First, the abstract appears to be a bit screwed up..... the first-stated intent of the study is to compare the inverse agonist with its major metabolite, but then we never hear about the metabolite in the conclusions. Then there's a "however" that seems out of context??
Are you asking if 103 might also lock the receptor into its inactive form, and thus contribute to cardio side-effects? I believe that the answer is "yes", but we don't know anything more from this abstract than before?? I guess that I don't understand what you're asking.... we knew that 103 was an inverse agonist, and we knew that 2A is expressed on cv tissue.
Maybe this will help explain my confusion??.... arna, and a selective 2C agonist that nonetheless has agonist activity for 2A..... while 2B seems to be a focus of interest, we're nonetheless concerned about potential 2A-mediated cardiovascular damage.
So... agonist, antagonist, reverse agonist..... aren't we baseline concerned about cardio side effects, and don't we just need to design molecules and do the preclinical and clinical testing?
>> which is why I'm bringing to the attention of someone with a better background in the science <<
No. I have a better background in science, not THE science..... you and I have equivalent bkgds here.
Not trying, actively, to frustrate you.
:-)
Shopping for a four wheel drive Tacoma today. Somebody stop me.
Best! Rick
edit: guys like T'sdad and BJ might have a better bkgd here. Neuro certainly is concerned about distributions across bbb and about peripheral effects. PGS is an expert in vascular smooth muscle. Etc. You really do try to pump a dry well, ya know?? |
