MCPP

CYP2D6-mediated bioactivation of mCPP produces a reactive quinone imine intermediatesupported

mCPP, a major circulating metabolite, is bioactivated by CYP2D6 to a quinone imine intermediate. dmd.107.019471

Gaillard and colleagues reported the death of a 20-year-old male cocaine user with pre-existing allergic asthma who ingested approximately 20 mg of mCPP in a tablet sold as ecstasy (stamped with a "smiling sun" logo)supported

A 20-year-old asthmatic cocaine addict died after ingesting ~20mg mCPP in a tablet sold as ecstasy. j.1556-4029.2012.02254.x

A female patient ingested three tablets sold as ecstasy, achieving a plasma mCPP concentration of 320 ng/mL — approximately 6 times the upper range of trazodone-derived therapeutic levels (26–108 ng/mL)supported

female ingested three multi-coloured tablets... Plasma mCPP 320 ng/mL (6x therapeutic trazodone levels). ftd.0b013e318170a879

Baumann and colleagues demonstrated that repeated mCPP administration in rats produces large acute serotonin elevations (>5-fold over baseline) but does not cause long-term serotonin depletion at two-week follow-up, in direct contrast to fenfluramine and d-fenfluraminesupported

mCPP is a SERT substrate producing >5-fold elevations in extracellular 5-HT but does NOT cause long-term serotonin depletion 2 weeks after dosing (unlike fenfluramine/d-fenfluramine). npp.2013.331

Gobbi and colleagues confirmed that mCPP, as a non-neurotoxic SERT substrate, produces substantially lower synaptosome-level serotonin release than neurotoxic compounds such as MDMA or para-chloroamphetaminesupported

in synaptosomes induce much lower release than pCA and MDMA. mCPP is non-neurotoxic SERT substrate. pmid:12354291

mCPP's combined 5-HT receptor agonism and serotonin-releasing activity create significant pharmacological potential for serotonin syndrome when combined with other serotonergic agentssupported

risks of psychiatric disorders and serotonin syndrome must be taken into account. pmid:17348609

Kast argued that chronic mCPP generation from trazodone poses ongoing serotonergic risk that may be clinically underappreciated.supported

Clinically significant levels of m-CPP are generated in patients using trazodone for sleep and present 24h a day with potentially serious ill effects. 15622970902836022

Patients receiving therapeutic doses of trazodone, nefazodone, or etoperidone are continuously exposed to mCPP as an active metabolite via CYP3A4-mediated N-dealkylationsupported

Trazodone, nefazodone, and etoperidone are classified as atypical antidepressants belonging to the phenylpiperazine class. These antidepressants are primarily metabolized by CYP3A4 into m-chlorophenylpiperazine (mCPP). 03602532.2025.2465482

Kast estimated that clinically significant mCPP levels persist 24 hours per day in trazodone-treated patients and argued that the documented adverse effects may outweigh the benefits of trazodone given the availability of safer alternativessupported

Clinically significant levels of m-CPP are generated in patients using trazodone for sleep and present 24h a day with potentially serious ill effects. 15622970902836022

False-positive urine MDMA testing in trazodone patients is a documented forensic complication.supported

mCPP causes false-positive results on the urine EMIT test for MDMA. Significant crossreactivity of trazodone and mCPP on the Ecstasy EMIT II assay. pmid:21073812

Anxiety is the most consistently documented psychological effect of mCPP and represents a genuine clinical risk rather than merely an unpleasant side effectsupported

Various behavioral effects depending on population. pmid:1663792

In clinical challenge studies at doses of 0.08–0.5 mg/kg (oral and IV), mCPP reliably induces panic-like states, acute dysphoria, and depersonalization in both healthy volunteers and psychiatric patientssupported

mCPP induced depersonalization significantly more than placebo. Correlation between depersonalization and increase in panic. pmid:8570768

OCD patients experience acute symptom exacerbation at challenge doses.supported

Obsessive-compulsive symptoms increased markedly after mCPP. pmid:3036259

Individuals with pre-existing anxiety disorders, OCD, borderline personality disorder, or psychotic spectrum disorders are at heightened risk of severe psychological distress following mCPP exposuresupported

risks of psychiatric disorders and serotonin syndrome must be taken into account. pmid:17348609

