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PsychedeliaDokholyan Laboratory
Plate 506 of 545Verified

Tenocyclidine

Also known asTenociclidina · Tenocyclidinum · thienyl cyclohexylpiperidine · Thienylcyclidine · Thienylphencyclidine · 2-thienylphencyclidine · tenocyclidine-TCP · (3H)thienylcyclohexylpiperidine

1-(1-thiophen-2-ylcyclohexyl)piperidine

PubChem CID
62751
Measurements
4
InChIKey
JUZZEWSCNBCFRL-UHFFFAOYSA-N

I · Summary

What is known

Published passages, each quoted whole and attributed to the database that published it. Two blocks are written here rather than quoted, and both say so where they stand: the synthesized summary at the top, which may draw only on the passages beneath it, and the history note, which cites the works it came from. Every claim in either carries a marker to its source.

What it is

  • Tenocyclidine is a tertiary amino compound that consists of cyclohexane having piperidin-1-yl and thiophen-2-yl groups attached at position 1. A dissociative anaesthetic drug with halluccinogenic and stimulant effects. Its effects are similar to those of phencyclidine (PCP, an analogue with the thienyl group replaced by phenyl), but it is rather more potent. It has a role as a central nervous system stimulant, a hallucinogen, a NMDA receptor antagonist and a neuroprotective agent. It is a member of piperidines, a member of thiophenes and a tertiary amino compound.

    ChEBI

  • Tenocyclidine (TCP, thienyl cyclohexylpiperidine) is a dissociative anesthetic drug with stimulant and hallucinogenic effects. It is more potent than phencyclidine and hence, this drug was classified under the schedule 1 in 1970.

    DrugBank

Recognized use

  • /EXPL/ The objective of this study was to evaluate the efficacy of thienyl phencyclidine (tenocyclidine, TCP) and its newly synthesized adamantyl derivatives containing piperidine (TAPIP), pyrolidine (TAPIR) and morpholine (TAMORF) groups, which were tested with or without standard therapy in mice poisoned with organophosphates (OPs) and carbamates. These compounds with potential activity at the N-methyl- D-aspartate and muscarinic receptors showed low acute toxicity, having LD50 values varying from 106.00 mg/kg (TCP) to >504.00 mg/kg body weight (TAMORF). TCP and its adamantyl derivatives were administered intraperitoneally (2.5 mg/kg body weight) together with atropine (10.0 mg/kg body wei…

    Therapeutic Uses

    Hazardous Substances Data Bank (HSDB)PMID 11967623Skare D et al; Arch Toxicol 76 (3): 173-7 (2002); Erratum in: Arch Toxicol 76 (9): 552 (2002)

  • /EXPL/ The effects of soman, a potent irreversible inhibitor of acetylcholinesterase, on central neuropathology in rats were studied in relation with subsequent spatial memory impairments. In a first step, it was found that, without treatment, neuropathology and learning impairment were observed only in rats which experienced convulsions. Then, treatment consisting of atropine sulfate, and/or (N-[1-(2-thienyl)cyclohexyl]piperidine) (TCP) and/or NBQX was administered to intoxicated animals at infraanticonvulsant doses to obtain a graded subsequent neuropathology and to appreciate an eventual relation between neuropathology and spatial memory impairment. Thus, a correlation between neuropathol…

    Therapeutic Uses

    Hazardous Substances Data Bank (HSDB)PMID 10499353Filliat P et al; Neurotoxicology 20 (4): 535-49 (1999)

  • /EXPL/ Poisoning with the potent nerve agent soman produces a cascade of central nervous system (CNS) effects characterized by severe convulsions and eventually death. In animals that survive a soman intoxication, lesions in the amygdala, piriform cortex, hippocampus and thalamus can be observed. In order to examine the mechanisms involved in the effects of soman and to evaluate possible curative interventions, a series of behavioral, electrophysiological and neuropathological experiments were carried out in the guinea pig using the NMDA antagonist N-[1-(2-thienyl)cyclohexyl] piperidine (TCP) in conjunction with atropine and pyridostigmine. The NMDA antagonist TCP appeared to be very effecti…

    Therapeutic Uses

    Hazardous Substances Data Bank (HSDB)PMID 11920922de Groot DM et al; J Appl Toxicol 21 Suppl 1: S57-65 (2001)

  • Because of its high affinity for the phencyclidine binding site on the NMDA receptor, the 3H radiolabelled form of tenocyclidine is widely used in research into NMDA receptors.

