“For those of you in the know, is Leronlimab eve
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Posted On: 03/09/2024 9:50:49 PM
Re: BuckCYDYLong #141730
“For those of you in the know, is Leronlimab even on the radar of all this research? Given everything I've learned from the collective expertise of this board, seems like Leronlimab would be the "miracle" that these other 2 drugs are not?”
Cool when stuff like that happens, and AARP covers news in AD that’s in our wheelhouse. But to answer you question, I have to split it up a bit into different parts of a response.
First of all, I’m not so much in the know. Certainly when pertaining to investing, but I can kinda nerd out on the science.
The two drugs you mentioned (one of which got further delayed last week), are both attempting to clear Amyloid plaques from the brains and CNS of AD patients. These two may not do much good except delay progression by 6 months or so. They can do a lot of bad like brain swelling and bleeding. The delayed drug candidate for instance, is delayed because the risks have been determined to outway the limited rewards. In my limited opinion, the real problem with both of these drugs as well as the amyloid plaque clearing concept, is a amyloid plaques are a symptom of the disease, not the underlying cause. It’s kinda like frying in fish in the kitchen with the porch door open and complaining about the flies, instead of just frying the fish on the porch and closing the freaking door.
In all serious, nobody yet knows with proof that Leronlimab is a miracle drug for Alzheimer’s. But take a look at the 3 papers discussed this weekend. Ohm’s from Fall 2021, mightyCYDy’s from summer 2022, and dwfl28’s from end of last year. They all studied Maravoric in mice with some good results.
Maravoric isn’t an Amyloid Plaque focused drug. It’s an HIV drug with promising anti inflammatory properties (sorry, can’t describe its exact MOA, but I think an allosteric CCR5 inhibitor). It’s getting some really interesting results in mice (murine) studies over time in AD.
Leronlimab is a competitive CCR5 inhibitor, so similar to Maravoric. But better, in theory. We don’t cause kidney, or liver damage for instance. And we allow chemotaxis to continue, while antagonizing the receptor.
So is Leronlimab even on the radar of the people doing the research? If they are studying Maravoric in Alzheimer’s you can be damn sure they are aware of Leronlimab and probably would prefer to use it if they could in their studies.
Anything Maravoric can do, we can do better. Leronlimab limits adverse effects, while Maravoric makes them worse.
Think of it this way, Leronlimab fries the fish where the fish needs to be fried. And no flies!
Cool when stuff like that happens, and AARP covers news in AD that’s in our wheelhouse. But to answer you question, I have to split it up a bit into different parts of a response.
First of all, I’m not so much in the know. Certainly when pertaining to investing, but I can kinda nerd out on the science.
The two drugs you mentioned (one of which got further delayed last week), are both attempting to clear Amyloid plaques from the brains and CNS of AD patients. These two may not do much good except delay progression by 6 months or so. They can do a lot of bad like brain swelling and bleeding. The delayed drug candidate for instance, is delayed because the risks have been determined to outway the limited rewards. In my limited opinion, the real problem with both of these drugs as well as the amyloid plaque clearing concept, is a amyloid plaques are a symptom of the disease, not the underlying cause. It’s kinda like frying in fish in the kitchen with the porch door open and complaining about the flies, instead of just frying the fish on the porch and closing the freaking door.
In all serious, nobody yet knows with proof that Leronlimab is a miracle drug for Alzheimer’s. But take a look at the 3 papers discussed this weekend. Ohm’s from Fall 2021, mightyCYDy’s from summer 2022, and dwfl28’s from end of last year. They all studied Maravoric in mice with some good results.
Maravoric isn’t an Amyloid Plaque focused drug. It’s an HIV drug with promising anti inflammatory properties (sorry, can’t describe its exact MOA, but I think an allosteric CCR5 inhibitor). It’s getting some really interesting results in mice (murine) studies over time in AD.
Leronlimab is a competitive CCR5 inhibitor, so similar to Maravoric. But better, in theory. We don’t cause kidney, or liver damage for instance. And we allow chemotaxis to continue, while antagonizing the receptor.
So is Leronlimab even on the radar of the people doing the research? If they are studying Maravoric in Alzheimer’s you can be damn sure they are aware of Leronlimab and probably would prefer to use it if they could in their studies.
Anything Maravoric can do, we can do better. Leronlimab limits adverse effects, while Maravoric makes them worse.
Think of it this way, Leronlimab fries the fish where the fish needs to be fried. And no flies!
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