I know you have already received some answers (eve
Post# of 148175
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Posted On: 12/12/2019 11:52:26 AM
I know you have already received some answers (even some more science specific) but I wanted to add a blurb from the CytoDyn website that seemed appropriate:
What Makes Leronlimab Different
Leronlimab is a unique humanized monoclonal antibody. Leronlimab prevents HIV from using the CCR5 receptor as an entry gateway for healthy cells; preclinical research has also shown that Leronlimab blocks calcium channel signaling of the CCR5 receptor when present on the cancer cell surface. Calcium channel signaling of the CCR5 receptor is a crucial component to the spread of metastatic cancer.
Due to its selectivity and target specific mechanism of action, Leronlimab allows chemokine binding (CCL3, CCL4) at therapeutic doses and does not have agonist activity of the CCR5 receptor (it does not activate the immune function of the receptor). This target specificity separates Leronlimab from other CCR5 antagonists. Other advantages of Leronlimab include improved safety profile, longer half-life, and less frequent dosing.
In saying this, it will take time to determine one way or another if cancer will find another way to spread......but I think this is where it is important to point out that leronlimab has several (7 I believe) mechanisms of action. None of these directly attack the cancer itself, but helps to keep the cancer controlled and not spread, has synergistic effects with drugs that attack the cancer, promotes and helps the body maintain a competent immune system (which also helps to fight the cancer without chemo or other drugs) to name a few......all of this without a single drug relates SAE, negligible toxicity and zero resistance! Any other drug that did one of these mechanisms and was relatively safe would be huge all by itself. Leronlimab is truly a miracle IMO.
BTW HIV also mutates and eventually finds a way around CCR5 (X4 tropic). Dr. Sacha noted during one of the CC that all sexually transmitted HIV is CCR5. I'm sure trding or someone can enlighten us on how long or why HIV eventually transforms from R5 to X4 tropic?
What Makes Leronlimab Different
Leronlimab is a unique humanized monoclonal antibody. Leronlimab prevents HIV from using the CCR5 receptor as an entry gateway for healthy cells; preclinical research has also shown that Leronlimab blocks calcium channel signaling of the CCR5 receptor when present on the cancer cell surface. Calcium channel signaling of the CCR5 receptor is a crucial component to the spread of metastatic cancer.
Due to its selectivity and target specific mechanism of action, Leronlimab allows chemokine binding (CCL3, CCL4) at therapeutic doses and does not have agonist activity of the CCR5 receptor (it does not activate the immune function of the receptor). This target specificity separates Leronlimab from other CCR5 antagonists. Other advantages of Leronlimab include improved safety profile, longer half-life, and less frequent dosing.
In saying this, it will take time to determine one way or another if cancer will find another way to spread......but I think this is where it is important to point out that leronlimab has several (7 I believe) mechanisms of action. None of these directly attack the cancer itself, but helps to keep the cancer controlled and not spread, has synergistic effects with drugs that attack the cancer, promotes and helps the body maintain a competent immune system (which also helps to fight the cancer without chemo or other drugs) to name a few......all of this without a single drug relates SAE, negligible toxicity and zero resistance! Any other drug that did one of these mechanisms and was relatively safe would be huge all by itself. Leronlimab is truly a miracle IMO.
BTW HIV also mutates and eventually finds a way around CCR5 (X4 tropic). Dr. Sacha noted during one of the CC that all sexually transmitted HIV is CCR5. I'm sure trding or someone can enlighten us on how long or why HIV eventually transforms from R5 to X4 tropic?
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