    Drug Indication

    DrugBank

  • A dissociative anesthetic drug with stimulant and hallucinogenic effects

    Use Classification

    Hazardous Substances Data Bank (HSDB)Chemie; Encyclopedia of Chemistery. Tenocyclidine. Available from, as of Oct 31, 2008: https://www.chemie.de/lexikon/e/Tenocyclidine/

How it acts

  • The primary interactions are as a non-competitive antagonist at the 3A-subunit of the NMDAR in Homo sapiens. TCP is known to bind, with relatively high affinity, to the D1 subunit of the human DAT, in addition to displaying a positive antagonistic effect at the α7-subunit of the Nicotinic Acetylcholine Receptor (nAChR). It also binds to the mu-opioid receptor, which seems to be a central part of the mechanism of action of drugs in this class. (For example, Dizocilpine [MK-801] shows little appreciable analgesic effect despite having a high specificity for the NMDA-3A and NMDA-3B subunits - this may well be mediated by the lack of related efficacy at the mu-opioid receptor, though the NMDAR c…

    DrugBank

  • Phencyclidine induces a model psychosis which can persist for prolonged periods and presents a strong drug model of schizophrenia. When given continuously for several days to rats, phencyclidine and other N-methyl-D-aspartate (NMDA) antagonists induce neural degeneration in a variety of limbic structures, including retrosplenial cortex, hippocampus, septohippocampal projections, and piriform cortex. In an attempt to further clarify the mechanisms underlying these degeneration patterns, autoradiographic studies using a variety of receptor ligands were conducted in animals 21 days after an identical dosage of the continuous phencyclidine administration employed in the previous degeneration stu…

    Hazardous Substances Data Bank (HSDB)PMID 9974184Ellison G et al; Pharmacol Toxicol 84 (1): 9-17 (1999)

Behavior carries the pharmacological classes and the acute-effect durations, with plasma half-life kept separate from duration of effect.

History, discovery and cultural use

— Not in this archive. PubChem, ChEMBL and the Human Protein Atlas publish pharmacology, regulation and toxicology, and none of them publishes a heading for when Tenocyclidine was first made, by whom, or how it has been used. That is a gap in the databases this site reads and not a gap in the literature — the history of these compounds is written, at length and under peer review, in the works below. This site does not summarize them; it says where they are. Where a published passage above happens to touch origin or traditional use, it appears inside the entry that carries it.

Histories of this field

Scholarship on psychedelics generally, not on Tenocyclidine specifically. Whether any of these treats this compound is a question for the book, not for this page.

  • Mescaline: A Global History of the First Psychedelic

    Traces mescaline and the peyote and San Pedro cacti from pre-Columbian ritual use through nineteenth-century chemistry to twentieth-century psychiatry and the counterculture.

    Jay M. Mescaline: A Global History of the First Psychedelic. Yale University Press, New Haven and London; 2019. ISBN 9780300231076.

  • Expanding Mindscapes: A Global History of Psychedelicsopen access

    Essays on the international and cross-cultural history of psychedelic science, deliberately decentring the standard North American and European account.

    Dyck E, Elcock C, editors. Expanding Mindscapes: A Global History of Psychedelics. The MIT Press, Cambridge MA; 2023. ISBN 9780262546935 (paper), 9780262376891 (open access). doi:10.7551/mitpress/14417.001.0001.

  • Plants of the Gods: Their Sacred, Healing, and Hallucinogenic Powers

    Botany, ethnography and chemistry of the principal hallucinogenic plants, by the founder of modern ethnobotany and the chemist who first synthesized LSD.

    Schultes RE, Hofmann A, Rätsch C. Plants of the Gods: Their Sacred, Healing, and Hallucinogenic Powers. 2nd ed. Healing Arts Press, Rochester VT; 2001. ISBN 9780892819799.

  • Psychonauts: Drugs and the Making of the Modern Mind

    The tradition of scientific self-experimentation with psychoactive drugs, and its part in the emergence of psychology and of modernism.

