| Systematic (IUPAC) name | |
|---|---|
| 1-(3-chlorophenyl)piperazine | |
| Clinical data | |
| Pregnancy cat. | ? |
| Legal status | See below.. |
| Routes | Oral, Nasal, Rectal |
| Pharmacokinetic data | |
| Metabolism | Hepatic |
| Half-life | 2-6 hours |
| Excretion | Renal |
| Identifiers | |
| CAS number | 51639-49-7 |
| ATC code | None |
| PubChem | CID 1355 |
| IUPHAR ligand | 142 |
| ChemSpider | 1314 |
| ChEBI | CHEBI:10588 |
| ChEMBL | CHEMBL478 |
| Chemical data | |
| Formula | C10H13ClN2 |
| Mol. mass | 196.676 g/mol |
| SMILES | eMolecules & PubChem |
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meta-Chlorophenylpiperazine (mCPP) is a psychoactive drug of the phenylpiperazine class. It was initially developed in the late-1970s and used in scientific research before being sold as a designer drug in the mid-2000s.[1][2] It has been detected in pills touted as legal alternatives to illicit stimulants in New Zealand and pills sold as "ecstasy" in Europe and the United States.[3][4]
Despite its advertisement as a recreational substance, mCPP is actually generally considered to be an unpleasant experience and is not desired by drug users.[3] It lacks any reinforcing effects,[5] produces depressive and anxiogenic effects in rodents and humans,[6][7] and can induce panic attacks in individuals susceptible to them.[8][9][10][11] It also worsens obsessive-compulsive symptoms in people with the disorder.[12][13][14]
mCPP is known to induce headaches in humans and has been used for testing potential antimigraine medications.[15][16][17] It has potent anorectic effects and has encouraged the development of selective 5-HT2C receptor agonists for the treatment of obesity as well.[18][19][20][21]
Meta-chlorophenylpiperazine is a major metabolite of the psychotropic drug trazodone, and may be responsible for some of its side-effects, such as headaches and migraines induced many hours after initial consumption.
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mCPP possesses significant affinity for the 5-HT1A, 5-HT1B, 5-HT1D, 5-HT2A, 5-HT2B, 5-HT2C, 5-HT3, and 5-HT7 receptors, as well as the SERT.[22] It also has some affinity for α1-adrenergic, α2-adrenergic, H1, I1, and NET.[22][23] It behaves as an agonist at most or all serotonin receptors.[22][24][25] mCPP has been shown to act not only as a reuptake inhibitor of serotonin but as a releasing agent as well.[26]
mCPP's strongest actions are at the 5-HT2B and 5-HT2C receptors and its discriminative cue is mediated primarily by 5-HT2C.[22][27][28] Its negative effects such as anxiety, headaches, and appetite loss are likely mediated by its actions on the 5-HT2C receptor,[7][18][29] whereas its psychedelic effects at high doses are caused by 5-HT2A activation. Other effects of mCPP include nausea, hypoactivity, and penile erection, the latter two the result of increased 5-HT2C activity and the former likely via 5-HT3 stimulation.[30][31][32]
mCPP is metabolized via the CYP2D6 isoenzyme by hydroxylation to p-hydroxy-mCPP (OH-mCPP).[33] Caution should be exercised in coprescribing inhibitors or substrates of CYP2D6 with drugs such as Trazodone and Nefazodone that have mCPP as a metabolite.[33]
Based on the recommendation of the EACD, the New Zealand government has passed legislation which placed BZP, along with the other piperazine derivatives TFMPP, mCPP, pFPP, MeOPP and MBZP, into Class C of the New Zealand Misuse of Drugs Act 1975. A ban was intended to come into effect in New Zealand on December 18, 2007, but the law change did not go through until the following year, and the sale of BZP and the other listed piperazines became illegal in New Zealand as of 1 April 2008. An amnesty for possession and usage of these drugs remained until October 2008, at which point they became completely illegal.[38]
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