdose (C24hr)Cycle 1 Day 15137 ng/mLGeometric Coefficient of Variation 132
RET-mutation MTC With No Prior Cabozantinib or Vandetanib TreatmentPhase 1: Plasma Drug Concentration at 24 Hours Postdose (C24hr)Cycle 1 Day 1221 ng/mLGeometric Coefficient of Variation 64.2
RET-mutation MTC With No Prior Cabozantinib or Vandetanib TreatmentPhase 1: Plasma Drug Concentration at 24 Hours Postdose (C24hr)Cycle 1 Day 15713 ng/mLGeometric Coefficient of Variation 42.2
RET-fusion Positive TCPhase 1: Plasma Drug Concentration at 24 Hours Postdose (C24hr)Cycle 1 Day 1376 ng/mLGeometric Coefficient of Variation 74.1
RET-fusion Positive TCPhase 1: Plasma Drug Concentration at 24 Hours Postdose (C24hr)Cycle 1 Day 15977 ng/mLGeometric Coefficient of Variation 107
RET-fusion Positive Solid Tumors Other Than NSCLC and TCPhase 1: Plasma Drug Concentration at 24 Hours Postdose (C24hr)Cycle 1 Day 151950 ng/mL
RET-fusion Positive Solid Tumors Other Than NSCLC and TCPhase 1: Plasma Drug Concentration at 24 Hours Postdose (C24hr)Cycle 1 Day 1715 ng/mLGeometric Coefficient of Variation 75.9
Secondary

Phase 1: Terminal Elimination Half-Life (t½)

The maximum values for t1/2 slightly exceed 24 hours because the analysis used the actual time, i.e., the duration between dosing and actual sample collection, rather than the nominal sampling time of 24 hours specified in the protocol. The timeframe has been given as per nominal sampling timepoints pre-specified in the protocol. Number of participants in each arm of this OM is based on the actual treatment received. 1 participant originally assigned to the 200/100 mg arm received the 100/100 mg treatment and hence, was counted under the 100/100 mg arm for this OM.

Time frame: Predose on 0.5, 1, 2, 4, 6, 8 and 24 hours postdose on Days 1 and 15 of Cycle 1 (1 cycle = 28 days)

Population: PK evaluable population included all participants who received at least one dose of pralsetinib and from whom at least one post dose PK sample was collected. Overall number analyzed is the number of participants with data available for analysis. Number analyzed is the number of participants with data available for analysis at the specified timepoint.

ArmMeasureGroupValue (MEDIAN)
Phase 1: All Participants QDPhase 1: Terminal Elimination Half-Life (t½)Cycle 1 Day 116.3 hours
Phase 1: All Participants QDPhase 1: Terminal Elimination Half-Life (t½)Cycle 1 Day 1517.6 hours
Pralsetinib 400 mg QDPhase 1: Terminal Elimination Half-Life (t½)Cycle 1 Day 19.87 hours
Pralsetinib 400 mg QDPhase 1: Terminal Elimination Half-Life (t½)Cycle 1 Day 158.10 hours
Pralsetinib BID Dosing SchedulePhase 1: Terminal Elimination Half-Life (t½)Cycle 1 Day 1513.4 hours
Pralsetinib BID Dosing SchedulePhase 1: Terminal Elimination Half-Life (t½)Cycle 1 Day 114.3 hours
Pralsetinib All DosesPhase 1: Terminal Elimination Half-Life (t½)Cycle 1 Day 1513.2 hours
Pralsetinib All DosesPhase 1: Terminal Elimination Half-Life (t½)Cycle 1 Day 112.6 hours
RET-mutation MTC With No Prior Cabozantinib or Vandetanib TreatmentPhase 1: Terminal Elimination Half-Life (t½)Cycle 1 Day 112.2 hours
RET-mutation MTC With No Prior Cabozantinib or Vandetanib TreatmentPhase 1: Terminal Elimination Half-Life (t½)Cycle 1 Day 1520.4 hours
RET-fusion Positive TCPhase 1: Terminal Elimination Half-Life (t½)Cycle 1 Day 116.5 hours
RET-fusion Positive TCPhase 1: Terminal Elimination Half-Life (t½)Cycle 1 Day 1520.9 hours
RET-fusion Positive Solid Tumors Other Than NSCLC and TCPhase 1: Terminal Elimination Half-Life (t½)Cycle 1 Day 1513.0 hours
RET-fusion Positive Solid Tumors Other Than NSCLC and TCPhase 1: Terminal Elimination Half-Life (t½)Cycle 1 Day 119.7 hours
RET-mutation Positive Tumors Other Than MTCPhase 1: Terminal Elimination Half-Life (t½)Cycle 1 Day 110.7 hours
Secondary

Phase 1: Time of Last Quantifiable Plasma Drug Concentration (Tlast)

The maximum values for Tlast slightly exceed 24 hours because the analysis used the actual time, i.e., the duration between dosing and actual sample collection, rather than the nominal sampling time of 24 hours specified in the protocol. The timeframe has been given as per nominal sampling timepoints pre-specified in the protocol. Number of participants in each arm of this OM is based on the actual treatment received. 1 participant originally assigned to the 200/100 mg arm received the 100/100 mg treatment and hence, was counted under the 100/100 mg arm for this OM.