    Jay M. Psychonauts: Drugs and the Making of the Modern Mind. Yale University Press, New Haven; 2023. ISBN 9780300257946.

  • Ancient Psychoactive Substances

    Archaeological and bioarchaeological evidence for psychoactive plant use across the ancient world.

    Fitzpatrick SM, editor. Ancient Psychoactive Substances. University Press of Florida, Gainesville; 2018. ISBN 9780813056708.

  • History and Current Status of Psychedelics and Entactogens for the Treatment of Psychiatric Disorders

    A chapter tracing psychedelic and entactogen research from earlier ritual use through the mid-century research period to current clinical trials.

    Stroud C, Posey Norris SM, Matney C, editors. History and Current Status of Psychedelics and Entactogens for the Treatment of Psychiatric Disorders. In: Exploring Psychedelics and Entactogens as Treatments for Psychiatric Disorders: Proceedings of a Workshop. National Academies Press, Washington DC; 2022. NBK587225.

    Workshop proceedings record what participants said; they are not a consensus statement of the National Academies.

  • Pharmacokinetic and Pharmacodynamic Aspects of Peyote and Mescaline: Clinical and Forensic Repercussions

    Peer-reviewed review covering the isolation, synthesis, pharmacology and ritual use of peyote and mescaline.

    Dinis-Oliveira RJ, Pereira CL, da Silva DD. Pharmacokinetic and Pharmacodynamic Aspects of Peyote and Mescaline: Clinical and Forensic Repercussions. Current Molecular Pharmacology 12(3):184–194; 2019. doi:10.2174/1874467211666181010154139.

Institutional archives

  • Heffter Research Institute Funds and coordinates clinical research on psilocybin, and keeps records of the studies it has supported since 1993. Sponsors the research it archives.
  • Multidisciplinary Association for Psychedelic Studies (MAPS) Sponsors clinical research, chiefly on MDMA-assisted therapy, and publishes an archive of historical and contemporary documents. A sponsor and an advocacy organization, not a disinterested archive; its clinical programme has a commercial arm.

The rest of this dossier

  • Affinity — 4 measurements in this archive, equilibrium constants kept apart from functional readouts.
  • Toxicology — 1 published passage, plus any assay in this archive bearing on toxicity.
  • Legal — listed by the DEA among its drugs of concern, with no schedule stated in the record held here.

Passages via PubChem descriptive sections, aggregating DrugBank, LiverTox, FDA, DEA, HSDB, EPA. Each is quoted whole and attributed to the database that published it. The only prose written here about Tenocyclidine is the history note, which says so on its face and carries a reference for every claim in it.

II · Identity

Structure and descriptors

Descriptors are computed here with RDKit from the structure PubChem returns — not from the archive's stored copy, so an edited local structure cannot reach this table.

2D structural depiction of Tenocyclidine
Depiction served by PubChem for CID 62751. Not redrawn here, so the picture and the identity come from the same record.
Formula
C15H23NSR
Molecular weight
249.42g/molR
Exact mass
249.1551DaR
cLogP
4.39R
TPSA
3.2ŲR
H-bond donors
0R
H-bond acceptors
2R
Rotatable bonds
2R
Aromatic rings
1R
Heavy atoms
17R
Fraction sp³
0.733R
Formal charge
0R

Computed with RDKit 2025.09.2 from the SMILES returned by PubChem. Audit run 26/09/2026.

Bemis–Murcko scaffold

c1csc(C2(N3CCCCC3)CCCCC2)c1

Shared with Gacyclidine. All families

III · Behavior

Behavioral summary

Class, mechanism, and the duration of acute effects — each quoted from the record or trial that publishes it. Duration of effects and plasma half-life are shown separately, because they are different quantities and diverge by a factor of three or four.

Classification

Duration of acute subjective effects

—

No controlled human trial reporting a duration for this compound is cited here. The archive holds no other record of one either. A duration is not inferred from a chemical relative.

Plasma elimination half-life

How fast the body clears the drug — not how long the effects last. The two diverge sharply: LSD is cleared with a half-life of about 2.6 h while its subjective effects run 8–12 h.

No half-life is published for this compound in the sources this site reads.

