I've been working on a response to some jackass on
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Posted On: 02/17/2022 8:42:18 AM
I've been working on a response to some jackass on stocktwits about the MOA. They think Ohm is wrong about it. Here's what I have so far. Let me know what you think...
That was based on the original inventors premise and it's wrong. When leronlimab was originally invented a lot less was known about the CCR receptors. I think they based that on he fact that there was still immune activity so they thought the chemokines were not being blocked, not realizing that immune activity would still occur through the other receptors. I was the first one to point out that they were wrong and Dr. Recknor told me they were looking into the MOA and biomarkers.
My conclusion that it was wrong is very simple logic. If leronlimab allowed chemokine binding and regular immune activation it would have no activity against overinflammation and autoimmunity. The fact that both the chemokines and leronlimab bind to the n terminus and the chemokines cannot attach when leronlimab is already there is a straightforward proposition.
My thesis for how it's actually working I believe is the correct one. We know that all of the CCR receptors increase when an immune or injurious challenge is presented. CCR5 is by far the most prolific CCR receptor and is the main CCR mechanism in the immune system. The other receptors are mainly backups to it.
You have elevated CCR receptors, elevated chemokine levels and an overinflammatory/autoimmune response mainly due to the CCR5 receptor but also a lower level from the other CCR receptors. The other CCR receptors response in a normal state would be very low. In the elevated state of high immune response those other receptors would equate to a normal immune response due to increased expression. But then you have the CCR5 receptor on top of it with a massive immune response causing disarray. Effectively block the CCR5 receptor and only the normal level of immune response from the other receptors is left. In other words immune homeostasis.
That was based on the original inventors premise and it's wrong. When leronlimab was originally invented a lot less was known about the CCR receptors. I think they based that on he fact that there was still immune activity so they thought the chemokines were not being blocked, not realizing that immune activity would still occur through the other receptors. I was the first one to point out that they were wrong and Dr. Recknor told me they were looking into the MOA and biomarkers.
My conclusion that it was wrong is very simple logic. If leronlimab allowed chemokine binding and regular immune activation it would have no activity against overinflammation and autoimmunity. The fact that both the chemokines and leronlimab bind to the n terminus and the chemokines cannot attach when leronlimab is already there is a straightforward proposition.
My thesis for how it's actually working I believe is the correct one. We know that all of the CCR receptors increase when an immune or injurious challenge is presented. CCR5 is by far the most prolific CCR receptor and is the main CCR mechanism in the immune system. The other receptors are mainly backups to it.
You have elevated CCR receptors, elevated chemokine levels and an overinflammatory/autoimmune response mainly due to the CCR5 receptor but also a lower level from the other CCR receptors. The other CCR receptors response in a normal state would be very low. In the elevated state of high immune response those other receptors would equate to a normal immune response due to increased expression. But then you have the CCR5 receptor on top of it with a massive immune response causing disarray. Effectively block the CCR5 receptor and only the normal level of immune response from the other receptors is left. In other words immune homeostasis.
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