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Systematic (IUPAC) name
Clinical data
[[Regulation of therapeutic goods |Template:Engvar data]]
  • Not assigned, use not recommended
Routes of
Legal status
Legal status
  • UK: POM (Prescription only)
Pharmacokinetic data
Bioavailability Undetermined
Protein binding Nearly 100%
Metabolism Hepatic, CYP3A4 involved
Biological half-life Variable:
6 to 9 days with normal BMI
16 days if BMI >30
Excretion Fecal (86%) and renal (3%)
CAS Number 158681-13-1
ATC code A08AX01 (WHO)
PubChem CID 104850
ChemSpider 94641
Chemical data
Formula C22H21Cl3N4O
Molar mass 463.79 g/mol[[Script error: No such module "String".]]
Script error: No such module "TemplatePar".Expression error: Unexpected < operator.

Rimonabant (also known as SR141716; trade names Acomplia, Bethin, Monaslim, Remonabent, Riobant, Slimona, Rimoslim, Zimulti,[1] and Riomont) is an anorectic antiobesity drug. It is an inverse agonist for the cannabinoid receptor CB1.[2] Its main effect is reduction in appetite.

Rimonabant was the first selective CB1 receptor blocker to be approved for use anywhere in the world. In Europe, it was indicated for use in conjunction with diet and exercise for patients with a body mass index greater than 30 kg/m², or patients with a BMI greater than 27 kg/m² with associated risk factors, such as type 2 diabetes or dyslipidaemia. In the UK, it was available beginning in July 2006. As of 2008, the drug was available in 56 countries. On 23 October 2008, the European Medicines Agency (EMEA) issued a press release stating its Committee for Medical Products for Human Use (CHMP) had concluded the benefits of Acomplia no longer outweighed its risks, and subsequently recommended the product be suspended from the UK market. Sanofi-Aventis later released a press statement stating the drug had been suspended.[3][4] Approval of the drug was officially withdrawn by the EMEA on 16 January 2009.[5]


Despite the FDA's issuing an approvable letter in February 2006 for the obesity indication, and a nonapprovable letter for smoking cessation, the drug did not enter the market in the United States in 2006.[citation needed] The French pharma firm Sanofi-Aventis disclosed a complete response to the FDA's approvable letter was submitted on 26 October 2006, triggering a Class I (two-month) or Class II (six-month) review process. On 13 June 2007, FDA's Endocrine and Metabolic Drugs Advisory Committee (EMDAC) concluded the French manufacturer Sanofi-Aventis failed to demonstrate the safety of rimonabant and voted against recommending the anti-obesity treatment for approval.[6] Subsequently, Sanofi-Aventis announced it was suspending the new drug application (NDA) for rimonabant, and that it would resubmit an application at some point in the future.

On 21 June 2006, the European Commission approved the sale of rimonabant in the then-25-member European Union. Sanofi announced the first country in which Acomplia would be sold was the United Kingdom as a nonprescription drug. Sales began in July 2006. Sanofi also announced it projected that the drug would be sold shortly thereafter in Denmark, Ireland, Germany, Finland, and Norway. It was expected in Belgium[7] and Sweden in 2007. Ordinary obesity would, according to official medical recommendations, not be enough to acquire the prescription in Sweden; there would be additional requirements concerning abnormal blood lipid levels.[8]

The EU's approval was not a blanket approval, nor did it approve Acomplia for nonobesity-related problems, such as smoking cessation, although off-label use of the drug was still possible. The approval was, in combination with diet and exercise, for the treatment of obese patients (BMI greater than or equal to 30), or overweight patients (BMI greater than 27) with associated risk factors, such as type 2 diabetes or dyslipidaemia.

In October 2008, the European Medicines Agency recommended doctors not prescribe the drug due to the risk of serious psychiatric problems and even suicide. The drug was subsequently suspended.[9]

Side effects

Shortly after market introduction, press reports and independent studies suggested side effects occurred more intensely and more commonly than shown by the manufacturer in their clinical studies. Resulting from drug actions at CB1 receptors in the brain, reports of severe depression and suicidal thoughts are frequent.[10] As CB1 receptors are fairly ubiquitous throughout the central nervous system, it is not currently understood where exactly the inverse agonist is acting to cause these side-effects.

On 15 June 2007, BBC News reported[11] a committee advising the U.S. FDA had voted not to recommend the drug's approval because of concerns over suicidality, depression, and other related side effects associated with use of the drug.

