Posted by jamestheyonger on November 30, 2005, at 19:56:26
In reply to Desoxyn metabolism/pharmacology, posted by mike99 on November 30, 2005, at 13:35:02
> 3. Is the conversion to amphetamine clinically significant? My understanding is that one of the benefits of meth or standard amphetamine is that it is less peripherally acting...but if it's converted to amphetamine wouldn't this then have the same peripheral actions as dextro and/or levoamphetamine?
>
> Thanks a bunch
http://publib.upol.cz/~obd/fulltext/Chemica40/chem40-3.pdf
"In all cases, (–)-L-MAP, which is physiologically much less active, is excreted mainly in unchanged form, whereas the found concentrations of the opposite (+)-MAP
enantiomer are significantly lower. A maximum concentration of MAP in urine can be
found in about 12 hours after the oral administration, then its level decreases. It was
still possible to detect and separate MAP enantiomers 48 hours after the administration
of the drug. For the racemic MAP administered, the situation is very similar,(+)-D-MAP is more distributed and transformed in comparison to (–)-MAP.Amphetamine, the main metabolite of MAP, was also present in assayed urine samples. Again, the less active (–)-AP isomer was found in higher concentration. This isomer came exclusively from (–)-isomer of MAP, no cross isomerisation was observed. A maximum amount of AP enantiomers was found in 24 hours after administration of drug."
So phenylethylamine
http://www.chocolate.org/pea.htm) and both isomers of Amphetamine are the primary products of metabolism.I have read that it may well be Amphetamine is what provides the stimulation in MAP & that MAP
may not be active or very active in humans. In a study of experienced IV drug users they could not tell the difference between MAP and AP by injection. So MAP is "stronger" as it hangs around longer to be changed into AP. AP has a much shorter half life than MAP.
poster:jamestheyonger
thread:583104
URL: http://www.dr-bob.org/babble/20051126/msgs/583852.html