do you think that could be one of the reasons why
Post# of 153832
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do you think that could be one of the reasons why CytoDyn decided to do a pre-clinical with Trodelvy? We already know how it works with Keytruda, not so much with an ADC.
Trodelvy needs tumor cells that express TROP-2 to be effective since that's what it binds too. But TROP-2 will not necessarily express in all tumor cells even those which typically have a high expression level. Without that binding it cannot deliver it's DNA breaking drug payload. Leronlimab of course has a multitude of different ways of killing tumor cells that could finish off the job that Trodelvy started.
I do have to wonder if leronlimab's switch to the M1 macrophage type that increases PD-L1 from 30 to 90 days in response would also do the same with TROP-2. Both PD-L1 and TROP-2 are associated with the M2 macrophage phenotype which must be initially spiking because of the increase of M1 macrophages around the tumor. If so than leronlimab would increase Trodelvy's ability to kill along with leronlimab's ability to kill.
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What do you think the chances of a triple partnership would be such as G, Merck and CytoDyn?
I think very little of it. Why would Gilead or Merck partner with each other when they could just buy out Cytodyn. Merck's Keytruda is going off patent soon and there are a number of other PD-L1 inhibitors out there that leronlimab would work with. For instance dostarlimab seems superior to Keytruda. The same goes for Gilead there are other Trop-2 targeting drug delivery drugs around, some may be superior. The key to the triple drug cocktail would be leronlimab. Leronlimab has superior binding and no toxicity which all other CCR5 inhibitors lack in one or both cases.
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What do you think of Hope Rego being on both SABs of G and CytoDyn? She has extensive experience with Trodelvy. Do you think they could be considering a threesome? What about Pestell?
I think Dr. Pestell's wife would get upset if he joined a menage a trois.

