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Posted On: 07/26/2021 8:35:29 PM
Post# of 154979
CTMedic,
I have also been thinking of the intersection of Leronlimab and CCR5, and what advantage LL may have.
Can someone please post the very fist slide from Dr Scott Kelly's mTNBC presentation? Here he speaks of the picture "off to the right" - a close-up of the CCR5 receptor.
"CCR5 is a 352 amino acid structure that crossses the membrane seven times. It's important to note that Leronlimab binds to the N-terminus as well as the second Extra Cellular Loop, and this seperates it from other CCR5-antagonists. It is competitive, rather that an allosteric inhibiitor."
https://www.google.com/url?sa=t&rct=j&...4ZwQXGrNzd
What do we understand about 'competitive, rather than allosteric inhibitor?'
It seems to me this is the mechanical part that seperates us from the rest, but I don't fully understand the difference between competitive and allosteric, or even non-compateive for that matter though it doesn't apply to LL.
Thanks in Advance to any takers.
Chazzle
I have also been thinking of the intersection of Leronlimab and CCR5, and what advantage LL may have.
Can someone please post the very fist slide from Dr Scott Kelly's mTNBC presentation? Here he speaks of the picture "off to the right" - a close-up of the CCR5 receptor.
"CCR5 is a 352 amino acid structure that crossses the membrane seven times. It's important to note that Leronlimab binds to the N-terminus as well as the second Extra Cellular Loop, and this seperates it from other CCR5-antagonists. It is competitive, rather that an allosteric inhibiitor."
https://www.google.com/url?sa=t&rct=j&...4ZwQXGrNzd
What do we understand about 'competitive, rather than allosteric inhibitor?'
It seems to me this is the mechanical part that seperates us from the rest, but I don't fully understand the difference between competitive and allosteric, or even non-compateive for that matter though it doesn't apply to LL.
Thanks in Advance to any takers.
Chazzle
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