Ha, not an expert, just had a little time today to
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Posted On: 11/04/2021 4:27:39 PM
Ha, not an expert, just had a little time today to dig around some, for my own edification.
Re: the Q about 350 vs. 700, I recall that perhaps Recknor wanted to get some more biomarker data - was part of the rational NP gave for extending the trial. Who knows, maybe it will help the dose justification for HIV too. If we can get away with lower dose, that would help our profit margins. There may be possible safety reasons too where would want less.
I still go back to the idea that for cancer, want to inhibit TRegs traveling to the site of cancer yet allow CD4 and CD8 effector T-cells to be able to "rev up" the immune response to attack cancer, but for inflammatory and autoimmune diseases, want to do the opposite: allow TReg migration but inhibit effector T-cell migration. I wonder if 350 vs. 700 mg dose would make a difference in those indications? Patterson did mention something about CCR5 receptor density differences on T-reg vs. T-eff cells, but don't remember the details. Maybe TRegs had higher #CCR5 receptors, so would want higher dose of LL to cover that in cancer, and then also a lower dose for inflammatory disease? (But that I'm sure is overly simplistic and wanting higher dose in Covid does not fit that profile). I think we do miss some scientific expert opinions on such matters (such as from BP, not saying I want him involved anymore, just someone like him with good ideas and understanding to help out Recknor).
Hopefully Recknor gets some insight into things regarding dosing, biomarkers, and how our drugs work - hopefully well in all these various diseases.
Re: the Q about 350 vs. 700, I recall that perhaps Recknor wanted to get some more biomarker data - was part of the rational NP gave for extending the trial. Who knows, maybe it will help the dose justification for HIV too. If we can get away with lower dose, that would help our profit margins. There may be possible safety reasons too where would want less.
I still go back to the idea that for cancer, want to inhibit TRegs traveling to the site of cancer yet allow CD4 and CD8 effector T-cells to be able to "rev up" the immune response to attack cancer, but for inflammatory and autoimmune diseases, want to do the opposite: allow TReg migration but inhibit effector T-cell migration. I wonder if 350 vs. 700 mg dose would make a difference in those indications? Patterson did mention something about CCR5 receptor density differences on T-reg vs. T-eff cells, but don't remember the details. Maybe TRegs had higher #CCR5 receptors, so would want higher dose of LL to cover that in cancer, and then also a lower dose for inflammatory disease? (But that I'm sure is overly simplistic and wanting higher dose in Covid does not fit that profile). I think we do miss some scientific expert opinions on such matters (such as from BP, not saying I want him involved anymore, just someone like him with good ideas and understanding to help out Recknor).
Hopefully Recknor gets some insight into things regarding dosing, biomarkers, and how our drugs work - hopefully well in all these various diseases.
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