wonder how K will be used in AML- for induction or consolidation? I asked CEO and did not get a direct response. Perhaps for consolidation with/without Cytarabine? Will be interesting
Recently saw a potential candidate for K in this regard Much talk about performance status of patients over 60(or was it 65?) for aggressive AML treatments He came in with fatigue/SOB eventual diagnosis AML(monocytic)
An older pt with very decreased blood counts(hematocrit) renal failure etc, frail.
Great research again, slc. High death rate and myelosuppression at higher dosages for RG7388 in a fragile AML patient population. Also, a few complete responses but about 70% with progression of disease. I'm sure they were hoping for a lot better.
It appears that myelosuppression is enough of a problem with RG7388 that it is now entering a Phase 1 trial for polycythemia vera and essential thrombocythemia at a much, much lower dose (100mg/day vs. recommended Phase 2 AML dose of 1200 mg/day. I wonder if RG7388s impact is comparable on leukocytes and erythrocyes. Obviously, safety is still an issue.
I'm not aware that we've seen any myelosuppression with Kevetrin during Phase 1 and I have no idea what we'll see with multiple consecutive day dosing in Phase 2 at Univ of Bologna. Of course, I am hoping for more CRs and fewer deaths in both Kevetrin and Kevetrin/cytarabine arms.
Roche has spent a lot of money on nutlins and they are not performing as Roche would like. Also Roche is possibly only BP who is focused on P53 and for long.
So if K enters P2 with no toxicity and good UoB results - Roche could be the 1st BP to approach CTIX - they have gathered so much knowledge on P53 that they wpuld not like to utilize it with any drug that can be successful.
Yes, that PlosOne article is a real shot in the arm for Kevetrin. If it's right, then Kevetrin fits the bill perfectly since it activates both nuclear and mitochondrial p53, via transcription dependent and independent pathways respectively.