Depersonalization occurs significantly more frequently than with placebo across multiple clinical populations, correlating with panic induction but dissociable from baseline anxiety or depression severity.supported

mCPP induced depersonalization significantly more than placebo. Correlation between depersonalization and increase in panic, but not anxiety, sadness, depression, or drowsiness. pmid:8570768

The compound does not exhibit reinforcing properties in standard animal or human paradigmssupported

mCPP does not exhibit reinforcing effects. pmid:17348609

Claim in safety — inconclusiveinconclusiveworking →

Claim in safety — inconclusiveinconclusiveworking →

The MDMA interaction is documented clinically: prior MDMA use alters mCPP neuroendocrine responses, initially blunting and later enhancing them, consistent with MDMA-induced serotonergic neurotoxicitysupported

MDMA users showed altered neuroendocrine and behavioral responses to mCPP, suggesting functional consequences of MDMA-induced serotonin neurotoxic effects. pmid:10591869

The MDMA interaction is documented clinically: prior MDMA use alters mCPP neuroendocrine responses, initially blunting and later enhancing them, consistent with MDMA-induced serotonergic neurotoxicitysupported

Monkeys 2 weeks after MDMA: non-significant reduction in prolactin response to mCPP. Monkeys 3.5 years after MDMA: significantly increased prolactin responses. pmid:11842446

Cocaine inhibits CYP2D6, reducing mCPP hydroxylation and elevating plasma concentrationssupported

co-consumed cocaine and diltiazem as potential CYP2D6 inhibitors. pmid:17574934

A forensic case documented mCPP as an adulterant of cocaine, highlighting real-world exposure scenarios where both compounds are present simultaneouslysupported

Case describing unequivocal proof of mCPP intake. co-consumed cocaine and diltiazem as potential CYP2D6 inhibitors. pmid:17574934

Claim in safety — inconclusiveinconclusiveworking →

Patients receiving trazodone, nefazodone, or etoperidone are already generating mCPP via CYP3A4 metabolismsupported

Trazodone, nefazodone, and etoperidone...are primarily metabolized by CYP3A4 into m-chlorophenylpiperazine (mCPP). 03602532.2025.2465482

Kast estimated that trazodone-treated patients maintain clinically significant mCPP levels continuously.supported

Clinically significant levels of m-CPP are generated in patients using trazodone for sleep and present 24h a day. 15622970902836022

Alcohol was present (0.7 g/L) in the only documented non-fatal mCPP overdose casesupported

Also had amphetamine, benzoylecgonine, alcohol (0.7 g/L). ftd.0b013e318170a879

The single documented mCPP fatality occurred in a patient with pre-existing allergic asthma who ingested approximately 20 mg (oral)supported

A 20-year-old asthmatic cocaine addict died after ingesting ~20mg mCPP in a tablet sold as ecstasy. j.1556-4029.2012.02254.x

Pre-existing anxiety disorders, OCD, borderline personality disorder, and psychotic spectrum disorders increase the risk of severe psychological distress following mCPP exposure. mCPP reliably exacerbates OCD symptoms and induces depersonalization in vulnerable populationssupported

risks of psychiatric disorders and serotonin syndrome must be taken into account. pmid:17348609

Pre-existing anxiety disorders, OCD, borderline personality disorder, and psychotic spectrum disorders increase the risk of severe psychological distress following mCPP exposure. mCPP reliably exacerbates OCD symptoms and induces depersonalization in vulnerable populationssupported

OCD patients became significantly more anxious, depressed, and dysphoric after mCPP. Obsessive-compulsive symptoms increased markedly after mCPP. pmid:3036259

