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Posted On: 12/16/2023 3:12:12 AM
Post# of 148878
Re: KenChowder #140020
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I hope Leron will do much better. Ohm can probably tell us whether it will.
How leronlimab would work in glioblastoma is the same way it would work in any cancer.
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Leronlimab's MOAs for cancer - Leronlimab elicits an NKT cell response - promoting tumor cell death , upregulates CD8+ T cells, Inhibits angiogenesis, shuts down cancer reappearing through collagen downregulation, Stops the recruitment of Tregs to tumor sites (Tregs promote tumor immunity), inhibits tumor cell dna repair via GRP78 downregulation, inhibits IL-13 a tumor protectant, downregulates IL-4 (IL-4 promotes tumor immunity), upregulates IFN-gamma promoting tumor cell death, downregulates PD-1 -PD-L1's receptor, polarization of macrophages - promoting tumor cell death , downregulates calcium channel signaling, blocks CCL5 shutting down pathways for CTCs.
The only real world example we have is Nader's mother-in-law. Given only a few months to live with the main cancer being stage four breast cancer but with metastatic tumors throughout the body including glioblastoma. The brain tumors shrunk and some disappeared, I believe she survived for around another three years, which is astounding given the damage that must have already been done. If leronlimab can do that in a patient so near death it should do very well in a protocol where the patients aren't to that extreme.
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