Time frame: Predose on 0.5, 1, 2, 4, 6, 8 and 24 hours postdose on Days 1 and 15 of Cycle 1 (1 cycle = 28 days)

Population: PK evaluable population included all participants who received at least one dose of pralsetinib and from whom at least one post dose PK sample was collected. Number analyzed is the number of participants with data available for analysis at the specified timepoint.

ArmMeasureGroupValue (MEDIAN)
Phase 1: All Participants QDPhase 1: Time of Last Quantifiable Plasma Drug Concentration (Tlast)Cycle 1 Day 124.0 hours
Phase 1: All Participants QDPhase 1: Time of Last Quantifiable Plasma Drug Concentration (Tlast)Cycle 1 Day 1523.8 hours
Pralsetinib 400 mg QDPhase 1: Time of Last Quantifiable Plasma Drug Concentration (Tlast)Cycle 1 Day 124.0 hours
Pralsetinib 400 mg QDPhase 1: Time of Last Quantifiable Plasma Drug Concentration (Tlast)Cycle 1 Day 1524.1 hours
Pralsetinib BID Dosing SchedulePhase 1: Time of Last Quantifiable Plasma Drug Concentration (Tlast)Cycle 1 Day 124.0 hours
Pralsetinib BID Dosing SchedulePhase 1: Time of Last Quantifiable Plasma Drug Concentration (Tlast)Cycle 1 Day 1524.3 hours
Pralsetinib All DosesPhase 1: Time of Last Quantifiable Plasma Drug Concentration (Tlast)Cycle 1 Day 124.0 hours
Pralsetinib All DosesPhase 1: Time of Last Quantifiable Plasma Drug Concentration (Tlast)Cycle 1 Day 1524.0 hours
RET-mutation MTC With No Prior Cabozantinib or Vandetanib TreatmentPhase 1: Time of Last Quantifiable Plasma Drug Concentration (Tlast)Cycle 1 Day 123.8 hours
RET-mutation MTC With No Prior Cabozantinib or Vandetanib TreatmentPhase 1: Time of Last Quantifiable Plasma Drug Concentration (Tlast)Cycle 1 Day 1524.0 hours
RET-fusion Positive TCPhase 1: Time of Last Quantifiable Plasma Drug Concentration (Tlast)Cycle 1 Day 1524.0 hours
RET-fusion Positive TCPhase 1: Time of Last Quantifiable Plasma Drug Concentration (Tlast)Cycle 1 Day 123.8 hours
RET-fusion Positive Solid Tumors Other Than NSCLC and TCPhase 1: Time of Last Quantifiable Plasma Drug Concentration (Tlast)Cycle 1 Day 1524.1 hours
RET-fusion Positive Solid Tumors Other Than NSCLC and TCPhase 1: Time of Last Quantifiable Plasma Drug Concentration (Tlast)Cycle 1 Day 123.9 hours
RET-altered Solid Tumors Previously Treated With RET InhibitorPhase 1: Time of Last Quantifiable Plasma Drug Concentration (Tlast)Cycle 1 Day 112.5 hours
RET-altered Solid Tumors Previously Treated With RET InhibitorPhase 1: Time of Last Quantifiable Plasma Drug Concentration (Tlast)Cycle 1 Day 1512.2 hours
RET-mutation Positive Tumors Other Than MTCPhase 1: Time of Last Quantifiable Plasma Drug Concentration (Tlast)Cycle 1 Day 112.3 hours
RET-mutation Positive Tumors Other Than MTCPhase 1: Time of Last Quantifiable Plasma Drug Concentration (Tlast)Cycle 1 Day 1512.5 hours
Secondary

Phase 1: Time to Maximum Plasma Concentration (Tmax)

Number of participants in each arm of this OM is based on the actual treatment received. 1 participant originally assigned to the 200/100 mg arm received the 100/100 mg treatment and hence, was counted under the 100/100 mg arm for this OM.

Time frame: Predose on 0.5, 1, 2, 4, 6, 8 and 24 hours postdose on Days 1 and 15 of Cycle 1 (1 cycle = 28 days)

Population: PK evaluable population included all participants who received at least one dose of pralsetinib and from whom at least one post dose PK sample was collected. Number analyzed is the number of participants with data available for analysis at the specified timepoint.

