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All of their experimental ligands seem to be unknown "in the wild". However, I'm not sure whether the studies detailing the activities of mono-fluoro-amphetamines have screened for activity as direct agonists.

ebola
 
sekio said:
Not a journal article but interesting anyway

Derek Lowe - Chemical probes vs drugs

-snip-

Makes me think about, say, the NBOMes versus LSD.
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I'd like to think that more selective drug-like compounds would ultimately and necessarily mean better drugs. If any non-selective drug is effective due to interacting with multiple targets, then would those effects not be achievable with a cocktail of individual ligands?
 
Yes, but then instead of one ADME problem, you have n ADME problems that all depend on each other... unless those agents are perfectly selective and don't touch each others metabolism, you're probably better off with a monotherapy.
 
So why doesn't smoking tobacco also reduce alcohol consumption?
 
EtOH is such a goddamn dirty drug. Is there anything it doesn't interact with?
 
The great thing about EA is he's extremely knowledgeable, has a sense of humor, is helpful, AND is humble.

No hate towards the other mods/titans of add though, and special shout-out to seker the wrecker.

I wonder why in that study though the author didn't conclude the same about mixed amp salts. I was always under the impression that they're more effective for attention disorders than the piperazine-derived ones.

Also, why don't they use diethylpropion and phenmetrazine for attention disorders, as they have less potential for abuse and have more adrenergic and ne activity than their phenylethylamine-related counterparts?

And if cathinones are primarily releasers as Ebola said then why is bupropion basically strictly an ndri?

Feel free to correct anything I said.
 
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And if cathinones are primarily releasers as Ebola said then why is bupropion basically strictly an ndri?
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There are *always* exceptions. Usually, empirical observations of activity take precedence over assuming it "should" be a resleasing agent.

diethylpropion and phenmetrazine for attention disorders, as they have less potential for abuse
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Ask the Beatles about that one - esp. phenmetrazine.
 
1. Varenicline is a partial agonist at nicotinic receptors, so full agonists might not share this property and
2. the relationship between nicotine and alcohol consumption might differ between those with alcohol dependence and those without alcohol dependence. Anecdotally, we can refer to people who take up chain-smoking while beginning AA.

ebola
 
Ho-Chi-Minh said:
The great thing about EA is he's extremely knowledgeable, has a sense of humor, is helpful, AND is humble.

No hate towards the other mods/titans of add though, and special shout-out to seker the wrecker.

I wonder why in that study though the author didn't conclude the same about mixed amp salts. I was always under the impression that they're more effective for attention disorders than the piperazine-derived ones.

Also, why don't they use diethylpropion and phenmetrazine for attention disorders, as they have less potential for abuse and have more adrenergic and ne activity than their phenylethylamine-related counterparts?

And if cathinones are primarily releasers as Ebola said then why is bupropion basically strictly an ndri?

Feel free to correct anything I said.
Click to expand...

Awe thanks bro :) But lets not forget some of the ADD veterans like nuke, ebola?, the various Hamms, and some of the up and comers like gaius and cannibalsnail.

Bupropion is (according to my old British neuropharmacology prof) a NDRI likely because its too bulky to be transported into the cell via DAT/NET. This is the same logic some drug companies had when creating methylphenidate "yo bro lets make this amphetamine backbone bulky as hell and possibly charged so it can't diffuse through the membrane, that'll probably block catecholamine reuptake".
 
And if cathinones are primarily releasers as Ebola said then why is bupropion basically strictly an ndri?
Click to expand...

My point was actually that cathinones relatively close to the cathinone skeleton itself tend to be releasers. Put some bulk on that alpha-chain, and you wander into reuptake inhibition instead. I think that EA's explanation is sound, but I still wonder why alpha-substitutions tend to abolish releasing activity more effectively than ring-substitutions.

ebola
 
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