<<In that you found the 'early cohort p21 data' not impressive, what would you consider impressive p21 data? I do not know. It's complicated- more p21 may not be better for the patient. Patient response and tumor markers are easier for me to understand.>>
We have indeed discussed Aprea, Nutlins, other p53 activating compounds, kevetrin MOA, and significance of p21 before, but who has time to go back and read every post before they became interested in a stock/company/message board?
Here's a link to some p21 discussion, with some further reading:
I agree that in the end what matters is increased survival (and QOL too, so QALY really should be the measure for all medical treatments, IMO) in these cancer patients. In prior animal work, kevetrin induced p21 increases were correlated with tumor suppression, so it's possibly a good biomarker, and good to look at. As biodoc said, p21 (and the whole of cancer biology in general) is complex. It isn't always that more p21 is better.
Aprea 246 started Phase I/II as a single agent (in blood and prostate cancers), as kevetrin is being studied in its Phase I trial (in Stage 4 solid tumors).
Kevetrin will soon be tried at U Bologna in combo with cytarabine, as the first kevetrin Phase Ib(II?) study.
Perhaps instead kevetrin should be combined with something that reduces p21, as SLC's link to the Cell/Colorado study showed, and as noted here for AML (p53 activator, p21 inhibitor), as previously discussed, without perhaps any need for chemotoxic drugs (hah, didn't say chemo! or did I?):