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PsychedeliaDokholyan Laboratory
Plate 493 of 545Verified

Rimonabant

Also known asAcomplia · Zimulti · rimonabantum · A08AX01 · Rimonabant free base · Rimoslim · C22H21Cl3N4O · Acomplia (TN)

5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-N-piperidin-1-ylpyrazole-3-carboxamide

PubChem CID
104850
ChEMBL
CHEMBL111
Measurements
120
InChIKey
JZCPYUJPEARBJL-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

  • Rimonabant is a carbohydrazide obtained by formal condensation of the carboxy group of 5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxylic acid with the amino group of 1-aminopiperidine. It is a potent and selective cannabinoid receptor 1 (CB1R) antagonist. Besides its antagonistic properties, numerous studies have shown that, at micromolar concentrations rimonabant behaves as an inverse agonist at CB1 receptors. The drug was the first selective CB1 antagonist/inverse agonist introduced into clinical practice to treat obesity and metabolic-related disorders. It was later withdrawn from market due to CNS-related adverse effects including depression and suicidal ideatio…

    ChEBI

  • Rimonabant is an anorectic anti-obesity drug produced and marketed by Sanofi-Aventis. It is an inverse agonist for the cannabinoid receptor CB1. Its main avenue of effect is reduction in appetite. Rimonabant is the first selective CB1 receptor blocker to be approved for use anywhere in the world. Rimonabant is approved in 38 countries including the E.U., Mexico, and Brazil. It was rejected for approval for use in the United States. This decision was made after a U.S. advisory panel recommended the medicine not be approved because it may increase suicidal thinking and depression.

    DrugBank

  • A pyrazole and piperidine derivative that acts as a selective cannabinoid type-1 receptor (CB1 RECEPTOR) antagonist. It inhibits the proliferation and maturation of ADIPOCYTES, improves lipid and glucose metabolism, and regulates food intake and energy balance. It is used in the management of OBESITY.

    Medical Subject Headings (MeSH)

Recognized use

  • For use in conjunction with diet and exercise for patients with a body mass index greater than 30 kg/m2, or patients wih a BMI greater than 27 kg/m2 with associated risk factors, such as type 2 diabetes or dyslipidaemia.

    DrugBank

How it acts

  • Rimonabant is a specific CB1 cannabinoid receptor antagonist. There is considerable evidence that the endocannabinoid (endogenous cannabinoid) system plays a significant role in appetitive drive and associated behaviours. It is therefore reasonable to hypothesize that the attenuation of the activity of this system would have therapeutic benefit in treating disorders that might have a component of excess appetitive drive or over-activity of the endocannabinoid system, such as obesity, ethanol and other drug abuse, and a variety of central nervous system and other disorders.

    DrugBank

  • In the RIO-North America trial, 3040 patients were randomized to receive either placebo or one of two doses of rimonabant (5 mg or 20 mg per day). Patients taking 20 mg rimonabant had significant weigh loss, decrease in waist circumference, improved insulin sensitivity, and increases in HDL cholesterol, compared to patients on placebo.

    DrugBank

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 Rimonabant 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 Rimonabant 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 — 120 measurements in this archive, equilibrium constants kept apart from functional readouts.
  • Toxicology — nothing published for Rimonabant. An absent record is an absence of study, not evidence of safety.
  • Legal — no DEA record is held here — which is not a finding that this compound is uncontrolled.
  • Systems — where this compound’s targets are transcribed, by brain region and tissue.

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 Rimonabant 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 Rimonabant
Depiction served by PubChem for CID 104850. Not redrawn here, so the picture and the identity come from the same record.
Formula
C22H21Cl3N4OR
Molecular weight
463.80g/molR
Exact mass
462.0781DaR
cLogP
5.94R
TPSA
50.2ŲR
H-bond donors
1R
H-bond acceptors
4R
Rotatable bonds
4R
Aromatic rings
3R
Heavy atoms
30R
Fraction sp³
0.273R
Formal charge
0R

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

Bemis–Murcko scaffold

O=C(NN1CCCCC1)c1cc(-c2ccccc2)n(-c2ccccc2)n1

Shared with AM-251. 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.

  • 6 to 9 days with normal BMI and 16 days if BMI is greater than 30
    DrugBank

Primary pharmacological drivers

Mechanism, as published

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

  • Rimonabant is a specific CB1 cannabinoid receptor antagonist. There is considerable evidence that the endocannabinoid (endogenous cannabinoid) system plays a significant role in appetitive drive and associated behaviours. It is therefore reasonable to hypothesize that the attenuation of the activity of this system would have therapeutic b…
    DrugBank
  • In the RIO-North America trial, 3040 patients were randomized to receive either placebo or one of two doses of rimonabant (5 mg or 20 mg per day). Patients taking 20 mg rimonabant had significant weigh loss, decrease in waist circumference, improved insulin sensitivity, and increases in HDL cholesterol, compared to patients on placebo.
    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 3 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.

V · Systems

Systems physiology

Where the targets this compound binds are transcribed — brain regions on the left, peripheral and autonomic tissues on the right. A join of two measurements, not a claim about what the compound does to either.

