Was just reading sox's nice Q&A with a p53 expert, David Lane.
He talked about the first approach for non-mutated (wild-type) p53. Then mutated p53:
"The second area we’re focused on is trying to target those tumors where p53 gene function is lost. We’re currently investigating a variety of different approaches there – one, and perhaps the most challenging, is trying to get the mutant protein to work again."
Sox said he thought Kevetrin would degrade, or get rid of mutant p53. David Lane says the approach he's thinking is important is to "get the mutant protein to work again" or to restore the lost function. He mentioned the Swedish company and drug APR-246 (PRIMA-1-met), which restores mutant p53 function.
I was just pointing out that we should probably be hoping Kevetrin restores the lost function of mutant p53 instead of degrading this mutated protein. I was mentioning that Kevetrin posters presented at cancer meetings claimed Kevetrin did both things (1) restored mutant p53 function, and (2) degraded mutant p53. Maybe both are important, but it's nice to see an expert's opinion that restoration of function of mutant p53 is the way to go.
It's also nice to follow along with what the competition is doing.
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