AI
Saturday, January 12, 2019 4:20:29 PM
As the Vice Chairman, he will advance and accelerate the Company’s initiatives in seeking non-dilutive licensing opportunities in cancer and immunology. His expanded leadership role will further leverage the Company’s ability to form strategic partnerships and further the clinical development of leronlimab (PRO 140) in cancer and immunology.
I agree NP has some issues with reality not matching his statements, though you might not want brutal honesty in that situation. From listening to his responses in the ccs, he lacks tact and patience.
Here is my take on the money issue though. The CCR5/HIV funding is dead, even with a more seasoned CEO, I'm not sure how successful in the past they would have been. Just like cypto was hot last year, CCR5/HIV was hot in the early 2000s after the CCR5/HIV link along with CCR5-delta 32 was found. BP was putting big money into it, many different compounds were developed, refined. GSK with aplaviroc, Schering-Plough with vicriviroc, and Pfizer with maraviroc.
Aplaviroc had liver toxicity and poor efficacy and discontinued their trails.
http://www.thebody.com/content/art39205.html
Vicriviroc was canceled phase 3 for possibly both side-effects and efficacy.
Maraviroc was approved but sales never reached full potential.
After these failures, concerns with bad side-effects with all these ccr5 antagonist, BP gave up on CCR5/HIV. They have been very skeptical on success. Pro 140 was picked up cheap, because it had been shelved. Few was believing the CCR5 story could be successful.
Where BP was wrong (IMO).
This paper hit it on the head:
https://www.sciencedirect.com/science/article/pii/S1093326307001891
Paraphrase from wiki:
To limit the toxicity and side effects of CCR5 antagonists it would be ideal to be able to preserve the chemokine receptor function. Consequently, it should be of interest to design inhibitors that specifically disrupt CCR5–gp120 binding but do not affect the CCR5 chemokine activation
So a partial CCR5 inhibitor allowing chemokine activity instead of a full antagonist.
Unlike those, Leronlimab is a monoclonal antibody, is a partial inhibitor, is competitive rather than allosteric. We now have mono trial results are shown with 90% for 700mg, the safety allowing a large enough dose to reach a good efficacy. Once the pivotal trial is approved, the BP assumptions will be proven wrong.
Interesting enough Leronlimab allows chemokine reaction. The current research suggests this activity enables cancer metastasis. So one might expect Leronlimab would not work well with cancer as the other full CCR5 antagonists, as it does not block the activity.
But RP last year, did his DD before joining CYDY, testing Leronlimab with both colon and breast cancer.
https://www.cytodyn.com/media/press-releases/detail/280/new-research-supports-potential-for-cytodyns-pro-140-to
The blocking of breast cancer invasion with PRO 140 was as effective as with small molecule CCR5 inhibitors in our prior published studies.
https://www.cytodyn.com/media/press-releases/detail/288/cytodyn-announces-strong-preclinical-results-using-pro-140
PRO 140 extended the life of treated mice and decreased tumor growth compared to control mice by greater than 50%, which was statistically significant. These results were dose dependent and were repeated in separate experiments.
Why does it work? Seemly the holy grail, little side effects allowing chemokine activity to function as normal, but still works with cancer and GvHD. Kind of a mystery to me.
RP also announced in the last PR they are trying to figure out why:
Current ongoing preclinical studies are defining the mechanisms involved in the anti-tumor efficacy of PRO 140.
Last (too long didn't read version): CCR5/Cancer is hot in 2019 with BP. Luckily CYDY will be in a hot financial spot, with some good TNBC results, we should be flush with cash opportunities, especially with RP at the helm with those opportunities. Also the HIV/CCR5 story will be resurrected with the pivotal mono trial, against BP assumptions from their past research.
