I disagree that Pourhassan, Kelly, or anyone else at Cytodyn lacks the education, experience or training to instantly appreciate the potential importance of leronlmab suppressing PDL1 expresion in cancer cells.
Between the two of them they have at least an order of magnitude more experience, training, and education than I do.
As has been amply demonstrated, I am but a mere stone's throw from clueless.
If someone tells me that leronlimab kills PDL1 expression its the intellectual equivalent of getting bashed in the head by a 2x4.
Keytruda/Opdivo does one and only one thing: it binds to a receptor.
Leronlimab does one and only one thing: it binds to a receptor.
Everyone at Cytodyn knows that LL binds to a receptor.
Keytruda/Opdivo is the biggest news in medicine in the last decade.
Everyone at Cytodyn knows that Keytruda/Opdivo binds to a receptor because IT WORKS EXACTLY LIKE LERONLIMAB.
Receptor bound by mab. Its automatic to everyone at Cytodyn.
So they all know that Keytruda/Opdivo saves cancer patients because the receptor is blocked from the problem molecule.
What Pourhassan and Kelly have not been alerted to is that LL may kill the problem molecule before it gets to the Keytruda/Opdivo blocked receptor.
This is a no-brainer.
This is not "How does LL cross the blood brain barier?" where no one has a clue.
This could be so easy its like falling off a chair.
If PDL1, the problem molecule, circulates in the bloodstream then it is measureable with a blood test. Needle in arm. Withdraw 4 milliliters. Don't even need Patterson for this one.
If LL suppresses PDL1 expression by cancer cells, when you give the patient LL, the PDL1 concentration in the bloodstream will decrease.
Administer LL. Wait one week. Needle in arm. Withdraw 4 milliliters.
Is the bloodstream PDL1 now lower or higher than a week ago before the patient got LL?
The math on this one is even easier than CD12.
There could be problems. Chemotherapy may prevent PDL1 equilibrium from ever being achieved in blood. Maybe PDL1 expression is localized in the tumor and doesn't really go to the blood.
But I don't believe for one minute that any CYDY engineer fails to understand the identical mechamisms of Keytruda/Opdivo/LL.
And I simalrly beleive that every engineer at CYDY would have the same reaction when informed that LL stops PDL1 expression in cancer cells: "Surely you must be kidding."
Between the two of them they have at least an order of magnitude more experience, training, and education than I do.
As has been amply demonstrated, I am but a mere stone's throw from clueless.
If someone tells me that leronlimab kills PDL1 expression its the intellectual equivalent of getting bashed in the head by a 2x4.
Keytruda/Opdivo does one and only one thing: it binds to a receptor.
Leronlimab does one and only one thing: it binds to a receptor.
Everyone at Cytodyn knows that LL binds to a receptor.
Keytruda/Opdivo is the biggest news in medicine in the last decade.
Everyone at Cytodyn knows that Keytruda/Opdivo binds to a receptor because IT WORKS EXACTLY LIKE LERONLIMAB.
Receptor bound by mab. Its automatic to everyone at Cytodyn.
So they all know that Keytruda/Opdivo saves cancer patients because the receptor is blocked from the problem molecule.
What Pourhassan and Kelly have not been alerted to is that LL may kill the problem molecule before it gets to the Keytruda/Opdivo blocked receptor.
This is a no-brainer.
This is not "How does LL cross the blood brain barier?" where no one has a clue.
This could be so easy its like falling off a chair.
If PDL1, the problem molecule, circulates in the bloodstream then it is measureable with a blood test. Needle in arm. Withdraw 4 milliliters. Don't even need Patterson for this one.
If LL suppresses PDL1 expression by cancer cells, when you give the patient LL, the PDL1 concentration in the bloodstream will decrease.
Administer LL. Wait one week. Needle in arm. Withdraw 4 milliliters.
Is the bloodstream PDL1 now lower or higher than a week ago before the patient got LL?
The math on this one is even easier than CD12.
There could be problems. Chemotherapy may prevent PDL1 equilibrium from ever being achieved in blood. Maybe PDL1 expression is localized in the tumor and doesn't really go to the blood.
But I don't believe for one minute that any CYDY engineer fails to understand the identical mechamisms of Keytruda/Opdivo/LL.
And I simalrly beleive that every engineer at CYDY would have the same reaction when informed that LL stops PDL1 expression in cancer cells: "Surely you must be kidding."
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