I hope you don't think I'm about throwing anythi

I hope you don't think I'm about throwing anything up on the board for any self centered reason. This is not about me whatsoever, not one iota. I got a PM from someone asking "What's my story?" "Like I seem to know a lot". I haven't replied yet, but I want to answer, "What difference does that make at all" I'm nothing. I'm just telling it like I see it. I seek to elevate my confidence in the molecule by whatever means I can. If I have to piece together puzzle pieces together in the forms of comments to understand the molecule, that's what I will do.

All my statements are my educated guesses.

In commenting on CytoDyn's new expert, Dr. Paul Edison, I wanted to bring up the impetus for his hiring and what I felt, he wil be involved in. What I wrote was:

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Dr. Paul Edison, more than likely brought on board for the indication of Alzheimer's Disease and possibly epilepsy. His work in assessing microglial activation and amyloid load showed that both these are increased in Alzheimer's disease, and microglial activation correlates with cognition, while amyloid load does not correlate with cognition. https://www.imperial.nhs.uk/consultant-directory/paul-edison


Remember, Leronlimab crosses the blood brain barrier. Microglial cells contain CCR5. Therefore LL will block the activation of microglial cells.

As in NASH, he will likely advise the employment of Brain MRI in determining Leronlimab's effectiveness by measuring reduction in Alzheimer's plaques . He is now evaluating the relationship between neuroinflammation, tau, glucose metabolism, and structural and functional changes measured by MRI . He is evaluating novel microglial agents in mild cognitive impairment and Alzheimer's disease.

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Regarding NASH, What I said was:

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We all know the outcome of mTNBC, where we beat SOC by 1/2 month, 12 months to our 12.5 months overall survivability, so BTC was denied, but our trial had continued. In June, ASCO will be presenting a discussion on our Breast Cancer trials, 3 of them. Comparisons with current treatments and their effectiveness will be made with Leronlimab's effectiveness. If a minimum of 14 of the 28 patients of the mTNBC trial remain alive by the date of that conference, Leronlimab will be sporting an overall survivability of 18 months. 1.5 years where SOC is only 12 months (and Gilead spent 3 years on that trial trying to maximize that overall survivability, but, 1 year was the best it could do, that's Trodelvy.).

The results of the Basket Trial have not yet been released. https://clinicaltrials.gov/ct2/show/NCT04504942

(Estimated Study Completion Date : March 15, 2022)

More than likely, it has been completed. We know that the mechanism of action of all solid tumors is roughly the same and it was for that reason why this study was put together. Since LL worked so well in mTNBC, we can assume, it will work just as well in the majority of other solid tumors. In addition, we know LL crosses the BBB, so, it was found also to cure brain metastasis and brain tumors. Tumors all over the body just shrink because the blood supply to them dwindles and they die off for lack of nourishment and lack of oxygenation.

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I base my estimates on the outcomes of the NASH 700 on what we learned from NASH 350. 350mg was 1/2 dosing. Nader said that 50% of the patients had an 80ms drop in cT1. That correlates to about a 3.5 basis point drop in NAS score. With 1/2 dosing of Leronlimab, 50% of patients dropped their NAS by 3.5-4 basis points. Further, 80% of patients had a 50ms drop in cT1, so therefore, 80% of these patients dropped their NAS score by 2-3 basis points with LL 1/2 dosing.

Use the following for reference:

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https://tpis.upmc.com/changebody.cfm?url=/tpi...LD2006.jsp



Scoring interpretation: Total NAS score represents the sum of scores for steatosis, lobular inflammation, and ballooning, and ranges from 0-8. Diagnosis of NASH (or, alternatively, fatty liver not diagnostic of NASH) should be made first, then NAS is used to grade activity. In the reference study, NAS scores of 0-2 occurred in cases largely considered not diagnostic of NASH, scores of 3-4 were evenly divided among those considered not diagnostic, borderline, or positive for NASH. Scores of 5-8 occurred in cases that were largely considered diagnostic of NASH

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I feel I was justified in this reasonable statement:

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So far, LL has not induced disease. So far, LL is side effect free. The LL version of human immunoregulatory control so far is 81% effective with a p value of 0.0032 with HIV. We have also measured LL effectiveness in mTNBC and more than likely we will see it increase Overall Survivability from the current SOC Trodelvy of 1 year to 1.5 years... yet to come. In NASH, wait and see... I believe it will show that it can completely eradicate NASH, even from a NAS of 8, (cirrhosis) and bring it all the way down to a healthy liver, NAS of 0, even in 14 doses. That's what I see.

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Since 1/2 dosing drops NAS by 3-4 basis points, (and we have learned how difficult a disease NASH is to treat, as there exist exactly 0 approved drugs on this indication, so therefore, wouldn't you think it would take a strong dose of medication to eradicate it?), wouldn't you think that doubling the dose may likely double the efficacy thereby dropping NAS by 6-8 basis points? 8 basis points eradicates NASH even from its maximum level.