Primary pharmacological drivers

ChEMBL holds no curated mechanism-of-action record for this compound. The measured affinities below are the evidence this archive has for what it binds.

Mechanism, as published

Quoted verbatim from the database named after each passage, never summarized.

  • Phencyclidine induces a model psychosis which can persist for prolonged periods and presents a strong drug model of schizophrenia. When given continuously for several days to rats, phencyclidine and other N-methyl-D-aspartate (NMDA) antagonists induce neural degeneration in a variety of limbic structures, including retrosplenial cortex, h…
    Hazardous Substances Data Bank (HSDB)PMID 9974184Ellison G et al; Pharmacol Toxicol 84 (1): 9-17 (1999)
  • 1-[1-(2-thienyl)cyclohexyl]piperidine (TCP) and its derivative gacyclidine (+/- GK11) are high-affinity non-competitive antagonists of N-methyl-D-aspartate (NMDA) receptors (NMDARs) and as such exhibit significant neuroprotective properties. These compounds also bind with a low affinity to binding sites whose pharmacological profiles are…
    Hazardous Substances Data Bank (HSDB)PMID 12111860Hirbec H et al; J Neurosci Res 68 (3): 305-14 (2002)
  • The voltage-dependent block of NMDA channels by Mg2+ is an important functional element of NMDA receptors, since relief of block by depolarization plays a key role in some forms of ischemic neurodegeneration and synaptic plasticity. To identify the relevant structural domains responsible for block by Mg2+ and TCP, ... site-directed mutage…
    Hazardous Substances Data Bank (HSDB)PMID 8107974Kawajiri S, Dingledine R; Neuropharmacology 32 (11): 1203-11 (1993)
  • The primary interactions are as a non-competitive antagonist at the 3A-subunit of the NMDAR in Homo sapiens. TCP is known to bind, with relatively high affinity, to the D1 subunit of the human DAT, in addition to displaying a positive antagonistic effect at the α7-subunit of the Nicotinic Acetylcholine Receptor (nAChR). It also binds to t…
    DrugBank
  • When compared to phencyclidine, tenocyclidine presents more affinity for NMDA receptors and less affinity for sigma receptors.
    DrugBank

IV · Clinical

Clinical description

Where this compound's substance class sits in ICD-11 and DSM-5-TR, and how much of the recorded literature speaks to each domain of a mental status examination.

No diagnostic chapter is shown for this compound. Either PubChem records no MeSH pharmacological class for it, or the class it records is not one of the substance classes ICD-11 gives a chapter to. Inferring a chapter from the compound’s name or its binding profile would be a diagnosis this archive is in no position to make.

How much has been written about each domain

The clinical domains, and how many of the records this archive holds for this compound say something under each. What the terms mean, and the word list behind every spoke, are set out in the method.

None of the 6 records this archive holds for this compound uses a term from any of the clinical domains. That is a statement about the literature recorded here, not about the compound.

VI · Profile

Affinity rosette

The strongest measurement at each of 2 molecular targets. Cell-line and whole-organism screens are excluded here — they carry no affinity — and appear in the table below.

Sigma 1 — IC50 6.62 pXLysosomal Pro-X carboxypeptidase — IC50 7.70 pXSigma 1Lysosomal Pro-X …579
Fig. Radius is pX = −log₁₀(value in M), that is 9 − log₁₀(value in nM), computed from the normalized measurement. Hatched wedges are equilibrium binding constants (Ki, Kd); dashed outlines are functional readouts (IC₅₀, EC₅₀, AC₅₀, potency), which answer a different question and are not pooled with them. Rings mark whole pX units from 5 to 10, labeled every second ring in the gutter at the top. Where a target carries several measurements, the strongest is drawn.

VII · Toxicology

Toxicological profile

What has been measured, and what has been published — kept apart, and neither scored. There is no risk rating on this page; the archive once carried one, identical for every compound, produced by a stub.

Measured in this archive

Assays that bear on toxicity, drawn from the same ChEMBL records as everything else on this page. They are measurements of what a compound binds or does to cells — not verdicts about what it does to a person.

No hERG, cytochrome, cytotoxicity or transport measurement exists for Tenocyclidine in this archive.

As published

Quoted verbatim from the database named after each passage, never summarized — a summary of a toxicology statement is a new claim.

