Its not 44%, it could be 100%. Maybe these guys will save Pourhassan's bacon in the event of CD12 mortality missing the primary endpoint.
The study results for homozygotes are just as important as the study result for heterozygotes.
In this study, of the 294 patients who had covid, zero were CCR5delta32 homozygotes.
As the study notes, the frequency of CCR5delta32 homozygotes in the general population is roughly 1%.
Thus the probability of selecting 294 patients at random from the general population while obtaining zero homozygotes is 0.052.
This is apparently the first study to check the frequency of CCR5delta32 mutation in covid patients.
Cytodyn should have done this six months ago. Its a dirt cheap study.
But of course CYDY should have done dose escalation and intravenous delivery as well because both of those bring LL treatment closer to homozygous CCR5delta32
I vaguely remember someone else doing this type of study but google scholar search turns up nil.
This study is so persuasive it could make up for Cytodyn's botched RO testing.
There is no doubt that CYDY will be pushing the data from this study if CD12 misses primary endpoint and CD12 turns into a debate with the FDA or even within the FDA.
The read-through to CD12 is not necessarily 44%, it could be 100%, but that would require 100% receptor occupancy with LL.
This study could be particularly powerful if CYDY has at least some RO data on the dose-response of leronlimab in CD12.
For example, if CYDY can show that every patient who achieved 95% (picking a number out of the air, it could be 99% I have no idea) RO was able to survive, then even if that data is only for a few patients the few patient problem is at least partly addressed by the data in this study.
The excerpt posted is CCR5delta32 heterozygotes.
CCR5 heterozygotes are people who have one of their two alleles as CCR5delta32. The other allele is normal so these people still produce CCR5, just not as high a quantity of people who have normal CCR5 for both alleles.
If CCR5delta32 heterozygotes produce 50% of the normal CCR5, that's 50% less CCR5 molecules that LL has to bind.
Here is the excerpt for the homozygotes:
"Of note, we did not find deletion-homozygotes among the patients compared to 1% among controls."
If leronlimab can achieve near 100% receptor occupancy, then that may be exactly the equivalent of a CCR5delta32 homozygote, and possibly a covid cure.
And that would be no surprise. Its an HIV cure as well. Not a treatment. A cure.
I would say this study waves a red flag, but its more like a nuclear missle launch.
But the key piece of data that you need to lock it down, and it can be locked down even in the face of a CD12 pirmary endpoint fail, is survival as a function of receptor occupancy.
With this new study, Cydy doesn't need RO for every patient.
Probably if you have even as few as ten patients who hit some magic number, like 95%, and they hit that number before some other disease severity milestone, and they all lived, then that's good enough.
But you need some RO data.
If CYDY has no CD12 RO data, this study still helps, but just get the damn data and lock the thing down.