no clue who JLang is, so had to look he/she seem
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Posted On: 06/01/2022 11:05:59 PM
no clue who JLang is, so had to look
he/she seems to be confident
everyone already thinks the posts are too long.
without making it excruciating long so it is crystal clear, I made it as short as I could, but yet it remains misunderstood
I thought I gleaned what ohm was trying to say through the few words used, but apparently, I misunderstood every line.
I am aware that our immune system undergoes regeneration.
How you state:
I said: "If we have to wait for the immune system to regenerate before LL works, this investment is worthless" I think I've proven why I made this reply to ohm. I know that old cells die off and new ones take their place. I knew they last for many months to many years depending on their rank. I know that if we have to wait for the generals in the immune system already bound with chemokines to die off so another unbound general can be born so LL may bind to it, then I stated, the drug is worthless.
I hope everyone understands that I completely do not believe that is the case.
LL has the greatest affinity to CCR5 bar none. LL dislodges any chemokine out of its binding with CCR5 and immediately takes residence there in. Certainly LL does not require waiting for unbound CCR5 to become available on newborn cells. To LL, every CCR5 receptor in the human body is available. There is 100% RO after LL is fully dosed.
LL works immediately. Its mechanism of action has nothing to do with "regeneration". If it did, we wouldn't have what we know it is, what it proves itself to be. Once bound to CCR5, LL won't let it go either. Not like the muscarinc receptors you discuss. It's bound till it degenerates, about a month to 2 months 1/2 life depending on dosage and length of time patient on the drug. After all, it is a -mab. It will degenerate and become metabolized.
Only then will that CCR5 be again available to chemokines or another molecule of LL.
I will only discuss LL and not other drug MOA, even this is becoming burdensome.
he/she seems to be confident
everyone already thinks the posts are too long.
without making it excruciating long so it is crystal clear, I made it as short as I could, but yet it remains misunderstood
I thought I gleaned what ohm was trying to say through the few words used, but apparently, I misunderstood every line.
I am aware that our immune system undergoes regeneration.
Quote:
These methods were later used to confirm that memory T cells live for six months or less in healthy humans (Westera et al., 2013), whereas naive T cells can live for up to nine years (Vrisekoop et al., 2008). Thus, a long life is not a key characteristic of memory T cells. Instead, immunological memory, which can last for a lifetime (Crotty and Ahmed, 2004), is maintained by relatively short-lived cells.
How you state:
Quote:
It reads like you believe the body has a finite number of cells and actions. Things regenerate, drugs leave the body at various rates for various reasons. A receptor blocked today might not be blocked tomorrow. For instance there are more than one muscarinic receptors (M1-M5) located in various parts of the body, and blocking one versus another can have a wildly different effect. As can how you try to dose your anti-muscarinic, be it inhaled, injected, delivered transdermally, or wafted in your general direction by Tibetan Monks.
I said: "If we have to wait for the immune system to regenerate before LL works, this investment is worthless" I think I've proven why I made this reply to ohm. I know that old cells die off and new ones take their place. I knew they last for many months to many years depending on their rank. I know that if we have to wait for the generals in the immune system already bound with chemokines to die off so another unbound general can be born so LL may bind to it, then I stated, the drug is worthless.
I hope everyone understands that I completely do not believe that is the case.
LL has the greatest affinity to CCR5 bar none. LL dislodges any chemokine out of its binding with CCR5 and immediately takes residence there in. Certainly LL does not require waiting for unbound CCR5 to become available on newborn cells. To LL, every CCR5 receptor in the human body is available. There is 100% RO after LL is fully dosed.
LL works immediately. Its mechanism of action has nothing to do with "regeneration". If it did, we wouldn't have what we know it is, what it proves itself to be. Once bound to CCR5, LL won't let it go either. Not like the muscarinc receptors you discuss. It's bound till it degenerates, about a month to 2 months 1/2 life depending on dosage and length of time patient on the drug. After all, it is a -mab. It will degenerate and become metabolized.
Only then will that CCR5 be again available to chemokines or another molecule of LL.
I will only discuss LL and not other drug MOA, even this is becoming burdensome.
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