Pre-existing anxiety disorders, OCD, borderline personality disorder, and psychotic spectrum disorders increase the risk of severe psychological distress following mCPP exposure. mCPP reliably exacerbates OCD symptoms and induces depersonalization in vulnerable populationssupported

mCPP induced depersonalization significantly more than placebo. pmid:8570768

Claim in safety — inconclusiveinconclusiveworking →

Individuals with CYP2D6 poor metabolizer genotype or those taking CYP2D6 inhibitors will achieve substantially higher mCPP plasma concentrations from the same dose, increasing all dose-dependent riskssupported

mCPP/hydroxy-mCPP ratio indicated CYP2D6 metabolism; co-consumed cocaine and diltiazem as potential CYP2D6 inhibitors. pmid:17574934

Claim in safety — inconclusiveinconclusiveworking →

mCPP produces mild elevations in systolic and diastolic blood pressure and heart ratesupported

BP, heart rate, and temperature mildly elevated. pmid:12496949

Claim in safety — inconclusiveinconclusiveworking →

mCPP is a multi-target serotonergic compound whose primary pharmacological action is partial agonism at the 5-HT₂C receptorsupported

mCPP is a safe, reliable, direct 5-HT agonist. pmid:1663792

mCPP is a multi-target serotonergic compound whose primary pharmacological action is partial agonism at the 5-HT₂C receptorsupported

Confirms primary role for 5-HT2C receptor (not 5-HT2A or 5-HT2B) in mCPP-induced hypolocomotion. pmid:11856898

This has been established through multiple antagonist studies: the selective 5-HT₂C antagonist SB-242084 blocks mCPP-induced hypolocomotion in animal models, ritanserin (a 5-HT₂/₁C antagonist) attenuates mCPP-induced anxiety and prolactin release in humans, and metergoline (a non-selective 5-HT antagonist) fully blocks both behavioral and neuroendocrine effects in OCD patients.supported

m-CPP hypolocomotion not attenuated by 5-HT2A antagonists (MDL 100,907, ketanserin) or 5-HT2B antagonists. Reversed by selective 5-HT2C antagonist SB 242084. pmid:11856898

This has been established through multiple antagonist studies: the selective 5-HT₂C antagonist SB-242084 blocks mCPP-induced hypolocomotion in animal models, ritanserin (a 5-HT₂/₁C antagonist) attenuates mCPP-induced anxiety and prolactin release in humans, and metergoline (a non-selective 5-HT antagonist) fully blocks both behavioral and neuroendocrine effects in OCD patients.supported

Ritanserin attenuated mCPP-induced anxiety and prolactin, completely antagonized cortisol elevations. pmid:1754635

This has been established through multiple antagonist studies: the selective 5-HT₂C antagonist SB-242084 blocks mCPP-induced hypolocomotion in animal models, ritanserin (a 5-HT₂/₁C antagonist) attenuates mCPP-induced anxiety and prolactin release in humans, and metergoline (a non-selective 5-HT antagonist) fully blocks both behavioral and neuroendocrine effects in OCD patients.supported

Metergoline blocked mCPP-induced anxiety and OCD symptom exacerbation, confirming serotonergic mediation of mCPP effects including OCD symptom elicitation. pmid:2018816

Claim in pharmacology — inconclusiveinconclusiveworking →

Beyond direct receptor agonism, mCPP functions as a serotonin transporter (SERT) substrate, inducing transporter-mediated serotonin efflux — a mechanism shared with MDMA and fenfluramine but pharmacologically distinct from classical reuptake inhibitionsupported

mCPP confirmed as a SERT substrate releasing 5-HT from rat brain synaptosomes. mCPP included alongside fenfluramine, MDMA, 5-HT in dose-response assays for serotonin releasing activity. syn.20804

Beyond direct receptor agonism, mCPP functions as a serotonin transporter (SERT) substrate, inducing transporter-mediated serotonin efflux — a mechanism shared with MDMA and fenfluramine but pharmacologically distinct from classical reuptake inhibitionsupported

mCPP is a SERT substrate producing >5-fold elevations in extracellular 5-HT. npp.2013.331

This serotonin-releasing activity contributes to the compound's overall serotonergic load but, critically, does not produce the long-term serotonin depletion characteristic of neurotoxic releasing agents.supported

mCPP is a SERT substrate producing >5-fold elevations in extracellular 5-HT but does NOT cause long-term serotonin depletion 2 weeks after dosing (unlike fenfluramine/d-fenfluramine). npp.2013.331

