{"classes":[{"categories":[{"measurements":[{"groupId":"OG000","lowerLimit":"37.4","upperLimit":"69.3","value":"53.7"},{"groupId":"OG001","lowerLimit":"58.8","upperLimit":"86.5","value":"74.4"}]}],"denoms":[{"counts":[{"groupId":"OG000","value":"41"},{"groupId":"OG001","value":"43"}],"units":"Participants"}],"title":"M918T"},{"categories":[{"measurements":[{"groupId":"OG000","lowerLimit":"19.2","upperLimit":"74.9","value":"46.2"},{"groupId":"OG001","lowerLimit":"68.8","upperLimit":"97.5","value":"88.0"}]}],"denoms":[{"counts":[{"groupId":"OG000","value":"13"},{"groupId":"OG001","value":"25"}],"units":"Participants"}],"title":"Cysteine Rich Domain"},{"categories":[{"measurements":[{"groupId":"OG000","lowerLimit":"15.8","upperLimit":"100","value":"100"},{"comment":"Since only 1 participant was analyzed upper and lower limit of 95% CI was not evaluable.","groupId":"OG001","lowerLimit":"NA","upperLimit":"NA","value":"0"}]}],"denoms":[{"counts":[{"groupId":"OG000","value":"2"},{"groupId":"OG001","value":"1"}],"units":"Participants"}],"title":"V804X"},{"categories":[{"measurements":[{"groupId":"OG000","lowerLimit":"39.8","upperLimit":"100","value":"100"},{"groupId":"OG001","lowerLimit":"9.4","upperLimit":"99.2","value":"66.7"}]}],"denoms":[{"counts":[{"groupId":"OG000","value":"4"},{"groupId":"OG001","value":"3"}],"units":"Participants"}],"title":"Other"}],"denoms":[{"counts":[{"groupId":"OG000","value":"60"},{"groupId":"OG001","value":"72"}],"units":"Participants"}],"description":"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.","dispersionType":"95% Confidence Interval","groups":[{"description":"Participants who had RET- mutation positive MTC previously treated with either cabozantinib and/or vandetanib therapies received pralsetinib, 400 mg orally, QD until discontinuation due to toxicity, disease progression, or other reasons.","id":"OG000","title":"RET-mutation MTC With Prior Cabozantinib and/or Vandetanib Treatment"},{"description":"Participants who had RET- mutation positive MTC not previously treated with cabozantinib or vandetanib therapies received pralsetinib, 400 mg orally, QD until discontinuation due to toxicity, disease progression, or other reasons.","id":"OG001","title":"RET-mutation MTC With No Prior Cabozantinib or Vandetanib Treatment"}],"paramType":"NUMBER","populationDescription":"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.","reportingStatus":"POSTED","timeFrame":"Up to approximately 79.8 months","title":"Phase 1 and Phase 2: ORR in RET-mutation MTC Participants With Specific RET Gene Status","type":"SECONDARY","unitOfMeasure":"percentage of participants"}