2-Chloroamphetamine

2-Chloroamphetamine (2-CA), also known as ortho-chloroamphetamine (OCA), is a monoamine releasing agent (MRA) of the amphetamine family related to 2-fluoroamphetamine (2-FA).^[1]

2-Chloroamphetamine

Clinical data
Other names	2-CA; ortho-Chloroamphetamine; o-Chloroamphetamine; OCA; o-CA
Drug class	Monoamine releasing agent
Identifiers
IUPAC name 1-(2-chlorophenyl)propan-2-amine
CAS Number	21193-23-7
PubChem CID	152331
ChemSpider	134269
UNII	00Q9Z0HNOQ
ChEBI	CHEBI:180535
CompTox Dashboard (EPA)	DTXSID40943523
Chemical and physical data
Formula	C9H12ClN
Molar mass	169.65 g·mol−1
3D model (JSmol)	Interactive image
SMILES CC(CC1=CC=CC=C1Cl)N
InChI InChI=1S/C9H12ClN/c1-7(11)6-8-4-2-3-5-9(8)10/h2-5,7H,6,11H2,1H3 Key:IQHHOHJDIZRBGM-UHFFFAOYSA-N

Pharmacology

Pharmacodynamics

It has been found to induce the release of norepinephrine and dopamine in rat brain synaptosomes with EC₅₀Tooltip half-maximal effective concentration values of 19.1 and 62.4 nM, respectively, whereas serotonin was not reported.^[1] It has been found to also induce the release of serotonin in mouse brain slices to some degree,^[2] whereas it did not induce the release of serotonin in the brain in rats in vivo.^[3]

In contrast to amphetamine and para-chloroamphetamine (PCA; 4-chloroamphetamine), 2-CA does not appear to produce hyperlocomotion in mice, and instead has been found to decrease locomotor activity.^[4] However, it did potentiate the effects of levodopa similarly to amphetamine and PCA.^[4] On the other hand, like amphetamine but in contrast to PCA and 4-methylamphetamine (4-MA), 2-CA did not potentiate the effects of 5-hydroxytryptophan (5-HTP).^[4] Unlike PCA, 2-CA did not produce the head-twitch response, a behavioral proxy of psychedelic-like effects, in mice.^[4]

In contrast to PCA, but similarly to amphetamine, 2-CA does not appear to produce serotonergic neurotoxicity in rats or guinea pigs.^[5][6][3][7] While this could be attributed to rapid metabolism in the case of 3-chloroamphetamine (3-CA), 2-CA continued to lack serotonergic neurotoxicity even when its metabolism was inhibited by desipramine.^[6]