Glad to see u back too KMBJN - your analyses many pay grades above mine :) Is very interesting to read about these p53 combo-type approaches. Targeting the once-considered "undruggable"... seems we're getting closer and closer.
I recall this is where Aprea (APR-246 / PRIMA-1 MET) is headed as it seems their compound has some toxicity concerns (unlike Kevetrin) as a Monotherapy (like Nutlins) -- below articles, Wiman Group.
Also saw long dormant Aileron posted an abstract at ASCO. Their stapled-peptide approach.
"PRIMA-1 acts to restore the mutant p53 by modifying thiol groups in the core domains of the protein. Its success is well documented, with many studies in different cancer models proving its effectiveness. This, however, is not unanimous, with some questions being raised about its efficacy and other aspects such as possible resistance mechanisms as well as potentially harmful degradation products."
Thanks for posting. The links confirm the need to research basic cell biology in order to find treatments for cancer as well as other disorders.
The research is paying off now that pharmaceuticals such as monoclonal antibodies can be designed to interact with cells on the molecular level to modify pathologic processes.
Kevetrin was discovered in a traditional way by observation of its biologic effect.
It is remarkable how many molecular pathways are affected by Kevetrin. Hopefully the current FDA Phase 2 study will let CTIX further delineate the molecular basis of these interactions and this understanding will lead to better treatments for cancer and other disorders associated with abnormal p53.
Kevetrin's affect on P53, Mdm2, PARP, caspase3, HDAC and other molecules which lead to the death of malignant cells may be a corner stone in the custom design of many cancer treatments.
Links below to an early graphic of the molecular mechanisms of Kevetrin.
News 
Market Data 
Discover 
