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Again, you make ridiculous assumptions that leronlimab will have a miraculous impact on every single indication where ccr5 is highly expressed.

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I don't believe in miracles. I also don't think that high CCR5 expression itself is enough to make it on the disease list. For example there are no psychiatric disorders on there. There are confounding factors that don't give me high confidence even though it's quite possible leronlimab may be of some help. When I look at a disease the first thing I do is look at the disease itself. What are the causative factors, what are the biological signatures, what other drugs have proved successful and what do they counter there's a slew of things I look at. Then I look at any studies with other CCR5 blocking drugs. Then I look at specific pathways that leronlimab affects that could be helpful in the disease state. Lastly I look at everything that could hinder the effectiveness of leronlimab. It is a damn time consuming process.

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drug A down regulates X and that is proven to reduce cancer 1.
leronlimab can downregulate X so leronlimab will reduce cancer 1.

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When it comes to CCR5 blocking drugs like maraviroc which are not as effective as leronlimab that's a pretty clearcut pathway. When it comes to other drugs, if we have the same effect then outcomes should be similar. But those drugs all treat a very narrow aspect of the problem,

For example Keytruda - It blocks PD-1, leronlimab downregulates PD-1 and PD-L1. If that's all it did in cancer than it would be no better than Keytruda. But Keytruda strips away only one of the defense mechanisms of cancer. Leronlimab affects several, it also boosts NKT cells to help kill the tumor, it downregulates Ca2+ which aids in migration of metastasic cells and increases angiogenesis, inhibits DNA repair of damaged tumor cells leading to apoptosis, downregulates EFGR to reverse uncontrolled tumor growth and upregulates PPARy which helps control tumor cell growth, angiogenesis and metastasis.

So tell me why you think leronlimab wouldn't be a better drug than Keytruda.

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the fact remains though that in tnbc and MASH etc... leronlimab hasn't been miraculous and has clearly fallen short of your expectations in those.

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Fallen short? Give me a properly sized phase 3 trial and then tell me you still know what I think.

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seriously, you know TOO MUCH at this point to have a clear mind about certain aspects imo.

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You can never know too much. I have an inkling of how much I do not know. But that would take a very systematic approach and thousands of more hours to correct.

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btw the tnbc data presentation was utter crap and pfs was not 12+. go reread it and you will totally get it. ALL the data from that INCOMPLETE mish mash of trials was presented as subsets and even subsets of subsets. crazy cherry picking. the 12+ pfs was from 73% of the N=30 who responded I(more or less, even that is confusing)

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The mOS 12+ months was from 19 patients who received 525-700mg of leronlimab. Using the 350mg at all was a mistake that was assuredly forced upon us by the FDA. 350mg is worse receptor occupancy than maraviroc and why Progenics abandoned it. Even 525mg is sub-optimal but even with a sub-optimal dose in some patients it was still a better outcome then Trodelvy. I do wish it was a straight forward trial with more patients but with low cash flow what can one expect.

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