My answers to a few points made in a PM by an anti-CYDY scalawg.

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You make ridiculous assumptions that leronlimab will have a miraculous impact on every single indication where ccr5 is highly expressed. i don't think you understand the realities of "the science"

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You do not know all of what I know so you're speaking out of ignorance.

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if this were a miracle drug then a skewed enrollment in covid wouldnt have stopped it.

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Skewed enrollment didn't help but the primary reason was leronlimab only being allowed for two weeks. Many of the patients would have been on corticosteroids prior to leronlimab and almost certainly after the two weeks leronlimab was used. After two weeks the death toll rose considerably and the end results if I remember correctly were just slightly better than corticosteroids but not statistically significant. Do you really expect a drug to work when there is no drug present?

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if this were a miracle drug then you wouldn't be hoping that follow up data in tnbc would show that all patients were dead at 13-16 months instead of 8-12 months.

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I would hope that no patients were dead but that's not realistic in late stage cancer. "Instead of 8-12 months" is a false claim by you. Median overall survival was 12+ months.

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if this were a miracle drug then the 700mg MASH cohort wouldn't have failed.

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You must have missed this post -

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I decided to look back at leronlimab's trial in NASH to see if possibly my theory of a single allele CCR5 delta 32 deletion in some patients may be the cause. What is interesting is that in the 350mg arm there were 16 Hispanic/African American patients and 6 Caucasian, non-Hispanics. In the 750mg arm there were 9 Hispanics/ 0 African Americans and 13 Caucasian, non-Hispanics.

Hispanics and African Americans show around a 3% expression of a single allelle CCR5 delta 32 deletion vs. around 15% for Caucasian, non-Hispanics. With the much lower number of Caucasian, non-Hispanics in the 350mg arm and the higher number of Caucasian, non-Hispanics in the 750mg arm there is a very good chance that there were no single allele CCR5 delta 32 single allele patients in the 350mg arm and two single allele patients in the 750mg arm. With only 22 patients in each arm that could skew results dramatically.

Now I'd like to find out if they excluded only patients with the double allele or patients with the double allele and single allele. If they excluded only the double allele patients then we may have solved the problem of non-responders.

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if those trials hadn;t been run yet and someone on the board asked you if you thought leronlimab would work in those indications, then your analysis would conclude that leronlimab does everything that every single other drug has ever done well in those indications, plus more, and that it would help 90% of the patients and they would all pretty much be cured.

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If that was the case then my disease list would be much longer. 90 diseases (although there are a few I still have to take a deep dive into) isn't much compared to the number of diseases out there. The reason it is as long as it is is that so many diseases have an immune dysregulation / inflammatory pathology.

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in vitro and murine work does not translate cleanly or at all 90% of the time.

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No it doesn't, but I look at the totality of the evidence. I haven't spent well over 5,000 hours looking into things without learning a few things along the way.

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ps. From a completely different scalawag -

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BTW I read your conversation with JL, maybe you missed it: he was politely dismissive of "your work".

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Very strange since I've never had a conversation with Dr. Lalezari. Maybe he's following me around and is referring to a polite thank you I gave to the clerk at a gas station and his name was JL.