Brain

cerebral cortex — 18.6 nTPM, from CNR1, KCNH2, OPRK1cerebellum — 32.4 nTPM, from KCNH2, CNR1, OPRK1hippocampal formation — 13.2 nTPM, from CNR1, KCNH2, OPRK1amygdala — 13.3 nTPM, from CNR1, KCNH2, OPRK1hypothalamus — 14.4 nTPM, from KCNH2, CNR1, OPRK1thalamus — no resolved target expressed herebasal ganglia — 15.1 nTPM, from CNR1, KCNH2, OPRK1medulla oblongata — no resolved target expressed here

basal ganglia: drawn as the caudate nucleus, putamen and globus pallidus.

Measured but not drawn — this anatomogram has no outline for them: pituitary gland 41.5, midbrain 6.7, retina 5.3, spinal cord 4.0.

Body

heart — 28.4 nTPM, from KCNH2, CNR1, OPRK1smooth muscle — 7.0 nTPM, from KCNH2, CNR1lung — 2.8 nTPM, from CNR1, KCNH2, OPRK1liver — 0.2 nTPM, from KCNH2, CNR1, CNR2kidney — 1.1 nTPM, from KCNH2, CNR1stomach — 10.6 nTPM, from KCNH2, CNR1, CNR2duodenum — 2.4 nTPM, from KCNH2, CNR1, CNR2small intestine — 8.1 nTPM, from CNR1, KCNH2, CNR2colon — 36.0 nTPM, from KCNH2, CNR1, CNR2adrenal gland — 4.6 nTPM, from CNR1, KCNH2thyroid gland — 3.9 nTPM, from CNR1, CNR2, OPRK1pancreas — 3.2 nTPM, from KCNH2, CNR1urinary bladder — 13.4 nTPM, from KCNH2, CNR1, CNR2skeletal muscle — 1.8 nTPM, from CNR1, CNR2, OPRK1spleen — 8.4 nTPM, from CNR2, KCNH2, CNR1salivary gland — 1.8 nTPM, from CNR1, KCNH2, CNR2
042 nTPM

Square-root ramp · shared scale across both plates

Shading is transcript level — not affinity, and not affinity combined with expression. Outlined but unshaded organs hold none of this compound’s resolved targets above the atlas’s detection threshold. Anatomy from EMBL-EBI Anatomogram (Apache License 2.0); regions identified by Uberon (uberon.org), CC BY 3.0.

Brain regions

Regions where this compound's measured targets are transcribed. Linked from the plate above.

  1. pituitary gland

    41.5 nTPM

  2. cerebellum

    32.4 nTPM

  3. cerebral cortex

    18.6 nTPM

  4. basal ganglia

    15.1 nTPM

  5. hypothalamus

    14.4 nTPM

  6. amygdala

    13.3 nTPM

  7. hippocampal formation

    13.2 nTPM

  8. midbrain

    6.7 nTPM

  9. retina

    5.3 nTPM

  10. spinal cord

    4.0 nTPM

Peripheral & autonomic

Tissues outside the CNS expressing the same targets — where a compound's bodily effects become possible.

  1. colon

    36.0 nTPM

  2. heart muscle

    28.4 nTPM

  3. urinary bladder

    13.4 nTPM

  4. stomach 1

    10.6 nTPM

  5. spleen

    8.4 nTPM

  6. small intestine

    8.1 nTPM

  7. smooth muscle

    7.0 nTPM

  8. adrenal gland

    4.6 nTPM

  9. thyroid gland

    3.9 nTPM

  10. pancreas

    3.2 nTPM

  11. lung

    2.8 nTPM

  12. duodenum

    2.4 nTPM

  13. skeletal muscle

    1.8 nTPM

  14. salivary gland

    1.8 nTPM

  15. kidney

    1.1 nTPM

  16. liver

    0.2 nTPM

Each row joins two published measurements and nothing else: the affinity this archive holds for the compound at that target, and the transcript level the Human Protein Atlas reports for that target’s gene in that region. Bars scale with expression only. Expression is not activation — a receptor transcribed in a region is a receptor available to be bound there, which is a weaker and more defensible claim than saying the region is affected.

2 of this compound’s targets could not be resolved to a gene and are absent from both columns: Cannabinoid receptor, Sigma 1.

Expression data from Human Protein Atlas (CC BY-SA 3.0), RNA expression, nTPM (normalized transcripts per million), consensus tissue dataset. Uhlén M, et al. Tissue-based map of the human proteome. Science. 2015;347(6220):1260419.

VI · Profile

Affinity rosette

The strongest measurement at each of 6 molecular targets. Cell-line and whole-organism screens are excluded here — they carry no affinity — and appear in the table below.

KOR — Ki 7.24 pXSigma 1 — Ki 5.36 pXCB1 — Ki 9.72 pXCannabinoid receptor — Ki 7.37 pXCB2 — Ki 6.90 pXhERG — IC50 5.32 pXKORSigma 1CB1Cannabinoid rece…CB2hERG579
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.

hERG / cardiac ion channel 1

Block of the hERG potassium channel (KCNH2) is the standard in-vitro flag for QT prolongation. A measured affinity is not an arrhythmia risk, and this archive does not convert one into the other.

