MisterBlues schreef op 21 oktober 2020 10:42:
Finally, we have some evidence that RLF-100 is significantly better than Leronlimab (LL) for treating severe/critical Covid patients. This may not be exactly apples to apples, but anyone with half a brain can see that the RLF-100 is significantly better than LL when comparing our EAP study with LL’s compassionate use study that came out today. Here is the link to the LL study from today:
academic.oup.com/cid/advance-article/...Main items:
1. LL was given to 23 severe/critical Covid patients 22/23 were receiving supplemental oxygen (3/23 high flow, 7/23 mechanical ventilation). i.e. one was not even on oxygen, and only 7 were intubated.
2. After 30 days, 4 out 23 had died.
3. The high recovery rate suggested benefit, and those with lower inflammatory markers had better outcomes. Some but not all patients appeared to have dramatic clinical responses, indicating that unknown factors may determine responsiveness to leronlimab. Routine inflammatory and cell prognostic markers did not markedly change immediately after treatment, although IL-6 tended to fall. In some persons C-reactive protein clearly dropped only after the second leronlimab dose.
These results are good, but not great. In fact, I would argue that standard of care would have probably had not significantly worse outcomes. Most of these patients were severe, and less than half were critical. Probably would have seen a few extra deaths with SoC only, but these results are far from remarkable.
On the flip side, as we know in the RLF-100 EAP trial:
1. 21 patients all critical (all on mechanical ventilation and 5 on ECMO) with significant comorbidities were given RLF-100 via IV.
2. After 28 days, 2 out of 21 had died. After 60 days, 4 out of 21 had died (no 60 day follow up from CYDY). In our control group 83% died, while CYDY was using stats saying that expected deaths would have been around 50% (without a control arm though and without really substantiating those claims)
3. Virtually all showed dramatic clinical responses, including dramatic IL-6 changes as well as other inflammatory markers. X-ray images tell the whole story.
My observations:
1. There are several things that go in LL’s favor and several things that go against them when compared to RLF-100. E.g. Average age was higher for LL, but the patients were significantly less sick than the RLF-100 patients and also received treatment way earlier in the Covid disease cycle. Please read both studies to come to your own conclusions.
2. LL is a good drug, but it has it’s limitations. Only appears to work on a subset of the population, while RLF-100 appears to work on almost entire population.
3. People keep saying that we need many drugs to fight covid. I really don’t think we do. We just need ONE SILVER BULLET. I am hoping that RLF-100 is that silver bullet, but it could easily be a vaccine or some other drug.
4. The reason why RLF-100 is going to work for almost all people is because it is a peptide/hormone, just like insulin or human growth hormone. Imagine giving HGH to someone and not seeing any results at all. That is the likelihood of not seeing results when given RLF-100.
5. I never owned nor shorted $CYDY but I believe that the stock was riding high on the Covid hype, which is about to die out. I am expecting a lot of weakness for the stock in the near future. I am avoiding it like the plague for the time being.
6. I repeat, LL is a good drug. But it is not the knockout the world needs right now. It might be useful, but if RLF-100 gets approval and becomes SoC, then there is very little need for LL.
These are just my opinions, so please read both studies and come up with your own conclusions. I would love to hear other opinions here from those who read both studies.