Regarding the possible NASH pre-clinical trial, my understanding is this would be a small trial involving animals to help further elucidate Leron's NASH mechanism of action, and would most likely be done *IN TANDEM* with the bigger NASH phase2b/3 clinical trial (2b/3 trial protocol will likely be submitted to FDA in September, per Antonio on the conference call).
Thus, IF that small pre-clinical animal trial happens, it wouldn't slow anything down on the NASH front.
That said, can any of the science people on this board speculate as to why else a pre-clinical animal trial might be beneficial, given that CYDY already ran one? Details below...
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The potential for leronlimab in the treatment of NASH was demonstrated in a pre-clinical model of fatty liver disease. Immunodeficient, NOD-SCID Gamma (NSG) mice were fed a high-fat, NASH-inducing diet, transplanted with human stem cells to repopulate the deficient immune system, and treated with leronlimab. Sixteen (16) male NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ, commonly known as the NOD scid IL-2 receptor gamma knockout mice (NSG), were first humanized by intravenous inoculation with normal human umbilical cord blood cells (105). After five weeks on normal mouse chow, mice were successfully humanized, demonstrating >25% human CD45 cells in peripheral blood. Mice were switched to high fat (52%) high cholesterol (1.25%) diet (FPC diet: fructose, palmitate, cholesterol, trans-fat; Envigo-Teklad TD.160785). Leronlimab and control antibody (normal human IgG, Sigma) were administered i.p. at a dose of 2mg i.p. twice weekly, n=8 mice/group. The results showed that leronlimab inhibited fatty liver development, a key characteristic of early-stage NASH, such that treatment of humanized NSG mice with leronlimab caused a threefold reduction in hepatic steatosis compared to control in an animal model of high fructose, high palmitate, high cholesterol diet.
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And details on CYDY's (successful) NASH trial in humans:
https://www.biospace.com/article/cytodyn-post...eronlimab/
Thus, IF that small pre-clinical animal trial happens, it wouldn't slow anything down on the NASH front.
That said, can any of the science people on this board speculate as to why else a pre-clinical animal trial might be beneficial, given that CYDY already ran one? Details below...
_____________________________
The potential for leronlimab in the treatment of NASH was demonstrated in a pre-clinical model of fatty liver disease. Immunodeficient, NOD-SCID Gamma (NSG) mice were fed a high-fat, NASH-inducing diet, transplanted with human stem cells to repopulate the deficient immune system, and treated with leronlimab. Sixteen (16) male NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ, commonly known as the NOD scid IL-2 receptor gamma knockout mice (NSG), were first humanized by intravenous inoculation with normal human umbilical cord blood cells (105). After five weeks on normal mouse chow, mice were successfully humanized, demonstrating >25% human CD45 cells in peripheral blood. Mice were switched to high fat (52%) high cholesterol (1.25%) diet (FPC diet: fructose, palmitate, cholesterol, trans-fat; Envigo-Teklad TD.160785). Leronlimab and control antibody (normal human IgG, Sigma) were administered i.p. at a dose of 2mg i.p. twice weekly, n=8 mice/group. The results showed that leronlimab inhibited fatty liver development, a key characteristic of early-stage NASH, such that treatment of humanized NSG mice with leronlimab caused a threefold reduction in hepatic steatosis compared to control in an animal model of high fructose, high palmitate, high cholesterol diet.
______________________________________
And details on CYDY's (successful) NASH trial in humans:
https://www.biospace.com/article/cytodyn-post...eronlimab/
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