Lastly, the Company remains focused on the possibl

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Lastly, the Company remains focused on the possible use of leronlimab in the treatment of GBM. Preliminary results from a preclinical study performed at the Albert Einstein College of Medicine do not appear to show a difference in outcome with leronlimab compared to the control arm. The Company has committed to repeating the study based on unpublished observations by Dr. Pestell’s lab and will now employ a treatment sequence involving temozolomide and leronlimab.
https://www.cytodyn.com/newsroom/press-releas...areholders

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Mechanistically, C-C motif chemokine ligand 5 (CCL5) secreted by pericytes activates C-C motif chemokine receptor 5 (CCR5) on GBM cells to enable DNA-dependent protein kinase catalytic subunit (DNA-PKcs)-mediated DDR upon TMZ treatment. Disrupting CCL5-CCR5 paracrine signaling through the brain-penetrable CCR5 antagonist maraviroc (MVC) potently inhibits pericyte-promoted DDR and effectively improves the chemotherapeutic efficacy of TMZ. https://www.nature.com/articles/s41422-021-00528-3

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It would be interesting to look at the results of that GBM study from Montefiore.

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The results from this preliminary study demonstrated that high dose leronlimab was significantly better at reversing liver fibrosis compared to an IgG 4 isotype control and demonstrated a trend toward better fibrosis reversal compared to Resmetirom. The final results from that study have now also demonstrated that leronlimab (both high and low dose) was significantly better than Resmetirom at reversal of fat deposition (steatosis) in the liver.

The first follow-up study seeks to confirm the observations of the original study with larger cohorts of mice (12 versus the original 8/group) and will compare leronlimab with a GLP-1 agonist (Semaglutide) in addition to confirming the comparisons with Resmetirom.

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If leronlimab's ability to reverse fat deposits is as good as semaglutide we can do away with two drugs and their side effects.

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The second follow-up study involves the administration of CCL4, a drug that directly causes liver fibrosis in mice. This study will clarify if the observed reversal of liver fibrosis is restricted to the MASH/fat deposition pathway or might occur independently of the etiology of fibrosis (e.g. alcohol, viral hepatitis, etc.).

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Steatosis in MASH, alcoholism and hepatitis is all inflammation driven so it will work for all three. The challenge in hepatitis and ongoing alcoholism is the continuing presence of inflammatory drivers.

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Second, in September, CytoDyn applied to the NIH/RECOVER-TLC group for the potential inclusion of leronlimab in their next round of Long Covid treatment studies.

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A lot of potential pilot studies upcoming. Now who wants to say management has been doing nothing?