ArmMeasureGroupValue (MEDIAN)
Phase 1: All Participants QDPhase 1: Time to Maximum Plasma Concentration (Tmax)Cycle 1 Day 13.04 hour
Phase 1: All Participants QDPhase 1: Time to Maximum Plasma Concentration (Tmax)Cycle 1 Day 151.87 hour
Pralsetinib 400 mg QDPhase 1: Time to Maximum Plasma Concentration (Tmax)Cycle 1 Day 12.04 hour
Pralsetinib 400 mg QDPhase 1: Time to Maximum Plasma Concentration (Tmax)Cycle 1 Day 152.00 hour
Pralsetinib BID Dosing SchedulePhase 1: Time to Maximum Plasma Concentration (Tmax)Cycle 1 Day 12.03 hour
Pralsetinib BID Dosing SchedulePhase 1: Time to Maximum Plasma Concentration (Tmax)Cycle 1 Day 153.97 hour
Pralsetinib All DosesPhase 1: Time to Maximum Plasma Concentration (Tmax)Cycle 1 Day 12.07 hour
Pralsetinib All DosesPhase 1: Time to Maximum Plasma Concentration (Tmax)Cycle 1 Day 152.97 hour
RET-mutation MTC With No Prior Cabozantinib or Vandetanib TreatmentPhase 1: Time to Maximum Plasma Concentration (Tmax)Cycle 1 Day 12.02 hour
RET-mutation MTC With No Prior Cabozantinib or Vandetanib TreatmentPhase 1: Time to Maximum Plasma Concentration (Tmax)Cycle 1 Day 152.23 hour
RET-fusion Positive TCPhase 1: Time to Maximum Plasma Concentration (Tmax)Cycle 1 Day 153.03 hour
RET-fusion Positive TCPhase 1: Time to Maximum Plasma Concentration (Tmax)Cycle 1 Day 13.00 hour
RET-fusion Positive Solid Tumors Other Than NSCLC and TCPhase 1: Time to Maximum Plasma Concentration (Tmax)Cycle 1 Day 156.00 hour
RET-fusion Positive Solid Tumors Other Than NSCLC and TCPhase 1: Time to Maximum Plasma Concentration (Tmax)Cycle 1 Day 12.00 hour
RET-altered Solid Tumors Previously Treated With RET InhibitorPhase 1: Time to Maximum Plasma Concentration (Tmax)Cycle 1 Day 112.5 hour
RET-altered Solid Tumors Previously Treated With RET InhibitorPhase 1: Time to Maximum Plasma Concentration (Tmax)Cycle 1 Day 152.00 hour
RET-mutation Positive Tumors Other Than MTCPhase 1: Time to Maximum Plasma Concentration (Tmax)Cycle 1 Day 112.0 hour
RET-mutation Positive Tumors Other Than MTCPhase 1: Time to Maximum Plasma Concentration (Tmax)Cycle 1 Day 154.03 hour
Secondary

Phase 2: AUC0-24

Time frame: 24 hours postdose on Days 1 and 15 of Cycle 1 (1 cycle = 28 days)

Population: PK evaluable population included all participants who received at least one dose of pralsetinib and from whom at least one post dose PK sample was collected. Overall number analyzed is the number of participants with data available for analysis. Number analyzed is the number of participants with data available for analysis at the specified timepoint.

ArmMeasureGroupValue (GEOMETRIC_MEAN)Dispersion
Phase 1: All Participants QDPhase 2: AUC0-24Cycle 1 Day 120400 hours*ng/mLGeometric Coefficient of Variation 64.2
Phase 1: All Participants QDPhase 2: AUC0-24Cycle 1 Day 1540100 hours*ng/mLGeometric Coefficient of Variation 59.5
Pralsetinib 400 mg QDPhase 2: AUC0-24Cycle 1 Day 1533900 hours*ng/mLGeometric Coefficient of Variation 27.4
Pralsetinib 400 mg QDPhase 2: AUC0-24Cycle 1 Day 117400 hours*ng/mLGeometric Coefficient of Variation 152
Pralsetinib BID Dosing SchedulePhase 2: AUC0-24Cycle 1 Day 1103000 hours*ng/mL
Pralsetinib BID Dosing SchedulePhase 2: AUC0-24Cycle 1 Day 1591100 hours*ng/mLGeometric Coefficient of Variation 46.8
Pralsetinib All DosesPhase 2: AUC0-24Cycle 1 Day 118400 hours*ng/mLGeometric Coefficient of Variation 69.8
Pralsetinib All DosesPhase 2: AUC0-24Cycle 1 Day 1532000 hours*ng/mLGeometric Coefficient of Variation 90.8
Secondary

Phase 2: C24hr

Time frame: 24 hours postdose on Days 1 and 15 of Cycle 1 (1 cycle = 28 days)

Population: PK evaluable population included all participants who received at least one dose of pralsetinib and from whom at least one post dose PK sample was collected. Overall number analyzed is the number of participants with data available for analysis. Number analyzed is the number of participants with data available for analysis at the specified timepoint.

