Kevetrin does have the long lasting effect of “turning on” the genes in wild type p53. The wild type p53 genes are making functional p53 proteins, but they are blocked/suppressed by the MDM2 proteins. K is small enough to get in the middle of the p53-MDM2 complex, separate the two, thus freeing the p53 protein to do its job.

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I've also wondered if the impact of Kevetrin on the cellular machinery persists well beyond what one would expect based on half lives. In that they are seeing clinical effects with a once weekly dose perhaps suggests this may be the case. I have no idea. To demonstrate clinical efficacy, however, it makes sense to maximize tumor exposure to Kevetrin.

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