Yes, p53 is difficult to figure out. Since its discovery 35 years ago, over 65,000 papers have been written on it! BTW, that David Lane guy knows his stuff. See a recent review article from him about targeting p53:
Unfortunately, no mention of kevetrin there, as far as I saw.
Overall, I agree with you, that it doesn't make sense to want to degrade mutant p53, as then perhaps there would be no function and no apoptosis of tumor cells. This is the "loss of function" that we were thinking about for mutant p53, which would be nice to have restored.
But, biology is not that simple. After some further reading, I have come to understand how degradation of mutant p53 could be helpful. First thing to remember is that there are two alleles (two chromosomes, one each from mom and dad) in each cell, so if one had a mutation in p53, there could be mutant p53 protein and wild-type p53 protein in the same cell.
The mutant form, in addition to losing its function, appears to be more stable, and could interfere with the wild-type p53, as p53 forms into groups of 4 (tetramers). If so, I can see how it would be good to degrade the mutant p53, to allow the wild-type p53 to do its thing.
See the below article for a nice discussion of p53 mutations, and the different effects mutant p53 may have on the cell:
So mutant p53 is bad because: (1) loss of function of normal p53 for apoptosis (2) interference with wild-type p53 and causing it to lose function, thus even worse loss of p53 function in tumor cells (3) "gain of function" which promotes tumor growth in some other way - probably pretty rare, but recently discovered
A drug which "restores function" of mutant p53 would be best, as it would, presumably, take care of all 3 bad qualities of mutant p53 above. If a drug "degrades mutant p53," then it could still be beneficial by #s (2) and (3) above. No restoration of function, but at least it could let the remaining wild type p53 work, and protect from the further oncogenic harmful effects of mutant p53.
It took me a while to understand how degradation could be beneficial, but some of the articles above helped me understand.
I just wish it was clearer how kevetrin is supposed to work. I don't understand how in 2011 they say it stabilizes mutant p53 into a form which still functions, then in 2012 onward say it degrades mutant p53. It will be nice to see some papers published by kevetrin researchers with some further details and desctiptions of its mechanism(s) of action.
Another thing to keep in mind is that there are hundreds or thousands of different p53 mutations, and different drugs will act differently upon these different mutant forms. At some point, it won't be enough to just say p53 mutation, but I imagine they will be categorized, and different drugs will be used for each category of mutation.
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