Published toxicology

— None. The toxicology databases this site reads — HSDB, RTECS and LiverTox, by way of PubChem — hold no record for Rimonabant. They index compounds that have been studied for decades, so most of this archive has no entry. An absent record is an absence of study, not evidence of safety.

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.

Equilibrium binding constants 93

Ki and Kd — a concentration at equilibrium. Directly comparable across rows at the same target.

TargetClassTypeValue (nM)pXOrganismAssay
CB1Cannabinoid receptorsKi0.1909.72HUMANPMID 19102698
CB1Cannabinoid receptorsKi0.4009.40HUMANPMID 1775
CB1Cannabinoid receptorsKi0.7409.13HUMANPMID 20047779
CB1Cannabinoid receptorsKi0.9009.05Rattus norvegicusCHEMBL1042698
CB1Cannabinoid receptorsKi0.9009.05HUMANPMID 19102698
CB1Cannabinoid receptorsKi1.108.96HUMANPMID 17383180
CB1Cannabinoid receptorsKi1.188.93HUMANPMID 18512901
CB1Cannabinoid receptorsKi1.188.93Rattus norvegicusCHEMBL658893
CB1Cannabinoid receptorsKi1.308.89Rattus norvegicusCHEMBL659698
CB1Cannabinoid receptorsKi1.388.86Homo sapiensCHEMBL1111398
CB1Cannabinoid receptorsKi1.388.86UNDEFINEDPMID 19767206
CB1Cannabinoid receptorsKi1.408.85Homo sapiensCHEMBL1767553
CB1Cannabinoid receptorsKi1.508.82Mus musculusCHEMBL2343203
CB1Cannabinoid receptorsKi1.608.80HUMANPMID 19351113
CB1Cannabinoid receptorsKi1.608.80HUMANPMID 19683918
CB1Cannabinoid receptorsKi1.808.74UNDEFINEDPMID 19351113
CB1Cannabinoid receptorsKi1.808.74HUMANPMID 18083560
CB1Cannabinoid receptorsKi1.808.74Rattus norvegicusCHEMBL658896
CB1Cannabinoid receptorsKi1.808.74Mus musculusCHEMBL3857711
CB1Cannabinoid receptorsKi1.808.74Homo sapiensCHEMBL983966
CB1Cannabinoid receptorsKi1.908.72HUMANPMID 19520572
CB1Cannabinoid receptorsKi1.988.70Homo sapiensCHEMBL936658
CB1Cannabinoid receptorsKi1.988.70Homo sapiensCHEMBL3124129
CB1Cannabinoid receptorsKi1.988.70UNDEFINEDPMID 18363352
CB1Cannabinoid receptorsKi1.988.70Rattus norvegicusCHEMBL981471
CB1Cannabinoid receptorsKi2.008.70HUMANPMID 22085649
CB1Cannabinoid receptorsKi2.408.62HUMANPMID 18363352
CB1Cannabinoid receptorsKi2.408.62HUMANPMID 20018510
CB1Cannabinoid receptorsKi2.408.62Homo sapiensCHEMBL1070892
CB1Cannabinoid receptorsKi2.828.55Mus musculusCHEMBL3857709
CB1Cannabinoid receptorsKi4.508.35Mus musculusCHEMBL5366617
CB1Cannabinoid receptorsKi5.378.27Homo sapiensCHEMBL854385
CB1Cannabinoid receptorsKi5.608.25HUMANPMID 19095444
CB1Cannabinoid receptorsKi5.608.25Homo sapiensCHEMBL1034817
CB1Cannabinoid receptorsKi6.008.22HUMANPMID 18335976
CB1Cannabinoid receptorsKi6.008.22HUMANPMID 22085649
CB1Cannabinoid receptorsKi6.188.21HUMANPMID 18512901
CB1Cannabinoid receptorsKi6.188.21Rattus norvegicusCHEMBL658892
CB1Cannabinoid receptorsKi6.508.19Rattus norvegicusCHEMBL961196
CB1Cannabinoid receptorsKi7.008.15Homo sapiensCHEMBL5048445
CB1Cannabinoid receptorsKi7.308.14Homo sapiensCHEMBL2027598
CB1Cannabinoid receptorsKi7.308.14Homo sapiensCHEMBL2353263
CB1Cannabinoid receptorsKi8.008.10HUMANPMID 18579386
CB1Cannabinoid receptorsKi8.908.05Homo sapiensCHEMBL657906
CB1Cannabinoid receptorsKi9.808.01Homo sapiensCHEMBL5321837
CB1Cannabinoid receptorsKi10.607.97Homo sapiensCHEMBL2329722
CB1Cannabinoid receptorsKi11.507.94Rattus norvegicusCHEMBL658897
CB1Cannabinoid receptorsKi12.007.92Homo sapiensCHEMBL873196
CB1Cannabinoid receptorsKi12.007.92HUMANPMID 18293908
CB1Cannabinoid receptorsKi12.007.92HUMANPMID 19595596
CB1Cannabinoid receptorsKi12.007.92HUMANPMID 18680276
CB1Cannabinoid receptorsKi16.007.80HUMANPMID 17942307
CB1Cannabinoid receptorsKi18.007.74Rattus norvegicusCHEMBL5256688
CB1Cannabinoid receptorsKi20.007.70Homo sapiensCHEMBL5048447
CB1Cannabinoid receptorsKi25.007.60Homo sapiensCHEMBL5510359
CB1Cannabinoid receptorsKi25.007.60HUMANPMID 20363132
CB1Cannabinoid receptorsKi25.007.60HUMANPMID 15771428
CB1Cannabinoid receptorsKi25.007.60HUMANPMID 18342403
CB1Cannabinoid receptorsKi40.007.40HUMANPMID 18511157
Cannabinoid receptorCannabinoid receptorsKi43.007.37Rattus norvegicusCHEMBL4360722
CB1Cannabinoid receptorsKi47.007.33HUMANPMID 17979261
KOROpioid receptorsKi57.007.24RATPDSP
UncheckedUnclassifiedKi65.837.18— organism not recordedCHEMBL1636583
CB2Cannabinoid receptorsKi1266.90HUMANPMID 20047779
CB2Cannabinoid receptorsKi3136.50HUMANPMID 18512901
CB2Cannabinoid receptorsKi3136.50Homo sapiensCHEMBL659747
CB2Cannabinoid receptorsKi3756.43Mus musculusCHEMBL2343202
CB2Cannabinoid receptorsKi3986.40Homo sapiensCHEMBL1670561
CB2Cannabinoid receptorsKi5146.29Mus musculusCHEMBL3857712
CB2Cannabinoid receptorsKi5546.26HUMANPMID 18083560
CB2Cannabinoid receptorsKi5606.25Homo sapiensCHEMBL1070893
CB2Cannabinoid receptorsKi5606.25HUMANPMID 18363352
CB2Cannabinoid receptorsKi5606.25HUMANPMID 20018510
CB2Cannabinoid receptorsKi6976.16HUMANPMID 1775
CB2Cannabinoid receptorsKi7026.15HUMANPMID 22085649
CB2Cannabinoid receptorsKi7906.10HUMANPMID 18293908
CB2Cannabinoid receptorsKi7906.10HUMANPMID 18680276
CB2Cannabinoid receptorsKi7906.10HUMANPMID 18579386
CB2Cannabinoid receptorsKi7906.10HUMANPMID 19595596
CB2Cannabinoid receptorsKi9276.03Homo sapiensCHEMBL1767554
CB2Cannabinoid receptorsKi9276.03UNDEFINEDPMID 19767206
CB2Cannabinoid receptorsKi9276.03Homo sapiensCHEMBL1111399
CB2Cannabinoid receptorsKi1,0006.00UNDEFINEDPMID 18363352
CB2Cannabinoid receptorsKi1,0006.00HUMANPMID 19520572
CB2Cannabinoid receptorsKi1,5695.80Homo sapiensCHEMBL983967
CB2Cannabinoid receptorsKi1,5695.80UNDEFINEDPMID 19351113
CB2Cannabinoid receptorsKi1,5805.80Homo sapiensCHEMBL5510360
CB2Cannabinoid receptorsKi1,5805.80HUMANPMID 20363132
CB2Cannabinoid receptorsKi1,5805.80HUMANPMID 18342403
CB2Cannabinoid receptorsKi1,5805.80HUMANPMID 15771428
CB2Cannabinoid receptorsKi1,6405.79HUMANPMID 17942307
CB2Cannabinoid receptorsKi1,9905.70HUMANPMID 17979261
Sigma 1Sigma receptorsKi4,3505.36RATPDSP

