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Systematic (IUPAC) name
CAS number 158681-13-1
ATC code A08AX01
PubChem 104850
ChemSpider 94641
Chemical data
Formula C22H21Cl3N4O 
Mol. mass 463.79 g/mol
Pharmacokinetic data
Bioavailability Undetermined
Protein binding Nearly 100%
Metabolism Hepatic, CYP3A4 involved
Half life Variable:
6 to 9 days with normal BMI
16 days if BMI >30
Excretion Fecal (86%) and renal (3%)
Therapeutic considerations
Licence data

EU EMEA:link

Pregnancy cat. Not assigned. Use not recommended
Legal status POM (UK)
Routes Oral
 Yes check.svgY(what is this?)  (verify)

Rimonabant (also known as SR141716, Acomplia, Bethin, Monaslim, Remonabent, Riobant, Slimona, Rimoslim, and Zimulti[1], Riomont) is an anorectic anti-obesity drug. It is an inverse agonist for the cannabinoid receptor CB1.[2] Its main avenue of 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 October 23, 2008, the European Medicines Agency (EMEA) released a press release stating that its Committee for Medical Products for Human Use (CHMP) had concluded that the benefits of Acomplia no longer outweighed its risks and subsequently recommended that the product be suspended from the UK market. Sanofi-Aventis later released a press statement stating that the drug had been suspended.[3][4] Approval of the drug was officially withdrawn by the EMEA on January 16, 2009.[5]



Despite the FDA's issuing an approvable letter in February 2006 for the obesity indication and a non-approvable 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 that a complete response to the FDA's approvable letter was submitted on October 26, 2006, triggering a Class I (two-month) or Class II (six-month) review process. On June 13, 2007, FDA's Endocrine and Metabolic Drugs Advisory Committee (EMDAC) concluded that 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 that 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 that the first country in which Acomplia would be sold was the United Kingdom as a non-prescription drug. Sales began in July 2006. Sanofi also announced that 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 non-obesity-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 that doctors not prescribe the drug due to the risk of serious psychiatric problems and even suicide. The drug was subsequently suspended.[9]


Shortly after market introduction, press reports and independent studies suggest that side-effects occur stronger and more commonly than shown by the manufacturer in their clinical studies. Reports of severe depression are frequent. This is deemed to result from the drug's being active in the central nervous system, an area of human physiology so complex that the effects of a drug are extremely difficult to predict or anticipate.[10]

Because the drug has the opposite effects of cannabinoid receptor agonists such as tetrahydrocannabinol (THC), one of the substances found in marijuana, which is neuroprotective against excitotoxicity,[11] it can be theorized that rimonabant promotes the development of neurodegenerative diseases of the central nervous system such as multiple sclerosis, Alzheimer's disease, amyotrophic lateral sclerosis (ALS), Parkinson's disease, and Huntington's disease in persons that are susceptible.[12] The reported development of previously clinically-silent multiple sclerosis in one patient taking rimonabant suggests that any patients with an underlying neurological condition should not take rimonabant, given the neuroprotective role of the endocannabinoid system in many experimental paradigms of neurological disease.

On June 15, 2007, BBC News reported[13] that 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 that 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 1/2-fold".[14]


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.[15]


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.[16]

Blockade of Cannabis effects

Rimonabant blocks the psychoactive and some of the cardiovascular effects of Δ9-tetrahydrocannabinol (THC) in humans without affecting the pharmacokinetics.[17]

Effect on physical activity

Rimonabant reduces voluntary wheel running in laboratory mice.[18] Apparently, the possibility of such effects in human beings has not been studied.


  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. ^ Fong TM, Heymsfield SB (September 2009). "Cannabinoid-1 receptor inverse agonists: current understanding of mechanism of action and unanswered questions". Int J Obes (Lond) 33 (9): 947–55. doi:10.1038/ijo.2009.132. PMID 19597516. 
  3. ^ "European Medicines Agency". 2010-02-15. Retrieved 2010-03-19. 
  4. ^ "Sanofi-aventis - A diversified healthcare company, focused on patients’ needs". 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". 2007-06-13. Retrieved 2010-03-19. 
  7. ^ Auteur: Femke Gebruers. "Article from the Belgian newspaper De Standaard". Retrieved 2010-03-19. 
  8. ^ "Article from the Swedish TV station TV 4 website". 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". 2006-10-17.,,OID6010180,00.html. Retrieved 2007-06-13. 
  11. ^ Van Der Stelt, M; Veldhuis, WB; Bär, PR; Veldink, GA; Vliegenthart, JF; Nicolay, K (2001). "Neuroprotection by Delta9-tetrahydrocannabinol, the main active compound in marijuana, against ouabain-induced in vivo excitotoxicity.". The Journal of neuroscience : the official journal of the Society for Neuroscience 21 (17): 6475–9. PMID 11517236.  edit
  12. ^ Kim AH, Kerchner GA, and Choi DW. Blocking Excitotoxicity. Chapter 1 in CNS Neuroproteciton. Marcoux FW and Choi DW, editors. Springer, New York. 2002. Pages 3-36
  13. ^ "Suicide risk fears over diet pill". BBC News. 15 June 2007. Retrieved 4 March 2010. 
  14. ^ 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. 
  15. ^ 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. 
  16. ^ 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. 
  17. ^ 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. 
  18. ^ Keeney BK, Raichlen DA, Meek TH, Wijeratne RS, Middleton KM, Gerdeman GL, Garland T, Jr. (2008). "Differential response to a selective cannabinoid receptor antagonist (SR141716: rimonabant) in female mice from lines selectively bred for high voluntary wheel-running behavior". Behavioural Pharmacology 19: 812–820. 

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