Editing Amphetamine (section)

===Related endogenous compounds===
{{Further|topic=related compounds|Trace amine}}
Amphetamine has a very similar structure and function to the [[wikt:endogenous|endogenous]] trace amines, which are naturally occurring [[neuromodulator]] molecules produced in the human body and brain.<ref name="Miller" /><ref name="Trace Amines" /><ref name="Human trace amines and hTAARs October 2016 review">{{cite journal | vauthors = Khan MZ, Nawaz W | title = The emerging roles of human trace amines and human trace amine-associated receptors (hTAARs) in central nervous system | journal =Biomedicine & Pharmacotherapy| volume = 83 | pages = 439–449 | date = October 2016 | pmid = 27424325 | doi = 10.1016/j.biopha.2016.07.002 }}</ref> Among this group, the most closely related compounds are [[phenethylamine]], the parent compound of amphetamine, and {{nowrap|[[N-methylphenethylamine|''N''-methylphenethylamine]]}}, a structural [[isomer]] of amphetamine (i.e., it has an identical molecular formula).<ref name="Miller" /><ref name="Trace Amines" /><ref name="Renaissance GPCR">{{cite journal |vauthors=Lindemann L, Hoener MC |title=A renaissance in trace amines inspired by a novel GPCR family |journal=Trends in Pharmacological Sciences|volume=26 |issue=5 |pages=274–281 |date=May 2005 |pmid=15860375 |doi=10.1016/j.tips.2005.03.007 | quote = <!-- In addition to the main metabolic pathway, TAs can also be converted by nonspecific ''N''-methyltransferase (NMT) [22] and phenylethanolamine ''N''-methyltransferase (PNMT) [23] to the corresponding secondary amines (e.g. synephrine [14], ''N''-methylphenylethylamine and ''N''-methyltyramine [15]), which display similar activities on TAAR1 (TA1) as their primary amine precursors. -->}}</ref> In humans, phenethylamine is produced directly from {{nowrap|[[L-phenylalanine|<small>L</small>-phenylalanine]]}} by the [[aromatic amino acid decarboxylase]] (AADC) enzyme, which converts {{nowrap|[[L-DOPA|<small>L</small>-DOPA]]}} into dopamine as well.<ref name="Trace Amines" /><ref name="Renaissance GPCR" /> In turn, {{nowrap|''N''-methylphenethylamine}} is metabolized from phenethylamine by [[phenylethanolamine N-methyltransferase|phenylethanolamine ''N''-methyltransferase]], the same enzyme that metabolizes norepinephrine into epinephrine.<ref name="Trace Amines">{{cite journal | author = Broadley KJ | title = The vascular effects of trace amines and amphetamines | journal =Pharmacology & Therapeutics| volume = 125 | issue = 3 | pages = 363–375 |date=March 2010 | pmid = 19948186 | doi = 10.1016/j.pharmthera.2009.11.005 | quote = <!-- '''Fig. 2.''' Synthetic and metabolic pathways for endogenous and exogenously administered trace amines and sympathomimetic amines&nbsp;...<br /> Trace amines are metabolized in the mammalian body via monoamine oxidase (MAO; EC 1.4.3.4) (Berry, 2004) (Fig. 2)&nbsp;... It deaminates primary and secondary amines that are free in the neuronal cytoplasm but not those bound in storage vesicles of the sympathetic neurone&nbsp;...<br />Thus, MAO inhibitors potentiate the peripheral effects of indirectly acting sympathomimetic amines&nbsp;... this potentiation occurs irrespective of whether the amine is a substrate for MAO. An α-methyl group on the side chain, as in amphetamine and ephedrine, renders the amine immune to deamination so that they are not metabolized in the gut. Similarly, β-PEA would not be deaminated in the gut as it is a selective substrate for MAO-B which is not found in the gut&nbsp;...<br /> Brain levels of endogenous trace amines are several hundred-fold below those for the classical neurotransmitters noradrenaline, dopamine and serotonin but their rates of synthesis are equivalent to those of noradrenaline and dopamine and they have a very rapid turnover rate (Berry, 2004). Endogenous extracellular tissue levels of trace amines measured in the brain are in the low nanomolar range. These low concentrations arise because of their very short half-life&nbsp;... -->}}</ref><ref name="Renaissance GPCR" /> Like amphetamine, both phenethylamine and {{nowrap|''N''-methylphenethylamine}} regulate monoamine neurotransmission via {{abbr|TAAR1|trace amine-associated receptor 1}};<ref name="Miller" /><ref name="Human trace amines and hTAARs October 2016 review" /><ref name="Renaissance GPCR" /> unlike amphetamine, both of these substances are broken down by [[monoamine oxidase B]], and therefore have a shorter half-life than amphetamine.<ref name="Trace Amines" /><ref name="Renaissance GPCR" />