Functional readouts 27

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

TargetClassTypeValue (nM)pXOrganismAssay
CB1Cannabinoid receptorsEC500.1709.77Rattus norvegicusCHEMBL966862
CB1Cannabinoid receptorsIC501.508.82Homo sapiensCHEMBL5357863
CB1Cannabinoid receptorsIC501.908.72Rattus norvegicusCHEMBL988123
CB1Cannabinoid receptorsIC502.508.60Rattus norvegicusCHEMBL1212387
CB1Cannabinoid receptorsIC503.208.49Homo sapiensCHEMBL5357864
CB1Cannabinoid receptorsIC504.508.35Rattus norvegicusCHEMBL950210
CB1Cannabinoid receptorsIC504.508.35Homo sapiensCHEMBL5357862
CB1Cannabinoid receptorsIC504.538.34Rattus norvegicusCHEMBL1227203
CB1Cannabinoid receptorsIC504.538.34Rattus norvegicusCHEMBL1074127
CB1Cannabinoid receptorsIC504.538.34Rattus norvegicusCHEMBL940410
CB1Cannabinoid receptorsIC505.008.30Rattus norvegicusCHEMBL983945
CB1Cannabinoid receptorsIC505.008.30Rattus norvegicusCHEMBL957519
CB1Cannabinoid receptorsIC505.008.30Rattus norvegicusCHEMBL1038201
CB1Cannabinoid receptorsIC505.008.30Rattus norvegicusCHEMBL963901
CB1Cannabinoid receptorsIC505.008.30Rattus norvegicusCHEMBL1060016
CB1Cannabinoid receptorsIC505.208.28Rattus norvegicusCHEMBL981471
CB1Cannabinoid receptorsIC506.208.21Homo sapiensCHEMBL827163
CB1Cannabinoid receptorsIC5013.507.87Homo sapiensCHEMBL5153410
CB1Cannabinoid receptorsIC5018.007.74Rattus norvegicusCHEMBL1816969
CB1Cannabinoid receptorsIC5025.007.60Mus musculusCHEMBL5366620
CB1Cannabinoid receptorsIC5060.007.22Rattus norvegicusCHEMBL5341191
CB1Cannabinoid receptorsIC5063.107.20Rattus norvegicusCHEMBL5341191
CB2Cannabinoid receptorsIC502,6005.59Homo sapiensCHEMBL5357865
CB1Cannabinoid receptorsEC503,0865.51Rattus norvegicusCHEMBL5256689
hERGIon channelsIC504,8005.32Homo sapiensCHEMBL1227232
UncheckedUnclassifiedPotency14,1254.85— organism not recordedCHEMBL3214913
UncheckedUnclassifiedPotency15,8494.80— organism not recordedCHEMBL3215169
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.

