Quote:
slcimmuno Member Level Friday, 05/26/17 06:11:38 PM
Re: farrell90 post# 183401
Post # of 183419

Indeed - Kevetrin is one of the few promising drug candidates still in the p53 race. And things seem to be getting more exciting as the pathway analyses presented in the 2017 AACR abstract reveals. Kevetrin seems to working on many molecular levels.

http://www.cellceutix.com/s/AACR-2017-complet...7MAR30.pdf

Kevetrin Patent
https://www.google.com/patents/US8338454

Kevetrin vs Cisplatin
https://goo.gl/images/GvfCAG

I keep thinking back to the p53 expert I reached out to a few years back who was less interested in Aprea than Kevetrin, which piqued his attn given it is active in wt and mut p53.

Below his direct comments (luckily never delete most emails) -- that the 1st MDM2 inhibitor (which Kevetrin is, potentially among many other things) approved will change the world.

Now if we could only Partner or Sell Prurisol and/or Brilacidin to go Big with Kevetrin. Would so like to see how K could perform particularly if the oral formulation comes thru.

http://www.cellceutix.com/new-events-and-pres...uppression

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QUOTE

After thoroughly searching the Cellceutix website I could not find how exactly Kevetrin works. The fact that it activates wild type p53 while at the same time inducing degradation of mutant p53 is intriguing and provocative, but without a detailed explanation of the molecular mechanism of action, I can't give an informed opinion.

I am more familiar with PRIMA-1, the parent drug described in Aprea. I am not impressed. The claim is that it specifically reactivates mutant p53, but other have shown that it is not so specific after all, being instead a rather non-specific electrophilic compound with many targets.

I would stick to the various MDM2 inhibitors currently being tested in clinical trials, the first one to gain FDA approval will change the world:

https://www.clinicaltrials.gov/ct2/results?te...rch=Search