Re: adding a good CEO would be a positive sign
Alan I agree. But I really donít see a point of a CEO at this moment. What would that accomplish? Faster data? No. New trials? No. New direction? No.
Maybe a more respected figurehead in the industry? Perhaps. Which might make some street investors more confident. But without data that would just be money wasted. CEOís define a companies path. At this moment we wait on data and no amount of new leadership will change how fast that comes at this point. In fact, if mgt says they will report on all P1ís by end of 1st qtr 2021....then recruitment in all P1ís should be finished because to report end of P1 trials you would have had to had path to ORR and OS data in place in order to have end of P1 meetings with the FDA. Though the P1 trials on clinicaltrials.gov do not indicate full recruitment per their initial N advertised..,I assume they report on what they have recruited 1st qtr next year on what they did recruit in order to talk to the FDA on future P2/P3 rolling trials....which I expect will be funded by big pharma as a codevelopment deal...if big pharma thinks all the P1ís data and all the independent data interesting.
If I recall, in a week or so at ESMO we report more data on melanoma studies. I would like to see data on stage III combo ORR and not just more PFS and OS data on stage IV combo. For me, stage III ORR data might portend future OS and PFS efficacy. Because in past stage IV in combo with Keytruda...all PV-10 injected lesions in that combo resulted in 75% CR. Uninjected lesions only had 8% CR...which gave the logic to back up and inject stage III where all lesions would be injected. This giving the logic of treating in transit mets by first injecting all lesions with combo PV-10 and then adding Keytruda. The further logic is that stage III intransit mets not injected donít get PV-10 and that those intransit mets through the lymph drainage system donít see PV-10 or in systemic drugs until they reach the lymph nodes. They then advance to stage IV. Thatís the theory. Treat earlier in stage III where all lesions can be injected and add Keytruda before traveling to the lymph nodes becomes a problem. Sound logic.
Digressing....most of the industry is on the antibody bandwagon. Targeted antibodies. There is logic to that when you target specific antigens. But what is an antigen? Itís a quality control protein peptide sample of a RNA transcription brought to the cell surface by MHC in order for the immune system to surveillance the inner workings of cell protein manufacturing in order to decide that the cell is working correctly internally. It is the ISO 9000 quality control protocol of the cells RNA transcription code of making correct proteins.
However....what defective gene caused a defective RNA transcription that caused a defective protein being produced that causes breast cancer...doesnít equate to the defective liver cancer gene causing a defective RNA transcription to mfg a defective protein that cause a sample of that to bind to MHC to be brought to the cell surface as a quality control sample known as an antigen.
Thus making specific antibodies is just that....specific. Unless that defective gene is shared between cancers.
Now to circle all this around to our drug. By injecting solid tumors wit PV-10....it kills the solid tumors...they rot...they dissolve..,they release all cancer specific antigens...and start all systemic cascades....which need to be addressed by all checkpoint inhibitors...or also maybe systemic Rose Bengal in the blood stream...which may become a checkpoint inhibitor on its own as far as anti-CTLA4.
Now to agree with you Alan before you criticize. Yes mgt needs to prove and publish all what I posted...or provide another cascade approach I might have missed which shows I missed something.