47T

Registered studies

1T

Open or ongoing

47T

With a phase recorded

By phase

A study may carry two phase codes at once, so these count studies bearing each phase and do not sum to the total.

  • Phase 14
  • Phase 27
  • Phase 335
  • Phase 42
  • Not applicable1

By status

The registry’s own status for each record. Withdrawn and terminated studies are counted here rather than hidden — a stopped trial is part of what is known.

  • Completed25
  • Terminated18
  • Unknown status2
  • Active, not recruiting1
  • Withdrawn1

The 25 most recently started, of 47

Newest first by start date. Each identifier opens the registry record it came from; the title is the sponsor’s own, quoted.

  • NCT07843108Active, not recruiting · Phase 1 / Phase 2

    Effect of Rimonabant on Hand Function in Patients With Spinal Cord Injury

    Enrollment
    8Testimated
    Started
    2026-05-13
    Sponsor
    Sinfatin S.L

    Conditions Cervical Spinal Cord Injury

    Matched “Rimonabant” in the study’s intervention “Rimonabant”

  • NCT05622994Unknown status · Phase 2

    Effects of CB1 Antagonist/Reverse Agonist Rimonabant on Walking Abilities in Incomplete Spinal Cord Injury

    Enrollment
    80Testimated
    Started
    2022-11
    Sponsor
    Hospital Nacional de Parapléjicos de Toledo

    Conditions Spinal Cord Injuries

    Matched “Rimonabant” in the study’s intervention “Rimonabant”

  • NCT05398913Completed · Phase 1 / Phase 2

    Effects of Rimonabant on Walking Abilities in Incomplete Spinal Cord Injury

    Enrollment
    8Tactual
    Started
    2021-05-12
    Sponsor
    Hospital Nacional de Parapléjicos de Toledo

    Conditions Spinal Cord Injuries

    Matched “Rimonabant” in the study’s intervention “Rimonabant”

  • NCT00754689Withdrawn · Phase 3

    Study of Rimonabant/Metformin Combinations to Investigate Diabetes (Blood Sugar) Control in Patients With Type 2 Diabetes

    Enrollment
    0Tactual
    Started
    2008-09
    Sponsor
    Sanofi

    Conditions Diabetes Mellitus, Type 2

    Matched “Rimonabant” in the study’s intervention “Rimonabant”

  • NCT00750347Completed · Phase 1

    Antagonistic Interaction CB1-paracetamol

    Enrollment
    24Testimated
    Started
    2008-09
    Sponsor
    University Hospital, Clermont-Ferrand

    Conditions Pain

    Matched “Rimonabant” in the study’s intervention “Rimonabant and Paracetamol and placebo”

  • NCT00690456Terminated · Phase 3

    Effect of Rimonabant and Metformin Combination on Glycemic Control in Patients With Type 2 Diabetes

    Enrollment
    403Tactual
    Started
    2008-05
    Sponsor
    Sanofi

    Conditions Diabetes Mellitus, Type 2

    Matched “Rimonabant” in the study’s intervention “Rimonabant”

  • NCT00656487Completed · Phase 2

    Clinical and Neurobiological Effects of Cannabis Dependence in Young Adults

    Enrollment
    66Tactual
    Started
    2008-04-30
    Sponsor
    The Scripps Research Institute

    Conditions Cannabis Dependence · Cannabis Withdrawal

    Matched “Rimonabant” in the study’s intervention “rimonabant”

  • NCT00678483Terminated · Phase 3

    Long-Term Effect of 10 mg Versus 20 mg Rimonabant in Overweight or Obese Patients

    Enrollment
    331Tactual
    Started
    2008-04
    Sponsor
    Sanofi

    Conditions Obesity · Weight Loss

    Matched “Rimonabant” in the study’s intervention “rimonabant (SR141716)”

  • NCT00734123Unknown status · Phase 4

    Early Detection of Atherosclerosis: a Randomized Trial in the Primary Prevention of Cardiovascular Diseases.

