The scalawag strikes again. I'm sure he sent this

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its just that there is evidence is multiple indications that inhibiting ccr5v is not enough and that either ccr1 or ccr2 must also be blocked to get anywhere.

ccr5 by itself has plenty of good indications, but it isn't always enough vs those redundancies.

and beyond that have you ever wondered why you claim it does everything better than everything else and accomplishes everything that every single competing drug does and also does it 10x better, but when it is trialed it not clearly better than other drugs?

if its so damn amazing then why does the data never smash the competition?
it might, eventually, but right now i see that happening perhaps in GBM. nothing else with any confidence yet. severe covid seemed like a great indication. trial design and execution failed. fda and amarex certainly didn't help mitigate those weaknesses. leronlimab MIGHT be a winner in many indications, but so far its just not enough.

great potential in long covid, hiv cure, hiv fucntional cure, HIV cure via bone marrow transplant, cancer metastasis, etc.

CRC the basket study data indicates difficulty with durability. alzheimer's the rap-103 therapy indicates possible limits to ccr5 inhibition efficacy. MASH is too competitive. long oovid, fibrosis and inflammation too early to say obviously.

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its just that there is evidence is multiple indications that inhibiting ccr5v is not enough and that either ccr1 or ccr2 must also be blocked to get anywhere.

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You are making that claim, show me the evidence.

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and beyond that have you ever wondered why you claim it does everything better than everything else and accomplishes everything that every single competing drug does and also does it 10x better, but when it is trialed it not clearly better than other drugs?

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Where have I said it does it 10X better? Where leronlimab outclasses so many drugs is because it does what the other drug does and a host of other factors involving the disease. Take for example Keytruda. Keytruda blocks PD-L1 from binding to it's receptor PD-1. Very nice, it eliminates one of the tumor protective factors. Leronlimab downregulates PD-1 and PD-L1 and other tumor protectant factors. On top of inhibiting angiogenesis, tumor DNA repair, metastasis, Tregs, CDK2/4/6, cyclin D1, cyclin E, and PCNA and upregulates tumor destroying T-cells.

What you fail to understand is that so many diseases are caused by a dysregulated immune system and the accompanying inflammation and that leronlimab can fix that rather than just targeting one single factor.

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CRC the basket study data indicates difficulty with durability

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Where are you seeing the data on that?

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alzheimer's the rap-103 therapy indicates possible limits to ccr5 inhibition efficacy.

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It most certainly doesn't. RAP-103 has good binding to CCR2 but very weak binding to CCR5. As I've explained before CCR5 is more prolific than other CCR receptors and has higher binding efficiency for CCL5 than other receptors. CCR5 and CCL5 are the two most important factors in immune dysregulation. If you have little receptor occupancy for CCR5 your drug is not going to do much to correct dysregulation.

You keep coming at me with bullshit ramblings without having any understanding of the science.

ps. Have you seen the press release on mTNBC?

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