Expert Interview
A Third View: A discussion of KIT inhibitors in GIST, including ripretinib (Qinlock)
Ticker(s): DCPHInstitution: University of Miami
- Professor & Associate Director of Research at University of Miami.
- Research is on understanding the mechanisms of action and resistance of imatinib in GIST and other sarcomas with a focus on the discovery and detection of biomarkers for metastasis, progression and resistance to therapy in gastrointestinal stromal tumor (GIST) and other sarcomas including chondrosarcoma, dermatofibrosarcoma protuberans, myxoid liposarcoma, perivascular endothelial cell sarcoma (PEComa), angiomyolipoma, rhabdomyosarcoma and synovial sarcoma.
- Research studies involve the use of novel preoperative/postoperative clinical trials, prospectively acquired tumor tissue, cell lines, archival tissue, as well as collaborations with disciplines such as the genomics facility, surgical oncology, pathology, radiology and interventional radiology.
Why did Qinlock fail in all patients, and may it actually be effective in the subset of KIT Exon 11, and 17 18 mutants?
If Theseus runs a second line trial, beats Sunitinib, and its safety is okay, would 100% of your patients then go on that second line, or would there still be some Sunitinib patients?
Added By: wilson_adminWhat is your opinion regarding Exon nine? It was really striking where Sunitinib did 14 months, and Ripretinib only did 5.5 months on Exon nine.
Is it likely to be repeated when they were on that pivotal phase three study, again for Sunitinib with the selected patients?
Do you have any views on the supportive data of either of THE-630(pan-KIT) or Bezuclastinib(combination with Sunitinib) approaches, and do you think one is more likely than the other?
The company has mentioned second line against Sunitinib, just like Deciphera did. So what do you think this trial probability would be, given that molecule's differentiated platform? You think it would be more likely to be like Deciphera, or more likely that it could have some differentiated PFS?
What is your opinion about Bezuclastinib, to be able to inhibit seven eight, and just combine it with Sunitinib, so you have the same pan-KIT in two molecules?
Would efficacy determine which one you would use, or safety, since that you could avoid Sunitinib with equal, say, if they're equally efficacious, but more safe, would you use THE-630, or if efficacy was better with a Sunitinib Bezuclastinib combo, would that trump the safety advantage?
Do you know of other molecules in the second line GIST that are there already, or will be there soon that are promising?
Does NB003 look as good, or better than THE-630?
Could an ORR of 20%, and some duration, six months get THE-630 approved in a single arm? Were those the right numbers, or the right benchmark that they would need?
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