Human Toxicity Excerpts

  • /ALTERNATIVE and IN VITRO TESTS/ ... In vitro interactions of Tenocyclidine (TCP)and its adamantane derivative--TAMORF with human erythrocyte acetylcholinesterase (AChE) /were investigated/. Moreover, their genotoxicity and radioprotective activity on human white blood cells were studied using the alkaline comet assay, viability testing and the analysis of the structural chromosome aberrations. The tested compounds…

    Hazardous Substances Data Bank (HSDB)PMID 16942853Radic B et al; Toxicol In Vitro 20 (8): 1455-64 (2006)

Published passages via PubChem toxicology sections, aggregating Hazardous Substances Data Bank (HSDB), RTECS, LiverTox. No figure on this page is scored, ranked or combined into a risk level.

VIII · Evidence

Every measurement

One row per published value. The identifier in the last column resolves to the ChEMBL assay record it was read from.

Functional readouts 4

IC₅₀, EC₅₀, AC₅₀ and potency. Assay-dependent, and not interchangeable with a binding constant.

TargetClassTypeValue (nM)pXOrganismAssay
Lysosomal Pro-X carboxypeptidaseEnzymesIC5020.007.70Homo sapiensCHEMBL764432
Sigma 1Sigma receptorsIC502406.62Rattus norvegicusCHEMBL808179
Sigma 1Sigma receptorsIC501,1005.96Homo sapiensCHEMBL846627
Sigma 1Sigma receptorsIC502,0605.69Homo sapiensCHEMBL846484
P
PubChem
C
ChEMBL
R
Computed here with RDKit
D
Derived here from the stored measurement

IX · Trials

Registered clinical trials

Studies filed with ClinicalTrials.gov that name this compound as an intervention. A registered trial is a protocol, not a result — status and enrollment are printed beside every row, and withdrawn studies are counted rather than hidden.

— No registered study names Tenocyclidine as an intervention. That is an absence of registered research, not evidence about the compound. Most of this archive has never been the subject of a registered trial.

Records from ClinicalTrials.gov (U.S. National Library of Medicine, NIH), API v2. A study is listed against a compound only when a verified name for that compound appears as a whole word in one of the study's own intervention names. A short code must appear as written, and a name the registry uses for something else (Aleph, a vaccine maker) is not matched. Title matches are not accepted. The matched name and the intervention text it matched are shown with every row.

Searched as Tenocyclidine · Tenociclidina · Tenocyclidinum. Run this search at the registry.

A registered trial is a protocol somebody filed with the registry. It is not a result, and nothing on this plate says whether Tenocyclidine worked.

XI · Literature

Sources behind this dossier

The papers this compound's values were read from, ranked by what each contributed. Not a review of the field.

Every paper below is one some value on this page came from — a binding constant, a passage of pharmacology or toxicology, or a measured duration. Each entry says what this archive took from it. Nothing else is claimed about any of them: the title is the study’s own account of itself, and a summary written here would be an assertion with no source behind it.

  1. 01

    In vitro biological efficiency of tenocyclidine-TCP and its adamantane derivative TAMORF

    Radić B, Vrdoljak AL, Petek MJ et al. · Toxicology in vitro : an international journal published in association with BIBRA 2006

    • · Human Toxicity Excerpts

    PMID 16942853

  2. 02

    Re-evaluation of phencyclidine low-affinity or "non-NMDA" binding sites

    Hirbec H, Mausset AL, Kamenka JM et al. · Journal of neuroscience research 2002

    • · Mechanism of Action

    PMID 12111860

  3. 03

    Long-term changes in brain following continuous phencyclidine administration: an autoradiographic study using flunitrazepam, ketanserin, mazindol, quinuclidinyl benzilate, piperidyl-3,4-3H(N)-TCP, and AMPA receptor ligands

    Ellison G, Keys A, Noguchi K · Pharmacology & toxicology 1999

    • · Mechanism of Action

    PMID 9974184

  4. 04

    Multiple structural determinants of voltage-dependent magnesium block in recombinant NMDA receptors

    Kawajiri S, Dingledine R · Neuropharmacology 1993

    • · Mechanism of Action

    PMID 8107974