    Enrollment
    2948Testimated
    Started
    2008-04
    Sponsor
    Hospital Arnau de Vilanova

    Conditions Atherosclerosis · Cardiovascular Diseases

    Matched “Rimonabant” in the study’s intervention “Rimonabant”

  • NCT00577148Terminated · Phase 3

    An Efficacy and Safety Study of Rimonabant for Treatment of Nonalcoholic Steatohepatitis (NASH) in Patients With Type 2 Diabetes

    Enrollment
    89Tactual
    Started
    2008-02
    Sponsor
    Sanofi

    Conditions Fatty Liver

    Matched “Rimonabant” in the study’s intervention “Rimonabant”

  • NCT00576667Terminated · Phase 3

    An Efficacy and Safety Study of Rimonabant for Treatment of Nonalcoholic Steatohepatitis (NASH) in Patients Without Diabetes

    Enrollment
    165Tactual
    Started
    2008-01
    Sponsor
    Sanofi

    Conditions Fatty Liver

    Matched “Rimonabant” in the study’s intervention “Rimonabant”

  • NCT00547118Terminated · Phase 2

    The Effects of Rimonabant, on Weight and Metabolic Risk Factors

    Enrollment
    17Tactual
    Started
    2007-11
    Sponsor
    University of Maryland, Baltimore

    Conditions Schizophrenia · Schizoaffective Disorder · Obesity · Hypertension · Smoking

    Matched “Rimonabant” in the study’s intervention “Rimonabant”

  • NCT00546325Completed · Phase 3

    REASSURE: The Effect of Rimonabant on HbA1c in Overweight or Obese Patients With Type 2 Diabetes Not Adequately Controlled on 2 Oral Antidiabetic Agents

    Enrollment
    358Tactual
    Started
    2007-10
    Sponsor
    Sanofi

    Conditions Diabetes Mellitus, Type 2

    Matched “Rimonabant” in the study’s intervention “Rimonabant”

  • NCT00603109Terminated · Phase 3

    Effect of Rimonabant on Weight Gain and Body Composition in Adults With Prader Willi Syndrome

    Enrollment
    10Tactual
    Started
    2007-08
    Sponsor
    Weill Medical College of Cornell University

    Conditions Prader-willi Syndrome

    Matched “Rimonabant” in the study’s intervention “rimonabant”

  • NCT00584389Terminated · Phase 4

    The Effect of Rimonabant on Energy Expenditure, Fat Metabolism and Body Composition

    Enrollment
    14Tactual
    Started
    2007-07
    Sponsor
    University of Surrey

    Conditions Obesity

    Matched “Rimonabant” in the study’s intervention “rimonabant”

  • NCT00478972Terminated · Phase 3

    Japanese Study With Rimonabant in Obese Type 2 Diabetic Patients on Diet and Exercise

    Enrollment
    321Tactual
    Started
    2007-04
    Sponsor
    Sanofi

    Conditions Obesity · Diabetes Mellitus Type 2

    Matched “Rimonabant” in the study’s intervention “Rimonabant”

  • NCT00478595Terminated · Phase 3

    Japanese Study With Rimonabant in Obese Type 2 Diabetic Patients With Oral Anti-diabetic Drug

    Enrollment
    458Tactual
    Started
    2007-04
    Sponsor
    Sanofi

    Conditions Obesity · Diabetes Mellitus Type 2

    Matched “Rimonabant” in the study’s intervention “Rimonabant”

  • NCT00458081Terminated · Phase 3

    Evaluation of the Rimonabant Impact on the Regression of Asymptomatic Damage Caused by Cardiovascular Risk Factors

    Enrollment
    174Tactual
    Started
    2007-03
    Sponsor
    Sanofi

    Conditions Obesity · Microalbuminuria · Diabetes Mellitus, Type 2 · Dyslipidemia

    Matched “Rimonabant” in the study’s intervention “Rimonabant”

  • NCT00449605Terminated · Phase 3

    A Glycemic Control Evaluation of Glimepiride Versus Rimonabant on Top of Metformin in Type 2 Diabetes

    Enrollment
    508Tactual
    Started
    2007-03
    Sponsor
    Sanofi

    Conditions Diabetes Mellitus, Type 2

    Matched “Rimonabant” in the study’s intervention “Rimonabant”

  • NCT00434096Terminated · Phase 3

    Japanese Study of Rimonabant in Obese Patients With Dyslipidemia (VENUS)

    Enrollment
    915Tactual
    Started
    2007-02
    Sponsor
    Sanofi

    Conditions Obesity

    Matched “Rimonabant” in the study’s intervention “rimonabant (SR141716)”

  • NCT00412698Terminated · Phase 3

    European Trial About Effect of RimoNabant on Abdominal Obese Patients With dysLipidemia

    Enrollment
    645Tactual
    Started
    2006-12
    Sponsor
    Sanofi

    Conditions Obesity · Dyslipidemias

    Matched “Rimonabant” in the study’s intervention “rimonabant”

  • NCT00405808Terminated · Phase 3

    Rimonabant in Abdominally Obese Patients With Impaired Fasting Blood Glucose

    Enrollment
    2666Tactual
    Started
    2006-12
    Sponsor
    Sanofi

    Conditions Obesity

    Matched “Rimonabant” in the study’s intervention “Rimonabant”

  • NCT00408148Terminated · Phase 3

    High Density Lipoprotein Turnover

    Enrollment
    64Tactual
    Started
    2006-10
    Sponsor
    Sanofi

    Conditions Obesity

    Matched “Rimonabant” in the study’s intervention “Rimonabant”