ArmMeasureGroupValue (GEOMETRIC_MEAN)Dispersion
Phase 1: All Participants QDPhase 2: C24hrCycle 1 Day 1540 ng/mLGeometric Coefficient of Variation 75.4
Phase 1: All Participants QDPhase 2: C24hrCycle 1 Day 151150 ng/mLGeometric Coefficient of Variation 69
Pralsetinib 400 mg QDPhase 2: C24hrCycle 1 Day 15797 ng/mLGeometric Coefficient of Variation 42.8
Pralsetinib 400 mg QDPhase 2: C24hrCycle 1 Day 1519 ng/mLGeometric Coefficient of Variation 197
Pralsetinib BID Dosing SchedulePhase 2: C24hrCycle 1 Day 11020 ng/mLGeometric Coefficient of Variation 225
Pralsetinib BID Dosing SchedulePhase 2: C24hrCycle 1 Day 151400 ng/mLGeometric Coefficient of Variation 207
Pralsetinib All DosesPhase 2: C24hrCycle 1 Day 1415 ng/mLGeometric Coefficient of Variation 140
Pralsetinib All DosesPhase 2: C24hrCycle 1 Day 151050 ng/mLGeometric Coefficient of Variation 94
Secondary

Phase 2: CBR

CBR was defined as the percentage of participants with CR or PR, or SD which has been lasting at least 16 weeks (i.e. 4 cycles if 28 days are in one cycle) from the first dose date. CR was defined as the disappearance of all target lesions or any pathological lymph nodes (whether target or non-target) having a reduction in the short axis to \<10 mm. PR was defined as at least a 30% decrease in the SOD of all target lesions, taking as reference the baseline SOD, in the absence of CR. SD was defined as neither sufficient shrinkage to qualify for CR or PR nor sufficient increase to qualify for PD. PD was defined as at least a 20% increase in SOD of target lesions, taking as reference the smallest SOD on study (including baseline). CBR and its two-sided 95% CI, which is based on the exact binomial distribution (Clopper-Pearson), were presented.

Time frame: Up to approximately 79.8 months

Population: RET-altered measurable disease population included participants in the efficacy population who have measurable (target) disease per RECIST v1.1, at baseline according to BICR and sufficient evidence of a RET alteration. As prespecified in the SAP, Phase 1 participants treated at 400 mg QD are pooled with Phase 2 participants for efficacy analysis.

ArmMeasureValue (NUMBER)
Phase 1: All Participants QDPhase 2: CBR74.6 percentage of participants
Pralsetinib 400 mg QDPhase 2: CBR78.3 percentage of participants
Pralsetinib BID Dosing SchedulePhase 2: CBR80.2 percentage of participants
Pralsetinib All DosesPhase 2: CBR80.0 percentage of participants
RET-mutation MTC With No Prior Cabozantinib or Vandetanib TreatmentPhase 2: CBR90.3 percentage of participants
RET-fusion Positive TCPhase 2: CBR85.2 percentage of participants
RET-fusion Positive Solid Tumors Other Than NSCLC and TCPhase 2: CBR60.7 percentage of participants
RET-altered Solid Tumors Previously Treated With RET InhibitorPhase 2: CBR28.6 percentage of participants
RET-mutation Positive Tumors Other Than MTCPhase 2: CBR23.1 percentage of participants
Secondary

Phase 2: CL/F

Time frame: Predose on 0.5, 1, 2, 4, 6, 8 and 24 hours postdose on Days 1 and 15 of Cycle 1 (1 cycle = 28 days)

Population: PK evaluable population included all participants who received at least one dose of pralsetinib and from whom at least one post dose PK sample was collected. Overall number analyzed is the number of participants with data available for analysis. Number analyzed is the number of participants with data available for analysis at the specified timepoint.

ArmMeasureGroupValue (GEOMETRIC_MEAN)Dispersion
Phase 1: All Participants QDPhase 2: CL/FCycle 1 Day 113.4 liters per hour (L/hour)Geometric Coefficient of Variation 56.8
Phase 1: All Participants QDPhase 2: CL/FCycle 1 Day 159.91 liters per hour (L/hour)Geometric Coefficient of Variation 58.9
Pralsetinib 400 mg QDPhase 2: CL/FCycle 1 Day 157.49 liters per hour (L/hour)Geometric Coefficient of Variation 64.4
Pralsetinib 400 mg QDPhase 2: CL/FCycle 1 Day 112.7 liters per hour (L/hour)Geometric Coefficient of Variation 347
Pralsetinib BID Dosing SchedulePhase 2: CL/FCycle 1 Day 12.00 liters per hour (L/hour)
Pralsetinib BID Dosing SchedulePhase 2: CL/FCycle 1 Day 152.92 liters per hour (L/hour)
Pralsetinib All DosesPhase 2: CL/FCycle 1 Day 116.1 liters per hour (L/hour)Geometric Coefficient of Variation 43.3
Pralsetinib All DosesPhase 2: CL/FCycle 1 Day 151.39 liters per hour (L/hour)Geometric Coefficient of Variation 1220
Secondary

Phase 2: Cmax

Time frame: Predose on 0.5, 1, 2, 4, 6, 8 and 24 hours postdose on Days 1 and 15 of Cycle 1 (1 cycle = 28 days)

Population: PK evaluable population included all participants who received at least one dose of pralsetinib and from whom at least one post dose PK sample was collected. Overall number analyzed is the number of participants with data available for analysis. Number analyzed is the number of participants with data available for analysis at the specified timepoint.

