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Research tools

RimonabantAlso known as SR141716, Acomplia

The first CB1 antagonist to be marketed (Acomplia, EU 2006), withdrawn in 2009 over psychiatric risk.

Unscheduled
Level of detail

C₂₂H₂₁Cl₃N₄O

CAS 168273-06-1

Family
ECS pharmacological toolAntagonist or inverse agonist
First described
1994
Molar mass
463.80 g/mol

Updated on

In plain terms

Rimonabant is a synthetic molecule that blocks the CB1 receptor. Authorised in Europe in 2006 for obesity, it was suspended in 2008 and withdrawn in 2009 because it roughly doubled the risk of psychiatric disorders, including depression. It remains a reference laboratory tool.

Receptors and activity

Target network

CB1Inverse agonistKi = 1.8 nM · mixed (rat, human)Ki range compiled from several studies (IUPHAR, table 1); inverse agonism: pEC50 8.26 on basal [35S]GTPγS binding, CHO-hCB1 (MacLennan 1998)
  • Blocks or inhibits

The lower the cited value, the closer the target sits to Rimonabant: one ring per factor of 100. A target with no measured value stays on the edge.

Where these targets live

Where each target has been found in humans, according to the cited studies. The map shows the target, not an effect of Rimonabant.

Brain, side view
Body, front view
Blood

CB1CB1 found in 7 regions of the body

  1. Basal gangliadenseMost dense in basal ganglia outflow nuclei1
  2. CerebellumdenseVery dense in the cerebellum1
  3. HippocampusdenseVery high concentrations in the hippocampus2
  4. AmygdaladenseHigh concentrations in the amygdala2
  5. CortexpresentPresent throughout the neocortex2
  6. Adipose tissuepresentExpressed in adipose tissue3
  7. GutpresentColonic epithelium, smooth muscle and plexus4

Map sources

  1. Herkenham M et al. Cannabinoid receptor localization in brain. Proc Natl Acad Sci U S A, 1990 (new tab)
  2. Glass M et al. Cannabinoid receptors in the human brain: a detailed anatomical and quantitative autoradiographic study in the fetal, neonatal and adult human brain. Neuroscience, 1997 (new tab)
  3. Engeli S et al. Activation of the peripheral endocannabinoid system in human obesity. Diabetes, 2005 (new tab)
  4. Wright K et al. Differential expression of cannabinoid receptors in the human colon: cannabinoids promote epithelial wound healing. Gastroenterology, 2005 (new tab)

Cited values

  1. CB1Inverse agonistKi = 1.8 nM · mixed (rat, human)79 out of 100

    Pertwee et al. 2010, Pharmacol Rev (new tab) · Ki range compiled from several studies (IUPHAR, table 1); inverse agonism: pEC50 8.26 on basal [35S]GTPγS binding, CHO-hCB1 (MacLennan 1998)

  2. CB2Inverse agonistKi = 514 nM · mixed (rat, human)38 out of 100

    Pertwee et al. 2010, Pharmacol Rev (new tab) · compiled Ki range (IUPHAR, table 1); inverse agonism: pEC50 6.00, basal [35S]GTPγS, CHO-hCB2 (MacLennan 1998)

Bar length follows the measured value (Ki, Kd, EC50 or IC50), on one scale shared by every entry, from 100 µM to 0.1 nM. A target with no cited value has no bar.

Measured effects

Not characterised. No placebo-controlled human trial has measured the effects of Rimonabant, so no level is shown.

Levels computed from placebo-controlled human trials: difference from placebo on 100, at the dose and route stated. Read the method

Pharmacology

Rimonabant (SR141716, Acomplia®) was described in 1994 by Sanofi Recherche (Montpellier) as the first selective, orally active antagonist of the central cannabinoid receptor (Rinaldi-Carmona et al. 1994). The European Commission authorised it on 19 June 2006, as an adjunct to diet and exercise, for obese or overweight patients with risk factors. In the RIO-Europe trial, the 20 mg/day dose produced a weight loss of 6.6 kg at one year versus 1.8 kg on placebo (Van Gaal et al. 2005). A meta-analysis of four trials (4105 participants) found 4.7 kg of additional loss and a 2.5-fold higher risk of stopping treatment because of depressive disorders (Christensen et al. 2007). On 23 October 2008 the CHMP concluded that the risk of psychiatric disorders was approximately doubled and recommended suspension; marketing was suspended on 13 November 2008 and the authorisation withdrawn on 16 January 2009. It was never authorised in the United States (Sam et al. 2011). It remains the reference CB1 antagonist in research (Pertwee et al. 2010).

Key sources.

Approved medicines

Acomplia

History

Source
Synthetic (Sanofi Recherche, Montpellier); withdrawn medicine

Origin

Research tool

None: a fully synthetic molecule (1,5-diarylpyrazole-3-carboxamide), described by Sanofi Recherche in 1994.

Classification

Family, origin and source verification

Family

ECS pharmacological tool › Antagonist or inverse agonist

Verification

Every fact on this entry was checked against its primary sources on 20 October 2026.

Wikipedia (English)

Rimonabant (new tab)

Article paired by the molecule's structure (InChIKey), revision read on 19 October 2026. Read as a second opinion, never cited as a source.

References

  1. Rinaldi-Carmona et al. 1994 · FEBS Lett 350:240 (new tab)PMID 8070571
  2. Van Gaal et al. 2005 · Lancet 365:1389 (RIO-Europe) (new tab)PMID 15836887
  3. Christensen et al. 2007 · Lancet 370:1706 (meta-analysis) (new tab)PMID 18022033
  4. MacLennan et al. 1998 · Br J Pharmacol 124:619 (new tab)PMID 9690851
  5. Pertwee et al. 2010 · Pharmacol Rev 62:588 (IUPHAR) (new tab)PMID 21079038
  6. EMA · Acomplia EPAR (EMEA/H/C/000666) and press release EMEA/CHMP/537777/2008 (new tab)
  7. Sam et al. 2011 · J Obes (Rimonabant: from RIO to ban) (new tab)PMID 21773005

Identifiers

Names

Common name
Rimonabant (SR141716, Acomplia)
IUPAC name
5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-N-piperidin-1-ylpyrazole-3-carboxamide
Other names
SR141716 · SR141716A (chlorhydrate) · Acomplia · Zimulti

Identifiers

Formula
C₂₂H₂₁Cl₃N₄O
CAS
168273-06-1
PubChem CID
104850(new tab)
ChEBI
CHEBI:34967(new tab)
InChIKey
JZCPYUJPEARBJL-UHFFFAOYSA-N
SMILES
CC1=C(N(N=C1C(=O)NN2CCCCC2)C3=C(C=C(C=C3)Cl)Cl)C4=CC=C(C=C4)Cl

Machine-readable entry (JSON)

LLM ingestion format: a structured superset of the entry (identifiers, binding, versioned legal status). Full corpus.