  • NCT00325650Terminated · Phase 3

    Rimonabant In Prediabetic Subjects To Delay Onset Of Type 2 Diabetes

    Enrollment
    2420Tactual
    Started
    2006-05
    Sponsor
    Sanofi

    Conditions Prediabetic State

    Matched “Rimonabant” in the study’s intervention “Rimonabant”

  • NCT01041170Completed · Phase 1

    Antagonist-Elicited Cannabis Withdrawal

    Enrollment
    — no enrollment recorded in the registry entry
    Started
    2006-04-16
    Sponsor
    National Institute on Drug Abuse (NIDA)

    Conditions Cannabis · Dependence

    Matched “Rimonabant” in the study’s intervention “Rimonabant”

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 Rimonabant · rimonabantum · Rimonabant free base. Run this search at the registry — it returns the unfiltered result, including studies this page rejected as belonging to a different molecule.

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

    Identification of novel cannabinoid CB1 receptor antagonists by using virtual screening with a pharmacophore model

    Wang H, Duffy RA, Boykow GC et al. · Journal of medicinal chemistry 2008

    • · 4 measurements at 2 targets (Ki), strongest CB1 at 8.70 pX

    PMID 18363352

  2. 02

    3-Substituted pyrazole analogs of the cannabinoid type 1 (CB₁) receptor antagonist rimonabant: cannabinoid agonist-like effects in mice via non-CB₁, non-CB₂ mechanism

    Wiley JL, Selley DE, Wang P et al. · The Journal of pharmacology and experimental therapeutics 2012

    • · 3 measurements at 2 targets (Ki), strongest CB1 at 8.70 pX

    PMID 22085649

  3. 03

    Discovery of 2-(2-chlorophenyl)-3-(4-chlorophenyl)-7-(2,2-difluoropropyl)-6,7-dihydro-2H-pyrazolo[3,4-f][1,4]oxazepin-8(5H)-one (PF-514273), a novel, bicyclic lactam-based cannabinoid-1 receptor antagonist for the treatment of obesity

    Dow RL, Carpino PA, Hadcock JR et al. · Journal of medicinal chemistry 2009

    • · 3 measurements at 2 targets (Ki), strongest CB1 at 8.80 pX

    PMID 19351113

  4. 04

    Conformationally constrained analogues of N-(piperidinyl)-5-(4-chlorophenyl)-1-(2,4- dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide (SR141716): design, synthesis, computational analysis, and biological evaluations

    Zhang Y, Burgess JP, Brackeen M et al. · Journal of medicinal chemistry 2008

    • · 3 measurements at 2 targets (Ki), strongest CB1 at 8.93 pX

    PMID 18512901

  5. 05

    Diaryl piperidines as CB1 receptor antagonists

    Scott JD, Li SW, Wang H et al. · Bioorganic & medicinal chemistry letters 2010

    • · 2 measurements at 2 targets (Ki), strongest CB1 at 8.62 pX

    PMID 20018510

  6. 06

    Discovery of benzhydrylpiperazine derivatives as CB1 receptor inverse agonists via privileged structure-based approach

    Meng T, Wang J, Peng H et al. · European journal of medicinal chemistry 2010

    • · 2 measurements at 2 targets (Ki), strongest CB1 at 9.13 pX

    PMID 20047779

  7. 07

    Probing the cannabinoid CB1/CB2 receptor subtype selectivity limits of 1,2-diarylimidazole-4-carboxamides by fine-tuning their 5-substitution pattern

    Lange JH, van der Neut MA, Borst AJ et al. · Bioorganic & medicinal chemistry letters 2010

    • · 2 measurements at 2 targets (Ki), strongest CB1 at 7.60 pX

    PMID 20363132

  8. 08

    Discovery and functional evaluation of diverse novel human CB(1) receptor ligands

    Foloppe N, Benwell K, Brooks TD et al. · Bioorganic & medicinal chemistry letters 2009

    • · 2 measurements at 2 targets (Ki), strongest CB1 at 8.72 pX

    PMID 19520572

  9. 09

    Discovery of 1-[9-(4-chlorophenyl)-8-(2-chlorophenyl)-9H-purin-6-yl]-4-ethylaminopiperidine-4-carboxylic acid amide hydrochloride (CP-945,598), a novel, potent, and selective cannabinoid type 1 receptor antagonist

    Griffith DA, Hadcock JR, Black SC et al. · Journal of medicinal chemistry 2009

    • · 2 measurements at 1 target (Ki), strongest CB1 at 9.72 pX

    PMID 19102698

  10. 10

    Synthesis and in vitro autoradiographic evaluation of a novel high-affinity radioiodinated ligand for imaging brain cannabinoid subtype-1 receptors

    Donohue SR, Varnäs K, Jia Z et al. · Bioorganic & medicinal chemistry letters 2009

    • · 2 measurements at 2 targets (Ki), strongest CB1 at 8.86 pX

    PMID 19767206

  11. 11

    Synthesis, cannabinoid receptor affinity, molecular modeling studies and in vivo pharmacological evaluation of new substituted 1-aryl-5-(1H-pyrrol-1-yl)-1H-pyrazole-3-carboxamides. 2. Effect of the 3-carboxamide substituent on the affinity and selectivity profile

    Silvestri R, Ligresti A, La Regina G et al. · Bioorganic & medicinal chemistry 2009