ArmMeasureGroupValue (GEOMETRIC_MEAN)Dispersion
Phase 1: All Participants QDPhase 2: CmaxCycle 1 Day 11680 ng/mLGeometric Coefficient of Variation 69.4
Phase 1: All Participants QDPhase 2: CmaxCycle 1 Day 152840 ng/mLGeometric Coefficient of Variation 50.7
Pralsetinib 400 mg QDPhase 2: CmaxCycle 1 Day 152200 ng/mLGeometric Coefficient of Variation 36.7
Pralsetinib 400 mg QDPhase 2: CmaxCycle 1 Day 11380 ng/mLGeometric Coefficient of Variation 65.4
Pralsetinib BID Dosing SchedulePhase 2: CmaxCycle 1 Day 12450 ng/mLGeometric Coefficient of Variation 164
Pralsetinib BID Dosing SchedulePhase 2: CmaxCycle 1 Day 153440 ng/mLGeometric Coefficient of Variation 93.9
Pralsetinib All DosesPhase 2: CmaxCycle 1 Day 11770 ng/mLGeometric Coefficient of Variation 87.2
Pralsetinib All DosesPhase 2: CmaxCycle 1 Day 152430 ng/mLGeometric Coefficient of Variation 55.3
Secondary

Phase 2: DCR

DCR was defined as the percentage of participants with a confirmed CR/PR, or SD, per RECIST v1.1. CR was defined as the disappearance of all target lesions or any pathological lymph nodes (whether target or non-target) having a reduction in the short axis to \<10 mm. PR was defined as at least a 30% decrease in the SOD of all target lesions, taking as reference the baseline SOD, in the absence of CR. SD was defined as neither sufficient shrinkage to qualify for CR or PR nor sufficient increase to qualify for PD. PD was defined as at least a 20% increase in SOD of target lesions, taking as reference the smallest SOD on study (including baseline). DCR and its two-sided 95% CI, which is based on the exact binomial distribution (Clopper-Pearson), were presented.

Time frame: Up to approximately 79.8 months

Population: RET-altered measurable disease population included participants in the efficacy population who have measurable (target) disease per RECIST v1.1, at baseline according to BICR and sufficient evidence of a RET alteration. As prespecified in the SAP, Phase 1 participants treated at 400 mg QD are pooled with Phase 2 participants for efficacy analysis.

ArmMeasureValue (NUMBER)
Phase 1: All Participants QDPhase 2: DCR91.5 percentage of participants
Pralsetinib 400 mg QDPhase 2: DCR91.3 percentage of participants
Pralsetinib BID Dosing SchedulePhase 2: DCR89.6 percentage of participants
Pralsetinib All DosesPhase 2: DCR95.0 percentage of participants
RET-mutation MTC With No Prior Cabozantinib or Vandetanib TreatmentPhase 2: DCR93.1 percentage of participants
RET-fusion Positive TCPhase 2: DCR96.3 percentage of participants
RET-fusion Positive Solid Tumors Other Than NSCLC and TCPhase 2: DCR75.0 percentage of participants
RET-altered Solid Tumors Previously Treated With RET InhibitorPhase 2: DCR42.9 percentage of participants
RET-mutation Positive Tumors Other Than MTCPhase 2: DCR69.2 percentage of participants
Secondary

Phase 2: DOR

DOR was defined as the time from first documented response (CR/PR) to the date of first documented PD or death due to any cause, whichever occurs first. CR was defined as the disappearance of all target lesions or any pathological lymph nodes (whether target or non-target) having a reduction in the short axis to \<10 mm. PR was defined as at least a 30% decrease in the SOD of all target lesions, taking as reference the baseline SOD, in the absence of CR. PD was defined as at least a 20% increase in SOD of target lesions, taking as reference the smallest SOD on study (including baseline). DOR was analyzed using the KM methods.

Time frame: Up to approximately 79.8 months

Population: RET-altered measurable disease population included participants in the efficacy population who have measurable (target) disease per RECIST v1.1, at baseline according to BICR \& sufficient evidence of a RET alteration. As prespecified in SAP, Phase 1 participants treated at 400 mg QD are pooled with Phase 2 participants for efficacy analysis. Participants who had a response of CR/PR were analyzed in this OM.

ArmMeasureValue (MEDIAN)
Phase 1: All Participants QDPhase 2: DOR31.8 months
Pralsetinib 400 mg QDPhase 2: DOR22.6 months
Pralsetinib BID Dosing SchedulePhase 2: DOR13.4 months
Pralsetinib All DosesPhase 2: DOR21.7 months
RET-mutation MTC With No Prior Cabozantinib or Vandetanib TreatmentPhase 2: DOR51.8 months
RET-fusion Positive TCPhase 2: DORNA months
RET-fusion Positive Solid Tumors Other Than NSCLC and TCPhase 2: DOR11.1 months
RET-altered Solid Tumors Previously Treated With RET InhibitorPhase 2: DORNA months
RET-mutation Positive Tumors Other Than MTCPhase 2: DOR5.5 months
Secondary

Phase 2: Intracranial CBR in RET-fusion Positive NSCLC CNS Metastases Participants

