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CytoDyn Inc CYDY
(Total Views: 415)
Posted On: 06/02/2025 6:47:24 PM
Post# of 153930
Posted By: MGK_2
Re: ohm20 #153790
Yes, I was also thinking that due to the stress response issued by the tumor cells, as a result of leronlimab's initial rampage, PD-L1 was upregulated by the tumor cells. I am also believing that the same "stress response" could cause a similar upregulation in the expression of TROP-2.

If that is found, then, subsequent treatment with Trodelvy assuredly would be better than without the initial leronlimab stressor.

We know that leronlimab reduces fibrosis and scar tissue. Therefore, if it gets rid of that which surrounds some tumors, then Trodelvy has better access.

On the flip side, leronlimab is a VEGF inhibitor and therefore cuts off the blood supply. If the blood supply is cut off, then how does Trodelvy access the interior of the tumor?

Merck and G do have a partnership . It is in HIV. Maybe it could be expanded to simply buy or license leronlimab.

If what we're proposing is correct, the cocktail for cure fails without leronlimab. We can get a cure without trodelvy as we already are. We could get a cure without keytruda, but we aren't sure yet, until the pre-clinical on the combo with Trodelvy pans out. But we can't get a cure without leronlimab.

Do you think Rego, Yam, or Tripathy or Pestell is considering what we're discussing here? Do you think they recommended the pre-clinical with Trodelvy based on what was seen with Keytruda?














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