PEA-P HCl, ≥98%

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N-substituted derivative of 2-Phenylethylamine, an endogenous trace amine.

Chemical Name3-[(2-phenylethyl)amino]-propanenitrile hydrochloride
Synonyms3-Phenethylamino-propionitrile hydrochloride; N-(2-Cyanoethyl)phenethylamine hydrochloride; "desmethyl fenproporex"; 1488-20-6
FormWhite to pale cream powder.
Molecular FormulaC11H14N2•HCl
Molecular Weight210.71 g/mol
SolubilitySoluble 50 mg / mL in water; Soluble to 50 mg / mL in ethanol.

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This Material is Sold For Research Use Only. Terms of Sale Apply. Not for Human Consumption, nor Medical, Veterinary, or Household Uses.

Chemical Information:

CAS Number:73605-24-0
Molecular Weight:210.71 g/mol
Melting Point:181-184°C
Molecular Formula:C11H14N2•HCl
Synonyms: 3-Phenethylamino-propionitrile hydrochloride; 3-[(2-phenylethyl)amino]-propanenitrile hydrochloride; N-(2-Cyanoethyl)phenethylamine hydrochloride; "desmethyl fenproporex"; 1488-20-6
PubChem CID:45074893


Technical Information:

Application:N-substituted derivative of 2-Phenylethylamine, an endogenous trace amine and monoamine releaser.
Appearance:White to pale cream powder
Physical State:Solid
Solubility:Soluble 50 mg / mL in water; Soluble to 50 mg / mL in ethanol.
Storage:Store at room temperature or cooler, in a sealed airtight container, protected from heat, light and humidity.
Stability:Stable for at least two years when stored as above.



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.



[1] Irsfeld, M., Spadafore, M., Prüß, B.M. (2013). β-phenylethylamine, a small molecule with a large impact. WebmedCentral, 4(9):4409.

[2] Coutts, R.T., Baker, G.B., Nazarali, A.J., Rao, T.S., Micetich, R.G., E.T.W. Hall. (1985). Chapter: Prodrugs of Trace Amines. In: Neuropsychopharmacology of the Trace Amines, pp. 175-80.

[3] Baker, G.B., Coutts, R.T., Rao, T.S. (1987). Neuropharmacological and neurochemical properties of N-(2-cyanoethyl)-2-phenylethylamine, a prodrug of 2-phenylethylamine. British Journal of Pharmacology, 92,243-255

Precaution and Disclaimer:

This Material is Sold For Research Use Only. Terms of Sale Apply. Not for Human Consumption, nor Medical, Veterinary, or Household Uses.

[PEA-P HCL Q1 2018] PEA-P HCL.20171202.pdf