CBR=percentage of participants with CR/PR/SD which has been lasting at least 16 weeks (i.e. 4 cycles if 28 days are in 1 cycle) from first dose date. CR=disappearance of all target CNS/brain lesion, including lesions in brain stem &/ cerebellum identified at baseline&disappearance of all non-target CNS/brain lesion at baseline & no identification of new CNS/brain lesion. PR=at least a 30% decrease in SOD of any CNS/brain lesion, identified as target lesions at baseline & if in absence of unequivocal progression of any non-target CNS/brain lesion at baseline, or identification of new CNS/brain lesion. SD=neither sufficient shrinkage for PR nor sufficient increase for PD for target/non-target CNS/brain lesion, taking as reference smallest SOD while on study. PD=either at least 20% increase in SOD of target CNS/brain lesion, taking as reference smallest sum on study. Unequivocal progression of any CNS/brain lesion nontarget lesions at baseline, or identification of new CNS/brain lesion.

Time frame: Up to approximately 79.8 months

Population: RET-altered measurable disease population included participants in the efficacy population who have measurable (target) disease per RECIST v1.1, at baseline according to BICR and sufficient evidence of a RET alteration. As specified in the SAP, CBR was to be assessed in RET-fusion CNS metastases sub-population (participants with CNS metastases) only. Hence only NSCLC arms are presented here. Phase 1 participants treated at 400 mg QD are pooled with Phase 2 participants for efficacy analysis.

ArmMeasureValue (NUMBER)
Phase 1: All Participants QDPhase 2: Intracranial CBR in RET-fusion Positive NSCLC CNS Metastases Participants61.5 percentage of participants
Pralsetinib 400 mg QDPhase 2: Intracranial CBR in RET-fusion Positive NSCLC CNS Metastases Participants100 percentage of participants
Pralsetinib BID Dosing SchedulePhase 2: Intracranial CBR in RET-fusion Positive NSCLC CNS Metastases Participants0 percentage of participants
Secondary

Phase 2: Intracranial DCR in RET-fusion Positive NSCLC CNS Metastases Participants

DCR=percentage of participants with a confirmed CR/PR, or SD. CR=disappearance of all target CNS/brain lesion, including lesions in brain stem &/or cerebellum identified at baseline & disappearance of all non-target CNS/brain lesion at baseline & no identification of new CNS/brain lesion. PR =at least a 30% decrease in the SOD of any CNS/brain lesion, identified as RECIST 1.1 target lesions at baseline & if in the absence of unequivocal progression of any non-target CNS/brain lesion at baseline, or the identification of new CNS/brain lesion. SD=neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD for target/non-target CNS/brain lesion, taking as reference the smallest SOD while on study. PD=either at least 20% increase in SOD of target CNS/brain lesion, taking as reference smallest sum on study. Unequivocal progression of any CNS/brain lesion nontarget lesions at baseline, or identification of new CNS/brain lesion.

Time frame: Up to approximately 79.8 months

Population: RET-altered measurable disease population included participants in the efficacy population who have measurable (target) disease per RECIST v1.1, at baseline according to BICR and sufficient evidence of a RET alteration. As specified in the SAP, DCR was to be assessed in RET-fusion CNS metastases sub-population (participants with CNS metastases) only. Hence only NSCLC arms are presented here. Phase 1 participants treated at 400 mg QD are pooled with Phase 2 participants for efficacy analysis.

ArmMeasureValue (NUMBER)
Phase 1: All Participants QDPhase 2: Intracranial DCR in RET-fusion Positive NSCLC CNS Metastases Participants76.9 percentage of participants
Pralsetinib 400 mg QDPhase 2: Intracranial DCR in RET-fusion Positive NSCLC CNS Metastases Participants100 percentage of participants
Pralsetinib BID Dosing SchedulePhase 2: Intracranial DCR in RET-fusion Positive NSCLC CNS Metastases Participants0 percentage of participants
Secondary

Phase 2: Intracranial DOR in RET-fusion Positive NSCLC CNS Metastases Participants

DOR=time from first documented CR/PR to the date of first documented PD/death due to any cause, whichever occurs first. CR=disappearance of all target CNS/brain lesion, including lesions in brain stem &/ cerebellum identified at baseline & disappearance of all non-target CNS/brain lesion at baseline & no identification of new CNS/brain lesion. PR=at least a 30% decrease in SOD of any CNS/brain lesion, identified as RECIST 1.1 target lesions at baseline & if in absence of unequivocal progression of any non-target CNS/brain lesion at baseline, or identification of new CNS/brain lesion. PD=either at least 20% increase in SOD of target CNS/brain lesion, taking as reference smallest sum on study. Unequivocal progression of any CNS/brain lesion nontarget lesions at baseline, or identification of new CNS/brain lesion. DOR was analyzed using the KM methods.

Time frame: Up to approximately 79.8 months

Population: RET-altered measurable disease population=participants in efficacy population who have measurable (target) disease per RECIST v1.1, at baseline according to BICR\&sufficient evidence of a RET alteration. As specified in SAP, DOR was to be assessed in RET-fusion CNS metastases sub-population only. Hence only NSCLC arms are presented here. Participants with a CR/PR were assessed for this OM. Phase 1 participants treated at 400 mg QD are pooled with Phase 2 participants for efficacy analysis.

