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Pharmaco-therapeutic group: Anti obesity agent

ATC code: A08AX01

Rimonabant is a selective cannabinoid-1 receptor (CB1) antagonist that inhibits the pharmacological effects of cannabinoid agonists in vitro and in vivo.

The endocannabinoid system is a physiological system present in brain and peripheral tissues (including adipocytes) that affects energy balance, glucose and lipid metabolism and body weight, and in neurons of the mesolimbic system modulates the intake of highly palatable, sweet or fatty foods.


Rimonabant (Acomplia) pharmacokinetics are fairly dose proportional up to about 20 mg. AUC increased less than in proportion to dose above 20 mg.


Rimonabant displays high in vitro permeability and is not a substrate of P-glycoprotein. The absolute bioavailability of rimonabant has not been determined. Following multiple once-daily doses of 20 mg to healthy subjects in the fasted state, maximum plasma concentrations of rimonabant are achieved in approximately 2 hours with steady state plasma levels achieved within 13 days (Cmax = 196 28.1 ng/ml; Ctrough = 91.6 14.1 ng/ml; AUC0-24 = 2960 268 ng.h/ml). Steady state Acomplia (Rimonabant) tablets exposures are 3.3-fold higher than those observed after the first dose. Population pharmacokinetic analysis demonstrated less fluctuation in peak to trough plasma concentration but no differences in steady state AUC as weight increases. As weight increases from 65 to 200 kg, Cmax is expected to decrease 24% and Ctrough is expected to increase by 5%. Time to steady state is longer in obese patients (25 days) as a consequence of the higher volume of distributionin these patients. Population pharmacokinetic analysis indicated that rimonabant pharmacokinetics are similar between healthy non-smoking subjects and patients who smoke.

Effect of food:

Administration of rimonabant to healthy subjects in the fasted state or with a high fat meal demonstrated that Cmax and AUC were increased 67% and 48% respectively, under fedconditions. In clinical studies, Rimonabant (Acomplia) tablets 20 mg was taken in the morning usually before breakfast.


The in vitro human plasma protein binding of rimonabant is high (> 99.9%) and non-saturable over a wide concentration range. The apparent peripheral volume of distribution of rimonabant appears to be related to body weight, with obese patients having a higher volume of distribution than normal-weight subjects.


Acomplia (Rimonabant) is metabolized by both CYP3A and amidohydrolase (predominantly hepatic) pathways in vitro. Circulating metabolites do not contribute to its pharmacologic activity.


Acomplia is mainly eliminated by metabolism and subsequent biliary excretion of metabolites. Only an approximate 3% of the dose of rimonabant is eliminated in the urine, while approximately 86% of the dose is excreted in the faeces as unchanged drug and metabolites. In obese patients, the elimination half-life is longer (about 16 days) than in non-obese patients (about 9 days) due to a larger volume of distribution.

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