This serotonin-releasing activity contributes to the compound's overall serotonergic load but, critically, does not produce the long-term serotonin depletion characteristic of neurotoxic releasing agents.supported

mCPP is non-neurotoxic SERT substrate. pmid:12354291

Claim in pharmacology — inconclusiveinconclusiveworking →

mCPP's anxiogenic effects in humans are mediated via 5-HT₂C receptor activation, consistent with its established efficacy as an anxiogenic probe in healthy volunteers and psychiatric patients.supported

Reviews in vitro and in vivo properties in animals, normal human subjects, and psychiatric patients. mCPP is a safe, reliable, direct 5-HT agonist. pmid:1663792

The only dedicated human pharmacokinetic study of mCPP was conducted by Feuchtl and colleagues, who administered the compound both intravenously and orally to healthy male volunteerssupported

Pharmacokinetics of m-chlorophenylpiperazine after intravenous and oral administration in healthy male volunteers. pmid:15467976

mCPP is metabolized primarily by CYP2D6 via ring hydroxylation to form para-hydroxy-mCPP (p-OH-mCPP) as the principal metabolitesupported

mCPP/hydroxy-mCPP ratio indicated CYP2D6 metabolism. pmid:17574934

CYP2D6 also bioactivates mCPP to a reactive quinone imine intermediate, raising theoretical hepatotoxicity concernssupported

mCPP, a major circulating metabolite, is bioactivated by CYP2D6 to a quinone imine intermediate. dmd.107.019471

When mCPP is generated as a metabolite of trazodone, the parent compound is converted via CYP3A4-mediated N-dealkylationsupported

These antidepressants are primarily metabolized by CYP3A4 into m-chlorophenylpiperazine (mCPP). 03602532.2025.2465482

CYP2D6 polymorphisms (poor metabolizer vs. extensive metabolizer phenotype) and co-administered CYP2D6 inhibitors (cocaine, diltiazem, paroxetine, fluoxetine) significantly alter mCPP plasma exposure.supported

mCPP/hydroxy-mCPP ratio indicated CYP2D6 metabolism; co-consumed cocaine and diltiazem as potential CYP2D6 inhibitors. pmid:17574934

Claim in pharmacology — inconclusiveinconclusiveworking →

Recreational users consistently report few positive subjective effects, and the compound does not support self-administration in standard preclinical modelssupported

mCPP does not exhibit reinforcing effects. pmid:17348609

The experiential profile is dominated by anxiety, dysphoria, and depersonalization, with minimal hedonic potentialsupported

Various behavioral effects depending on population. pmid:1663792

Claim in summary — inconclusiveinconclusiveworking →

Wicker Jr. at the University of Florida as a candidate antihistamine, mCPP became the most extensively used pharmacological probe of serotonin function in psychiatry by the early 1990s, with applications spanning obsessive-compulsive disorder, depression, eating disorders, and seasonal affective disordersupported

mCPP is the most extensively used probe of serotonin function in psychiatry. Reviews in vitro and in vivo properties in animals, normal human subjects, and psychiatric patients. pmid:1663792

The compound appeared on European recreational drug markets around 2004, frequently sold as MDMAsupported

Metachlorophenylpiperazine (mCPP) is a psychoactive substance that appeared in 2004 on the black market of illicit substances in Europe and France. pmid:17348609

It is also generated continuously as the primary active metabolite of the antidepressant trazodone via CYP3A4-mediated N-dealkylation.supported