ArmMeasureValue (MEDIAN)
Phase 1: All Participants QDPhase 2: Intracranial DOR in RET-fusion Positive NSCLC CNS Metastases Participants28.3 months
Pralsetinib 400 mg QDPhase 2: Intracranial DOR in RET-fusion Positive NSCLC CNS Metastases Participants11.3 months
Secondary

Phase 2: Intracranial ORR in RET-fusion Positive NSCLC Central Nervous System (CNS) Metastases Participants

ORR=percentage of participants with CR or PR for at least 2 assessments with at least 28 days apart & no PD in between. CR=disappearance of all target CNS/brain lesion, including lesions in brain stem &/or cerebellum identified at baseline & disappearance of all non-target CNS/brain lesion at baseline & no identification of new CNS/brain lesion. PR =at least a 30% decrease in the SOD of any CNS/brain lesion, identified as RECIST 1.1 target lesions at baseline & if in the absence of unequivocal progression of any non-target CNS/brain lesion at baseline, or the identification of new CNS/brain lesion. PD=either at least 20% increase in the SOD of target CNS/brain lesion, taking as reference the smallest sum on study. In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of at least 5mm or unequivocal progression of any CNS/brain lesion identified as RECIST 1.1 nontarget lesions at baseline, or the identification of new CNS/brain lesion.

Time frame: Up to approximately 79.8 months

Population: RET-altered measurable disease population included participants in the efficacy population who have measurable (target) disease per RECIST v1.1, at baseline according to BICR and sufficient evidence of a RET alteration. As specified in the SAP, ORR was to be assessed in RET-fusion CNS metastases sub-population (participants with CNS metastases) only. Hence only NSCLC arms are presented here. Phase 1 participants treated at 400 mg QD are pooled with Phase 2 participants for efficacy analysis.

ArmMeasureValue (NUMBER)
Phase 1: All Participants QDPhase 2: Intracranial ORR in RET-fusion Positive NSCLC Central Nervous System (CNS) Metastases Participants53.8 percentage of participants
Pralsetinib 400 mg QDPhase 2: Intracranial ORR in RET-fusion Positive NSCLC Central Nervous System (CNS) Metastases Participants100 percentage of participants
Pralsetinib BID Dosing SchedulePhase 2: Intracranial ORR in RET-fusion Positive NSCLC Central Nervous System (CNS) Metastases Participants0 percentage of participants
Secondary

Phase 2: Overall Survival (OS)

OS was defined as the time from the first dose of pralsetinib to the date of death due to any causes.

Time frame: Up to approximately 7 years

Population: Efficacy population included all participants who have been exposed to at least one dose of the study drug at the RP2D. As pre-specified in the SAP, OS was to be assessed in participants with RET-fusion positive NSCLC, RET-mutation MTC, RET-fusion TC, and RET-fusion solid tumors other than NSCLC and TC. Hence, only the data for these arms is presented here.

ArmMeasureValue (MEDIAN)
Phase 1: All Participants QDPhase 2: Overall Survival (OS)39.7 months
Pralsetinib 400 mg QDPhase 2: Overall Survival (OS)46.0 months
Pralsetinib BID Dosing SchedulePhase 2: Overall Survival (OS)50.1 months
Pralsetinib All DosesPhase 2: Overall Survival (OS)42.2 months
RET-mutation MTC With No Prior Cabozantinib or Vandetanib TreatmentPhase 2: Overall Survival (OS)NA months
RET-fusion Positive TCPhase 2: Overall Survival (OS)NA months
RET-fusion Positive Solid Tumors Other Than NSCLC and TCPhase 2: Overall Survival (OS)10.3 months
Secondary

Phase 2: Progression-free Survival (PFS)

PFS was defined as the time from the first dose of pralsetinib to the date of first documented PD or death due to any cause, whichever occurred first. PD was defined as at least a 20% increase in SOD of target lesions, taking as reference the smallest SOD on study (including baseline). PFS was analyzed using KM methods.

Time frame: Up to approximately 7 years

Population: Efficacy population included all participants who have been exposed to at least one dose of the study drug at the RP2D. As pre-specified in the SAP, PFS was to be assessed in participants with RET-fusion positive NSCLC, RET-mutation MTC, RET-fusion TC, and RET-fusion solid tumors other than NSCLC and TC. Hence, only the data for these arms is presented here. Overall number analyzed is the number of participants with data available for analysis.