    • · 2 measurements at 2 targets (Ki), strongest CB1 at 7.92 pX

    PMID 19595596

  12. 12

    Discovery of a novel class of selective human CB1 inverse agonists

    Foloppe N, Allen NH, Bentley CH et al. · Bioorganic & medicinal chemistry letters 2008

    • · 2 measurements at 2 targets (Ki), strongest CB1 at 8.74 pX

    PMID 18083560

  13. 13

    Investigations on the 4-quinolone-3-carboxylic acid motif. 2. Synthesis and structure-activity relationship of potent and selective cannabinoid-2 receptor agonists endowed with analgesic activity in vivo

    Pasquini S, Botta L, Semeraro T et al. · Journal of medicinal chemistry 2008

    • · 2 measurements at 2 targets (Ki), strongest CB1 at 7.92 pX

    PMID 18680276

  14. 14

    Novel sterically hindered cannabinoid CB1 receptor ligands

    Urbani P, Cascio MG, Ramunno A et al. · Bioorganic & medicinal chemistry 2008

    • · 2 measurements at 2 targets (Ki), strongest CB1 at 8.10 pX

    PMID 18579386

  15. 15

    Rational design, synthesis and biological evaluation of new 1,5-diarylpyrazole derivatives as CB1 receptor antagonists, structurally related to rimonabant

    Menozzi G, Fossa P, Cichero E et al. · European journal of medicinal chemistry 2008

    • · 2 measurements at 2 targets (Ki), strongest CB1 at 7.60 pX

    PMID 18342403

  16. 16

    Synthesis, cannabinoid receptor affinity, and molecular modeling studies of substituted 1-aryl-5-(1H-pyrrol-1-yl)-1H-pyrazole-3-carboxamides

    Silvestri R, Cascio MG, La Regina G et al. · Journal of medicinal chemistry 2008

    • · 2 measurements at 2 targets (Ki), strongest CB1 at 7.92 pX

    PMID 18293908

  17. 17

    Diaryl dihydropyrazole-3-carboxamides with significant in vivo antiobesity activity related to CB1 receptor antagonism: synthesis, biological evaluation, and molecular modeling in the homology model

    Srivastava BK, Joharapurkar A, Raval S et al. · Journal of medicinal chemistry 2007

    • · 2 measurements at 2 targets (Ki), strongest CB1 at 7.33 pX

    PMID 17979261

  18. 18

    New 1,8-naphthyridine and quinoline derivatives as CB2 selective agonists

    Manera C, Cascio MG, Benetti V et al. · Bioorganic & medicinal chemistry letters 2007

    • · 2 measurements at 2 targets (Ki), strongest CB1 at 7.80 pX

    PMID 17942307

  19. 19

    Bioisosteric replacements of the pyrazole moiety of rimonabant: synthesis, biological properties, and molecular modeling investigations of thiazoles, triazoles, and imidazoles as potent and selective CB1 cannabinoid receptor antagonists

    Lange JH, van Stuivenberg HH, Coolen HK et al. · Journal of medicinal chemistry 2005

    • · 2 measurements at 2 targets (Ki), strongest CB1 at 7.60 pX

    PMID 15771428

  20. 20

    Freezing and freeze-drying

    Rey L · Proceedings of the Royal Society of London. Series B, Biological sciences 1975

    • · 2 measurements at 2 targets (Ki), strongest CB1 at 9.40 pX

    PMID 1775

  21. 21

    1,2,3-Triazole derivatives as new cannabinoid CB1 receptor antagonists

    Hou DR, Alam S, Kuan TC et al. · Bioorganic & medicinal chemistry letters 2009

    • · 1 measurement at 1 target (Ki), strongest CB1 at 8.25 pX

    PMID 19095444

  22. 22

    Analogs of JHU75528, a PET ligand for imaging of cerebral cannabinoid receptors (CB1): development of ligands with optimized lipophilicity and binding affinity

    Fan H, Kotsikorou E, Hoffman AF et al. · European journal of medicinal chemistry 2009

    • · 1 measurement at 1 target (Ki), strongest CB1 at 7.40 pX

    PMID 18511157

  23. 23

    Bioisosteric replacement of the hydrazide pharmacophore of the cannabinoid-1 receptor antagonist SR141716A. Part I: potent, orally-active 1,4-disubstituted imidazoles

    Dow RL, Hadcock JR, Scott DO et al. · Bioorganic & medicinal chemistry letters 2009

    • · 1 measurement at 1 target (Ki), strongest CB1 at 8.80 pX

    PMID 19683918

  24. 24

    Benzodioxoles: novel cannabinoid-1 receptor inverse agonists for the treatment of obesity

    Alig L, Alsenz J, Andjelkovic M et al. · Journal of medicinal chemistry 2008

    • · 1 measurement at 1 target (Ki), strongest CB1 at 8.22 pX

    PMID 18335976

  25. 25

    Optimization of imidazole amide derivatives as cannabinoid-1 receptor antagonists for the treatment of obesity

    Smith RA, Fathi Z, Achebe F et al. · Bioorganic & medicinal chemistry letters 2007

    • · 1 measurement at 1 target (Ki), strongest CB1 at 8.96 pX

    PMID 17383180