Excepted the study doesn’t “show” it and Leronlimab has been pumped up by illegal stock promoters - welcome to their team$CYDY : IT’S ALL FAKE https://t.co/cZkOWl4dpJ
$CYDY baggies discovering that Loserlimab is no better than saline and maybe worse - this is a giant IQ test and the results are not pretty pic.twitter.com/8qgFWQOrkc
The questions are however valid and open for discussion. Asking on them does not mean we are jumping to conclusions; we are trying to be as unbiased as possible in analyzing the data. There may not be simple answers either. Ideally the management or Dr. Recknor should try explain the apparent discrepancy in the data with regard to CCR5/CCL5 in LH and the better response in cancer for those having <50%.
Can misiu or someone who has followed LL for multiple years comment on this?
Also, historically how was it established or concluded that Leronlimab is a CCR5 antagonist? I am sure it does this in vitro but has it been established in HIV or other patients that it acts this way?
In the case of covid, the most ccr5 activity is expected in critical patient; so for Long Haulers the MOA may be something else. Still that the placebo group has less CCL5 than Leronlimab seemed strange - although all this is anecdotal.