ArmMeasureValue (MEDIAN)
Phase 1: All Participants QDPhase 2: Progression-free Survival (PFS)16.4 months
Pralsetinib 400 mg QDPhase 2: Progression-free Survival (PFS)13.0 months
Pralsetinib BID Dosing SchedulePhase 2: Progression-free Survival (PFS)12.1 months
Pralsetinib All DosesPhase 2: Progression-free Survival (PFS)24.9 months
RET-mutation MTC With No Prior Cabozantinib or Vandetanib TreatmentPhase 2: Progression-free Survival (PFS)55.3 months
RET-fusion Positive TCPhase 2: Progression-free Survival (PFS)NA months
RET-fusion Positive Solid Tumors Other Than NSCLC and TCPhase 2: Progression-free Survival (PFS)7.0 months
Secondary

Phase 2: t½

The maximum values for t1/2 slightly exceed 24 hours because the analysis used the actual time, i.e., the duration between dosing and actual sample collection, rather than the nominal sampling time of 24 hours specified in the protocol. The timeframe has been given as per nominal sampling timepoints pre-specified in the protocol.

Time frame: Predose on 0.5, 1, 2, 4, 6, 8 and 24 hours postdose on Days 1 and 15 of Cycle 1 (1 cycle = 28 days)

Population: PK evaluable population included all participants who received at least one dose of pralsetinib and from whom at least one post dose PK sample was collected. Overall number analyzed is the number of participants with data available for analysis. Number analyzed is the number of participants with data available for analysis at the specified timepoint.

ArmMeasureGroupValue (GEOMETRIC_MEAN)Dispersion
Phase 1: All Participants QDPhase 2: t½Cycle 1 Day 113.4 hoursGeometric Coefficient of Variation 44.1
Phase 1: All Participants QDPhase 2: t½Cycle 1 Day 1517.9 hoursGeometric Coefficient of Variation 58.8
Pralsetinib 400 mg QDPhase 2: t½Cycle 1 Day 1516.5 hoursGeometric Coefficient of Variation 44.6
Pralsetinib 400 mg QDPhase 2: t½Cycle 1 Day 118.4 hoursGeometric Coefficient of Variation 98.8
Pralsetinib BID Dosing SchedulePhase 2: t½Cycle 1 Day 120.8 hours
Pralsetinib BID Dosing SchedulePhase 2: t½Cycle 1 Day 1525.8 hours
Pralsetinib All DosesPhase 2: t½Cycle 1 Day 111.0 hoursGeometric Coefficient of Variation 55.8
Pralsetinib All DosesPhase 2: t½Cycle 1 Day 1563.0 hoursGeometric Coefficient of Variation 882
Secondary

Phase 2: Tlast

The maximum values for Tlast slightly exceed 24 hours because the analysis used the actual time, i.e., the duration between dosing and actual sample collection, rather than the nominal sampling time of 24 hours specified in the protocol. The timeframe has been given as per nominal sampling timepoints pre-specified in the protocol.

Time frame: Predose on 0.5, 1, 2, 4, 6, 8 and 24 hours postdose on Days 1 and 15 of Cycle 1 (1 cycle = 28 days)

Population: PK evaluable population included all participants who received at least one dose of pralsetinib and from whom at least one post dose PK sample was collected. Overall number analyzed is the number of participants with data available for analysis. Number analyzed is the number of participants with data available for analysis at the specified timepoint.

ArmMeasureGroupValue (MEDIAN)
Phase 1: All Participants QDPhase 2: TlastCycle 1 Day 123.9 hours
Phase 1: All Participants QDPhase 2: TlastCycle 1 Day 1523.8 hours
Pralsetinib 400 mg QDPhase 2: TlastCycle 1 Day 1523.70 hours
Pralsetinib 400 mg QDPhase 2: TlastCycle 1 Day 18.00 hours
Pralsetinib BID Dosing SchedulePhase 2: TlastCycle 1 Day 123.10 hours
Pralsetinib BID Dosing SchedulePhase 2: TlastCycle 1 Day 1524.00 hours
Pralsetinib All DosesPhase 2: TlastCycle 1 Day 18.05 hours
Pralsetinib All DosesPhase 2: TlastCycle 1 Day 1524.00 hours
Secondary

Phase 2: Tmax

Time frame: Predose on 0.5, 1, 2, 4, 6, 8 and 24 hours postdose on Days 1 and 15 of Cycle 1 (1 cycle = 28 days)

Population: PK evaluable population included all participants who received at least one dose of pralsetinib and from whom at least one post dose PK sample was collected. Overall number analyzed is the number of participants with data available for analysis. Number analyzed is the number of participants with data available for analysis at the specified timepoint.

ArmMeasureGroupValue (MEDIAN)
Phase 1: All Participants QDPhase 2: TmaxCycle 1 Day 14.00 hours
Phase 1: All Participants QDPhase 2: TmaxCycle 1 Day 154.00 hours
Pralsetinib 400 mg QDPhase 2: TmaxCycle 1 Day 155.00 hours
Pralsetinib 400 mg QDPhase 2: TmaxCycle 1 Day 13.90 hours
Pralsetinib BID Dosing SchedulePhase 2: TmaxCycle 1 Day 14.0 hours
Pralsetinib BID Dosing SchedulePhase 2: TmaxCycle 1 Day 154.00 hours
Pralsetinib All DosesPhase 2: TmaxCycle 1 Day 12.05 hours
Pralsetinib All DosesPhase 2: TmaxCycle 1 Day 153.05 hours

Source: ClinicalTrials.gov · Data processed: May 29, 2026