These antidepressants are primarily metabolized by CYP3A4 into m-chlorophenylpiperazine (mCPP). 03602532.2025.2465482

mCPP binds 5-HT₂C with approximately 10-fold selectivity over 5-HT₂A (Ki ≈ 32.1 nM at 5-HT₂A) and functions as a serotonin transporter substrate, inducing transporter-mediated 5-HT efflux rather than classical reuptake inhibitionpartially supported

mCPP is a SERT substrate producing >5-fold elevations in extracellular 5-HT but does NOT cause long-term serotonin depletion 2 weeks after dosing. npp.2013.331

mCPP binds 5-HT₂C with approximately 10-fold selectivity over 5-HT₂A (Ki ≈ 32.1 nM at 5-HT₂A) and functions as a serotonin transporter substrate, inducing transporter-mediated 5-HT efflux rather than classical reuptake inhibitionpartially supported

mCPP is non-neurotoxic SERT substrate. pmid:12354291

Blocking studies using ritanserin, metergoline, and the selective 5-HT₂C antagonist SB-242084 confirm that behavioral, neuroendocrine, and anxiogenic effects are primarily 5-HT₂C-mediated.supported

Ritanserin attenuated mCPP-induced anxiety and prolactin, completely antagonized cortisol elevations. Confirms 5-HT1c/5-HT2 receptor role. pmid:1754635

Blocking studies using ritanserin, metergoline, and the selective 5-HT₂C antagonist SB-242084 confirm that behavioral, neuroendocrine, and anxiogenic effects are primarily 5-HT₂C-mediated.supported

Metergoline blocked mCPP-induced anxiety and OCD symptom exacerbation, confirming serotonergic mediation of mCPP effects including OCD symptom elicitation. pmid:2018816

Blocking studies using ritanserin, metergoline, and the selective 5-HT₂C antagonist SB-242084 confirm that behavioral, neuroendocrine, and anxiogenic effects are primarily 5-HT₂C-mediated.supported

Reversed by selective 5-HT2C antagonist SB 242084. Confirms primary role for 5-HT2C receptor (not 5-HT2A or 5-HT2B) in mCPP-induced hypolocomotion. pmid:11856898

Despite its serotonin-releasing activity, mCPP is classified as non-neurotoxic — unlike MDMA and fenfluramine, it does not cause long-term serotonin depletionsupported

mCPP is a SERT substrate producing >5-fold elevations in extracellular 5-HT but does NOT cause long-term serotonin depletion 2 weeks after dosing (unlike fenfluramine/d-fenfluramine). npp.2013.331

One fatality has been documented: a 20-year-old asthmatic male who died following cardiorespiratory arrest after ingesting approximately 20 mgsupported

A 20-year-old asthmatic cocaine addict died after ingesting ~20mg mCPP in a tablet sold as ecstasy. Severe asthma attack evolved into fatal cardiorespiratory arrest. j.1556-4029.2012.02254.x

Claim in summary — inconclusiveinconclusiveworking →

Thomas and colleagues demonstrated in two controlled studies that mCPP (0.5 mg/kg oral) reduced palatable food consumption and BOLD fMRI responses to food images in healthy female volunteers via 5-HT₂C-mediated mechanismssupported

Brain 5-HT2C receptors form part of a neural network that controls eating behaviour. 5-HT2C receptor agonists decrease food intake by activating proopiomelanocortin (POMC) neurons. s00213-017-4764-9

Claim in clinical-evidence — inconclusiveinconclusiveworking →

The most comprehensive review, by Kahn and Wetzler in 1991, synthesized evidence from dozens of challenge studies across multiple psychiatric conditions.supported

Reviews in vitro and in vivo properties in animals, normal human subjects, and psychiatric patients. pmid:1663792

Pigott and colleagues demonstrated that metergoline fully blocked mCPP's behavioral and neuroendocrine effects in OCD patients, confirming serotonergic mediationsupported

Metergoline blocked mCPP-induced anxiety and OCD symptom exacerbation, confirming serotonergic mediation of mCPP effects including OCD symptom elicitation. pmid:2018816

mCPP challenge produced significant increases in alcohol craving in recently detoxified alcoholics, contributing to understanding of serotonergic mechanisms in relapsesupported

When challenged with mCPP, alcoholics report increases in craving and desire for alcohol. Serotonergic system manipulation linked to alcohol craving. pmid:1845592

MDMA users demonstrated altered neuroendocrine responses to mCPP — initially blunted and later enhanced — providing evidence of MDMA-induced serotonergic neurotoxicity.supported

Monkeys 2 weeks after MDMA: non-significant reduction in prolactin response to mCPP. Monkeys 3.5 years after MDMA: significantly increased prolactin responses. pmid:11842446

