PEA-P HCl, ≥98%

Chemical Information:

Technical Information:

Background:

PEA-P (3-[(2-phenylethyl)amino]-propanenitrile hydrochloride) is an N-substituted derivate of the endogenous trace amine, 2-Phenylethylamine (PEA). PEA has several key functions in the human body, including acting as a neurotransmitter with stimulant effects and binding to TAAR1 proteins. It has been studied for its role in attention deficit disorder (ADD), depression, and schizophrenia.[1]

 The need for prodrugs of trace amines in the study of depression was first outlined by Coutts et al. in 1985.[2] Thus, PEA-P was initially developed as a possible means of studying the function of PEA in the central nervous system (CNS) and its potential role in depression, and the actions of antidepressant drugs.[3]

PEA has a very high affinity for monoamine oxidase type-B enzymes and a very short biological half-life, which makes using the amine itself difficult in studies.³ Furthermore, MAO inhibitors cause in increase in other several other amines, including epinephrine, norepinephrine and dopamine. Therefore, the researchers who initially designed PEA-P argued for the use of a ‘PEA prodrug’, to selectively elevate brain concentrations of PEA over a sustained period of time. [1]

The original article documenting the use of PEA-P found the following:

“Administration of PEA caused transient increases in PEA concentrations which decreased rapidly in brain and blood and at a slower rate in liver. Administration of [PEA-P] caused sustained elevations of PEA concentrations and elimination of PEA was markedly decreased in these tissues relative to the situation after administration of PEA itself…

Administration of [PEA-P] caused more prolonged decreases in brain noradrenaline, dopamine and 5-hydroxytryptamine concentrations than those observed after PEA administration, although values increased to control levels eventually.” [3]

Modes of action:

Compared to administration of PEA, PEA-P causes a much slower increase in brain PEA levels. 15 minutes after administration of 0.1 mmol / kg, i.p., PEA concentrations in the rat brain were 140 times greater than control. These concentrations decreased exponentially with a half-life of 22 minutes. Blood concentrations showed similar results – 130 times greater than control at 15 minutes after i.p. administration, with a half-life of 27 minutes. PEA-P causes a much greater increase in PEA concentration in the liver: 15 minutes post-administration, concentrations were 600 times greater than control. [3] 

Although PEA-P did not produce a significantly greater amount of PEA in the brain or blood than administration of PEA, it allowed relatively sustained elevations compared to PEA administration.³ PEA-P causes weak inhibition of MAO-A and MAO-B enzymes, with enzyme function returning to normal after 2 hours. Compared to PEA administration, PEA-P caused significantly less changes in concentration of other amines. [3]

Further Scientific research:

There is no further scientific research available for this compound.

Clinical Reviews:

No clinical reviews or meta-analyses have been performed for this compound, due to the relative lack of data.

Human studies:

No human studies have been performed using this compound.

Animal studies:

Apart from the initial study cited above, no further animal studies have been published using this compound.

Toxicity Cases:

No toxicity cases have been reported for this compound.

References: