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That doctor has mentioned leronlimab as a new promising drug before. Since he's talking about new treatments it's almost a certainty he'll mention it again.
Peak coverage for leronlimab is 3 days which goes all the way back to Progenics trials. So each day after injection should see a further improvement.
You've "talked" to Dr. Patterson you should have some idea. As a SMF, noMD you should be able to find those resources easily enough.
Dr. Patterson paper, EINDs are back and longhaulers trial on clinicaltrials, it's a very good day.
From a post I made in early October.
From a medical paper -
The graph is from the study. The table does not show elevation. It does show correlation of mortality with GM-CSF with an adjusted p= .05. It did not break down mortality and CCL5 in the table.
I don't believe Dr. Patterson has said CCR5 regulates GM-CSF. I tracked that down on my own. By the way CCR5 blockade does downregulate IL-10 also. What seems unknown to you is the enormous number of feedback loops in the immune system.
So I am right about Mars?
Does that look like GM-CSF is going up?
GM-CSF
It's putting restrictions on Duterte's Executive Order. That may make Duterte unhappy and you don't want to make Duterte unhappy.
How long before reverse split and more dumping? More likely they've ran through this scam and will transition to a Mars bulk transport company. Elon Musk will need one once he starts a colony there.
I'm not sure what contradiction you're referring too. My guess would be the importance of RANTES (CCL5). Well this study shows a massive increase in CCL5 to 50,000, even higher than ARDS and 50x the normal level. You'll also notice that GM-CSF comes crashing down all on it's own over time.
https://www.atsjournals.org/doi/pdf/10.1164/rccm.202005-1885OC
Spend a few thousand hours reading medical papers then you can catch up with me.
I provide quotes because you obviously didn't believe what I originally posted then you want to whine about it.
It wasn't a study, the EIND's were not done by Dr. Patterson and since it wasn't a study there was no timeline.
In a high inflammatory state the overexpression of IL-4 and IL-13 prevent the downregulation of CCR5 by GM-CSF. Why you make ask? Because the bodies response is to overexpress immune response in the face of a threat. As I said in my previous post leronlimab breaks the feedback cycles.
CCR5 doesn't downregulate GM-CSF? Also it should be said that leronlimab in HIV produces a far superior blockade compared to maraviroc.
GM-CSF affects a part of the equation in COVID-19. CCR5 blockade breaks down a myriad of feedback loops.
Maraviroc is in a trial for Covid. A black box warning for causing a rise in liver enzymes for a disease that causes a rise in liver enzymes is not ideal. We saved the patient but he might need a liver transplant is not good for the corporate image.
If you want an example of direct action CCR5 blockade downregulates IFNy, lowering IFNy downregulates IL33. IL33 is a driver of GM-CSF expression.
IL-4 and IL-13 prevent the downregulation of CCR5 by GM-CSF. So in a high inflammatory state GM-CSF does not affect CCR5. Conversely CCR5 blockade and downregulation of IL-4 and IL-13 does downregulate GM-CSF. Nice little interruption of a feedback loop by leronlimab.
They're a little late to the game.
All those patients with organ failure. We also have the results from all the remaining EINDs.
In severe/critical is the number of patients who do recover more important than the time it takes for those who do recover? If the patients who do recover do so more quickly but there's not a statistically significant amount of patients who do recover than time to recovery is moot.
The inflammation and consequent edema in the lungs is what leads to the lower oxygen levels.
If the trial involved all COVID-19 patients indeed you would need thousands. Not so for only severe/critical patients.
Did you want me to look at the one that most closely resembles the primary endpoint of the phase 3 trial? That doesn't look good.
Incidence of clinical improvement lenzilumab group - 11 (92%) control group 22 (81%) p = .43
Leronlimab gets patients in worse condition SaO2<93% rather than SaO2<=94% for HGEN. Leronlimab's inclusions/exclusions also favor patients in worse condition. This makes it a bit easier to show the differentiation between the drug and SOC.
I have to stop back occasionally for a good laugh.
I wouldn't say it's being pumped. Lenzulimab has a decent chance of making stat sig with full enrollment. There will be a better drug out there but both will be needed for the COVID-19 fight.
Yep, two weeks or so for full enrollment. A competitor should have a data lock on trial results slightly after that.
Time to ventilation or death is not statistically significant (p= .06) is the truth. That's from your own CEO.
I've been telling HGEN investors there was no EUA. Of course the non-statistical significance of p= .06, no 75% interim analysis and 90 more patients needed to fill the trial isn't doing HGEN any favors either.
My average is 40 cents and COVID Phase 3 trial will be locked in less than a month. I'm doing just fine.
Has that been peer reviewed? Any article can be posted there. There's even one that claims coconut oil cures HIV. Here's the clue it's a bit off the fusion mechanism of HIV is gp120.
One doesn't need to look them up. What shows the dissimilarity and is of importance is where the spikes bind too. In the case of COVID-19 the ACE2 receptor and more weakly to neuropilin 1. For HIV it binds to CCR5.