Across study populations, mCPP consistently produces dose-dependent elevations of ACTH, cortisol, prolactin, and growth hormonesupported

IV mCPP augmented prolactin, cortisol and growth hormone release. pmid:12496949

mCPP produces mild elevations in systolic and diastolic blood pressure and heart rate at IV challenge dosessupported

BP, heart rate, and temperature mildly elevated. pmid:12496949

fMRI studies demonstrate that mCPP (0.5 mg/kg oral) reduces BOLD responses to food images in reward-associated brain regions in healthy womensupported

The 5-HT2C receptor agonist meta-chlorophenylpiperazine (mCPP) reduces palatable food consumption and BOLD fMRI responses to food images in healthy female volunteers. s00213-017-4764-9

Claim in neuroscience — inconclusiveinconclusiveworking →

IV mCPP (0.08 mg/kg) produces a biphasic thermoregulatory response: initial hypothermia (−0.04°C at 12 minutes) followed by progressive hyperthermia (+0.17°C at 90 minutes), with concurrent elevation of plasma norepinephrinesupported

IV m-CPP (0.08 mg/kg) produced biphasic temperature changes: initial hypothermia (-0.04°C at 12 min) followed by hyperthermia (+0.17°C at 90 min). Also increased plasma norepinephrine. pmid:8597522

Claim in neuroscience — inconclusiveinconclusiveworking →

Unlike classical stimulants that potentiate dopaminergic reward pathways, mCPP produces minimal mesolimbic dopamine activation, consistent with its low reinforcing potential and the absence of self-administration behavior.supported

mCPP does not exhibit reinforcing effects. pmid:17348609

mCPP's anxiogenic effects represent one of the most reliably induced pharmacological anxiety states in human research, mediated by 5-HT₂C receptors in amygdala and prefrontal circuitssupported

mCPP is a safe, reliable, direct 5-HT agonist. Various behavioral effects depending on population. pmid:1663792

The mechanism of non-neurotoxicity — lower SERT-mediated ionic currents relative to neurotoxic substrates — has been characterized at the synaptosome level.supported

in synaptosomes induce much lower release than pCA and MDMA. mCPP is non-neurotoxic SERT substrate. pmid:12354291

Kahn and Wetzler described mCPP in 1991 as "the most extensively used probe of serotonin function in psychiatry", and through the period from approximately 1985 to 2005, the compound was administered to thousands of research participants across studies of OCD, major depression, bulimia nervosa, panic disorder, seasonal affective disorder, alcoholism, and cocaine dependence.supported

mCPP is the most extensively used probe of serotonin function in psychiatry. Reviews in vitro and in vivo properties in animals, normal human subjects, and psychiatric patients. pmid:1663792

Scientific interest emerged in the late 1970s and early 1980s, when mCPP was initially employed in veterinary medicine and subsequently recognized as a useful tool for probing central serotonin function in animal and then human paradigms.supported

mCPP, which was initially employed in veterinary medicine but has gained widespread use as a recreational drug globally. 03602532.2025.2465482

The utility of mCPP as a probe rested on its relatively selective 5-HT₂C agonism, which produced measurable neuroendocrine responses — elevations of cortisol, prolactin, ACTH, and growth hormone — that served as biomarkers for central serotonergic sensitivitysupported

Causes consistent dose-dependent elevation of ACTH, cortisol, and prolactin. pmid:1663792

It was widely distributed in tablets sold as MDMA (ecstasy), a misidentification facilitated by its piperazine-class stimulant properties and its appearance in pressed pill form indistinguishable from ecstasy tabletssupported

its initial misidentification as an MDMA substitute facilitated its unregulated distribution worldwide. 03602532.2025.2465482

It was widely distributed in tablets sold as MDMA (ecstasy), a misidentification facilitated by its piperazine-class stimulant properties and its appearance in pressed pill form indistinguishable from ecstasy tabletssupported

mCPP is emerging as an illicit recreational drug or MDMA/cocaine adulterant. pmid:21073812

As of the 2006 French review by Lecompte and colleagues, mCPP was not subject to any international regulation under the UN Conventions, and no subsequent UN scheduling has been identified.supported

Not subject to any international regulation as of 2006. pmid:17348609

In the documented overdose case, plasma mCPP reached 320 ng/mL — approximately 6 times the upper therapeutic range.supported

Plasma mCPP 320 ng/mL (6x therapeutic trazodone levels). ftd.0b013e318170a879

All human PK data derive from Feuchtl and colleagues' study in healthy male volunteers — the only dedicated human pharmacokinetic investigation of mCPP.supported

Pharmacokinetics of m-chlorophenylpiperazine after intravenous and oral administration in healthy male volunteers. pmid:15467976

Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →

CYP2D6 additionally catalyzes bioactivation of mCPP to a reactive quinone imine intermediate — a glutathione-trapped species whose formation has been documented in vitro but has not been linked to clinical hepatotoxicitysupported

Several new glutathione adducts of trazodone identified in human liver microsomal incubations. mCPP, a major circulating metabolite, is bioactivated by CYP2D6 to a quinone imine intermediate. dmd.107.019471

Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →

Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →

Claim in comparative-pharmacology — inconclusiveinconclusiveworking →

Claim in comparative-pharmacology — not_supportednot supportedworking →

Neurotoxicity: MDMA causes long-term serotonin depletion via high SERT-mediated ionic currents. mCPP does not — it induces lower SERT-mediated currents and is classified as non-neurotoxic.supported

in synaptosomes induce much lower release than pCA and MDMA. mCPP is non-neurotoxic SERT substrate. pmid:12354291

Claim in comparative-pharmacology — inconclusiveinconclusiveworking →

MDMA users show altered neuroendocrine responses to mCPP challenge — initially blunted and later enhancedsupported

MDMA users showed altered neuroendocrine and behavioral responses to mCPP, suggesting functional consequences of MDMA-induced serotonin neurotoxic effects. pmid:10591869

This selectivity has been confirmed functionally through antagonist studies — the 5-HT₂C-selective antagonist SB-242084 blocks mCPP-induced hypolocomotion, whereas 5-HT₂A- and 5-HT₂B-selective antagonists do not.supported

m-CPP hypolocomotion not attenuated by 5-HT2A antagonists (MDL 100,907, ketanserin) or 5-HT2B antagonists. Reversed by selective 5-HT2C antagonist SB 242084. pmid:11856898

The SERT substrate activity warrants distinction from classical reuptake inhibition. mCPP enters the serotonin transporter as a substrate and induces reverse transport (efflux) of serotonin from presynaptic terminals — a mechanism shared with MDMA and fenfluraminesupported

mCPP is a SERT substrate producing >5-fold elevations in extracellular 5-HT. npp.2013.331

However, mCPP induces substantially lower SERT-mediated ionic currents than neurotoxic compounds, which explains its non-neurotoxic profile despite robust acute serotonin release (>5-fold over baseline).supported

in synaptosomes induce much lower release than pCA and MDMA. mCPP is non-neurotoxic SERT substrate. pmid:12354291

No listing under the 1961, 1971, or 1988 UN Conventions has been identifiedsupported

Not subject to any international regulation as of 2006. pmid:17348609

mCPP's cross-reactivity with the Ecstasy EMIT II immunoassay produces false-positive MDMA results in standard urine drug testingsupported

mCPP causes false-positive results on the urine EMIT test for MDMA. Significant crossreactivity of trazodone and mCPP on the Ecstasy EMIT II assay. pmid:21073812

The phenylpiperazine class includes several compounds of pharmacological interest: 1-(3-trifluoromethylphenyl)piperazine (TFMPP), another recreational piperazine; and the antidepressant metabolites generated from nefazodone and trazodone. mCPP's position within this class is defined by the meta-chloro substitution on the phenyl ring, which confers the high 5-HT₂C affinity that distinguishes it from ortho- and para-substituted analogs.supported

Trazodone, nefazodone, and etoperidone are classified as atypical antidepressants belonging to the phenylpiperazine class. 03602532.2025.2465482