Not saying that link with mTOR is or isn't worth i
Post# of 155432
(Total Views: 999)
Posted On: 10/09/2020 3:10:57 AM
Not saying that link with mTOR is or isn't worth investigating, it does seem plausible.
But HIV *just happens* to use CCR5 as an entry point into the cell. Targeting CCR5 to block HIV is completely agnostic towards why CCR5 is there in the first place. FDA and/or anyone else doesn't generally need to know any more than that, in the context of HIV... HIV uses CCR5, LLMab prevents viral entry through CCR5 antagonism, done.
But this isn't the context of HIV anymore... We are now looking at CCR5's actual purpose as it pertains to chemotaxis and immune response.
Just the ability to repolarize immune cells, leaving them active but without shutting down the entire immune system, would have massive implications. Preventing mass migration of immune cells to areas under hyperimmune "Cytokine Storm" conditions would be phenomenal, breaking that feedback loop.
LLMab likely does all of that, and that's really all that's needed to downgrade severe reactions to "a common cold"... if it has an antiviral effect for CV19as well, it would boggle the mind. Said another way, the known proposed MOAs, along with the safety profile, suggests LLMab is the superior treatment option, by orders of magnitude... adding antiviral would render the whole class of (ineffective) antivirals moot as well.
Which would be wild. All for it. I just don't know if we need more than two near-miraculous MOAs to get approval. One alone should suffice, considering there are barely any valid MOA confirmation in what the FDA has greenlighted so far.
But HIV *just happens* to use CCR5 as an entry point into the cell. Targeting CCR5 to block HIV is completely agnostic towards why CCR5 is there in the first place. FDA and/or anyone else doesn't generally need to know any more than that, in the context of HIV... HIV uses CCR5, LLMab prevents viral entry through CCR5 antagonism, done.
But this isn't the context of HIV anymore... We are now looking at CCR5's actual purpose as it pertains to chemotaxis and immune response.
Just the ability to repolarize immune cells, leaving them active but without shutting down the entire immune system, would have massive implications. Preventing mass migration of immune cells to areas under hyperimmune "Cytokine Storm" conditions would be phenomenal, breaking that feedback loop.
LLMab likely does all of that, and that's really all that's needed to downgrade severe reactions to "a common cold"... if it has an antiviral effect for CV19as well, it would boggle the mind. Said another way, the known proposed MOAs, along with the safety profile, suggests LLMab is the superior treatment option, by orders of magnitude... adding antiviral would render the whole class of (ineffective) antivirals moot as well.
Which would be wild. All for it. I just don't know if we need more than two near-miraculous MOAs to get approval. One alone should suffice, considering there are barely any valid MOA confirmation in what the FDA has greenlighted so far.
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