Other uses

Smoking cessation

Rimonabant may also be found to be effective in assisting some smokers to quit smoking. Sanofi-Aventis is currently conducting studies to determine the possible value of rimonabant in smoking-cessation therapy. The Studies with Rimonabant and Tobacco Use (STRATUS) program involves more than 6,000 subjects. STRATUS is designed to explore two smoking-related therapies: first, to use rimonabant directly to aid in smoking cessation; second, to help prevent weight gain in former smokers. Initial results apparently suggest rimonabant is effective for both uses. However, the FDA has explicitly stated to Sanofi-Aventis that, without additional studies, rimonabant cannot be approved in the United States for smoking cessation therapy. According to a Cochrane review in 2007, rimonabant "may increase the odds of quitting approximately 11/2-fold".[12]


Rimonabant reduced resumption of cocaine-seeking responses triggered by two of the three most common triggers of relapse in humans, priming and cues. It may also reduce ethanol- and opiate-seeking behavior.[13]


Tetrahydrocannabinol (THC) is known to impair short-term memory. It was therefore hypothesised that rimonabant may improve short-term memory. Indeed, in animal studies, it significantly improved the performance of rats to encode information in the short-term memory.[14]

Blockage of cannabis effects

Rimonabant blocks the psychoactive and some of the cardiovascular effects of Δ9-tetrahydrocannabinol (THC) in humans without affecting the pharmacokinetics.[15]

Effect on physical activity

Rimonabant reduces voluntary wheel running in laboratory mice.[16] Apparently, the possibility of such effects in human beings has not been studied.


Rimonabant can be synthesized as follows:[17]



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de:Rimonabant fr:Rimonabant he:רימונבאנט nl:Rimonabant ja:リモナバン pl:Rimonabant pt:Rimonabanto

  1. Rimonabant is currently being sold in the United Kingdom by Sanofi-Aventis and in Denmark by Sanofi-Synthelabo under the trade name Acomplia, the name used in 18 countries, as of 2007. Bethin, Monaslim, Remonabent, Riobant, Slimona and Rimoslim are generic forms available in India. If approved in the United States, it is intended to be marketed under the name Zimulti.
  2. Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  3. "European Medicines Agency". Emea.europa.eu. 2010-02-15. Retrieved 2010-03-19. 
  4. "Sanofi-aventis - A diversified healthcare company, focused on patients' needs". En.sanofi-aventis.com. Retrieved 2010-03-19. 
  5. "Microsoft Word - Zimulti _Rimonabant_ Public Statement" (PDF). Retrieved 2010-03-19. 
  6. "Zimulti Acomplia Report - Diet Drug Acomplia / Zimulti Gets Thumbs Down From FDA Panel". Acompliareport.com. 2007-06-13. Retrieved 2010-03-19. 
  7. Auteur: Femke Gebruers. "Article from the Belgian newspaper De Standaard". Standaard.be. Retrieved 2010-03-19. 
  8. "Article from the Swedish TV station TV 4 website". Tv4.se. 2008-03-06. Retrieved 2010-03-19. 
  9. "Anti-obesity drug use suspended". BBC News. 23 October 2008. Retrieved 4 March 2010. 
  10. "Kassen müssen nicht für "Acomplia" zahlen". tagesschau.de. 2006-10-17. Retrieved 2007-06-13. 
  11. "Suicide risk fears over diet pill". BBC News. 15 June 2007. Retrieved 4 March 2010. 
  12. Cahill K, Ussher M (2007). "Cannabinoid type 1 receptor antagonists (rimonabant) for smoking cessation". Cochrane database of systematic reviews (Online) (4): CD005353. doi:10.1002/14651858.CD005353.pub3. PMID 17943852. 
  13. Maldonado R, Valverde O, Berrendero F (2006). "Involvement of the endocannabinoid system in drug addiction". Trends Neurosci. 29 (4): 225–32. doi:10.1016/j.tins.2006.01.008. PMID 16483675. 
  14. Deadwyler SA, Goonawardena AV, Hampson RE (2007). "Short-term memory is modulated by the spontaneous release of endocannabinoids: evidence from hippocampal population codes". Behavioural pharmacology. 18 (5-6): 571–80. doi:10.1097/FBP.0b013e3282ee2adb. PMID 17762525. 
  15. Huestis MA, Gorelick DA, Heishman SJ; et al. (2001). "Blockade of effects of smoked marijuana by the CB1-selective cannabinoid receptor antagonist SR141716". Arch. Gen. Psychiatry. 58 (4): 322–8. doi:10.1001/archpsyc.58.4.322. PMID 11296091. 
  16. Keeney BK, Raichlen DA, Meek TH, Wijeratne RS, Middleton KM, Gerdeman GL, Garland T, Jr. (2008). "antagonist (SR141716: rimonabant) in female mice from lines selectively bred". Behavioural Pharmacology. 19 (8): 812–820. doi:10.1097/FBP.0b013e32831c3b6b. PMID 19020416. 
  17. Yoshioka, T.; Fujita, T.; Kanai, T.; Aizawa, Y.; Kurumada, T.; Hasegawa, K.; Horikoshi, H. (1989). "Studies on hindered phenols and analogs. 1. Hypolipidemic and hypoglycemic agents with ability to inhibit lipid peroxidation". Journal of Medicinal Chemistry. 32 (2): 421. doi:10.1021/jm00122a022. PMID 2913302.  edit