N-Methyl-Tyrosine (NMTyr), also known as Surinamine, is an amino acid found in the Andira & Rhatany species of plant. This compound was recently released in a stimulant pre-workout formula as a component of the "Shred complex (1)." Ironically, N-Methyl-Tyrosine was investigated in the 1940's as an anti-stimulant.
As the name suggests, N-Methyl-Tyrosine is the N-methylated analogue of L-Tyrosine. Differing from L-Tyrosine in its pharmacokinetics however, NMTyr is unable to become hydroxylated on the meta position of the benzyl ring. This conversion would normally convert L-Tyrosine into L-Dopa via the enzyme Tyrosine Hydroxylase. In fact, N-Methyl-Tyrosine is still offered from various laboratories as a tyrosine hydroxylase inhibitor (2).
Without the ability to become a true catchol, the next step would normally be decarboxylation. Unfortunately, NMTyr is not a substrate for dopa decarboxylase, and therefore is a metabolic dead-end (3).
|The production of CO2 is an indicator of decarboxylase activity. N-methyl-tyrosine is unreactive.|
N-Methyl-Tyrosine possesses a carboxylic acid on the alpha carbon which prevents direct adrenergic receptor binding, in addition to deamination throught steric hindrance. The former modality creates a physiologic receptor antagonist via the law of mass action and vesicular depletion, and the latter increases its half-life, extending its enzymatic inhibition for a longer period of time. Even in the unlikely event of decarboxylation, NMTyr would simply yield non-beta-hydroxylated, para-hydroxylated, metabolites including NMT, which would only excacerbate its anti-adrenergic potential.
- Inhibits Tyrosine hydroxylase - Decreases the natural production of catecholamines/neurotransmitters
- Not a substrate for Dopa decarboxylase - No potential for metabolic improvement
- Competes for neuronal vesicular uptake with viable precursors (L-tyrosine, L-dopa, L-Phenylalanine) - Physiologic competitive antagonist