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Re: +++ MAO-A or B ? Gerovital (procaine) selectivity

Posted by undopaminergic on July 6, 2008, at 13:12:44

In reply to Re: +++ MAO-A or B ? Gerovital (procaine) selectivity » undopaminergic, posted by SLS on July 6, 2008, at 5:15:18

> It might be worth your looking into if it is important enough to you. I have. Clorgyline is a specific inhibitor of MAO-A. Just enter "clorgyline" and "specific" as keywords when performing a Medline search.
>

Unfortunately, you seem to be reading too much significance into the word "specific". In reality, clorgyline doesn't have perfect specificity, but rather a significant - and practically useful - preference for MAO-A over MAO-B. However, at higher doses, it binds to other targets as well, including at least MAO-B in a manner that inhibits its activity. There are few, if any, drugs that are perfectly specific for anything.

"rats were treated for 21 days with either deprenyl (0.25 mg/kg), TVP-1012 [0.05 mg/kg], an irreversible inhibitor of MAO-B that is not metabolized to amphetamines, clorgyline (0.2 mg/kg)"
"Chronic treatment with the MAO-B inhibitors reduced striatal MAO-B activity by 90%, with 15% (TVP-1012) or 40% (deprenyl) inhibition of MAO-A. Clorgyline inhibited MAO-A by 95%, with 30% inhibition of MAO-B."
(from http://www.ncbi.nlm.nih.gov/pubmed/8858937 )

> Just because clorgyline and selegiline are propargyl MAOIs doesn't guarantee any similarity in biological activity at all.
>

OK, but incidentally, I think the fact that both bind irreversibly to MAO enzymes already qualifies as substantial similarity in biological activity. I'm not denying that the similarity coexists with significant differences between the two compounds.

> Look at amineptine and tianeptine, for example. Tianeptine is a sister drug to amineptine, yet does not directly affect dopamine uptake at all.
>

I suspect that it does affect dopamine uptake at high doses, but that's another story.

> You might have to relegate yourself to the uncomfortable position of having to trust me on this one. Inhibition of MAO-A is of greater therapeutic effect than is inhibition of MAO-B in treating depression. In fact, inhibiting MAO-B might be counterproductive.
>

That's possible, but more counterproductive side effects are known for MAO-A inhibition than for MAO-B inhibition. Unfortunately, you are probably right in that considerable MAO-A inhibition is required. It might even be sufficient, but if that's the case, this isn't about dopamine or any of the three major monoamine neurotransmitter, but possibly about a trace amine or other substance potentiated by MAO-A inhibition, or about adaptive changes that occur within the cell and has some antidepressant effect in the long term. One proposal for the antidepressant trace substance is acetylserotonin, the melatonin precursor.



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