May 22, 2017
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Discontinued Warning IconPlease Note: This Brand Name drug is no longer available in the US.
(Generic versions may still be available.)



Cisapride is metabolized mainly via the cytochrome P450 3A4 enzyme. Cisapride is extensively metabolized; unchanged drug accounts for less than 10% of urinary and fecal recovery following oral administration. Norcisapride, formed by N-dealkylation, is the principal metabolite in plasma, feces, and urine. Cisapride is rapidly absorbed after oral administration; peak plasma concentrations are reached 1 to 1.5 hours after dosing. The absolute bioavailability of cisapride is 35-40%. When gastric acidity was reduced by high dose histamine H2 receptor blocker and sodium bicarbonate in fasting subjects, there was a decrease in the rate, and to a lesser degree the extent, of cisapride tablet absorption. (This has not been established for the suspension.) Cisapride binds to an extent of 97.5-98% to plasma proteins, mainly to albumin. The volume of distribution of cisapride is about 180 L, indicating extensive tissue distribution.

The plasma clearance of cisapride is about 100 ml/min. The mean terminal half-life reported for cisapride ranges from 6 to 12 hours; longer half-lives, up to 20 hours, have been reported following intravenous (IV) administration.

There was no unusual drug accumulation due to time-dependent or non-linear changes in pharmacokinetics. After cessation of the repeated dosing, the elimination half-lives (8 to 10 hr) were in the same order as after single dosing. The degree of accumulation of cisapride and/or its metabolites may be somewhat higher in patients with hepatic or renal impairment and in elderly patients compared to young healthy volunteers, but the differences are not consistent. Dose adjustments are recommended in patients with hepatic impairment. (See DOSAGE AND ADMINISTRATION.)

The pharmacokinetics of cisapride in pediatric patients are not well characterized. Therefore, it is unknown if the dose-response relationship in the adult population can be extrapolated to the pediatric population. (See PRECAUTIONS, Pediatric Use.)


The onset of pharmacological action of cisapride is approximately 30 to 60 minutes after oral administration.

Cisapride promotes gastric motility. The mechanism of action of cisapride is thought to be primarily enhancement of release of acetylcholine at the myenteric plexus. Cisapride does not induce muscarinic or nicotinic receptor stimulation, nor does it inhibit acetylcholinesterase activity. It is less potent than metoclopramide in dopamine receptor-blocking effects in rats. It does not increase or decrease basal or pentagastrin-induced gastric acid secretion.

In vitro studies have shown that cisapride is a serotonin-4 (5-HT4) receptor agonist.

Electrophysiological studies in in vivo anesthetized guinea pig and rabbit models and in vitro isolated rabbit Purkinje fibers and ventricular papillary muscle and isolated rabbit ventricular myocyte models, have shown that cisapride prolonged cardiac repolarization without slowing conduction by selectively blocking the rapid component of the delayed rectifying K+ current (lkr) which leads to a lengthening of the action potential (QT Syndrome).

Esophagus: Twenty milligrams oral cisapride given once to healthy volunteers increased LESP, starting 45 minutes after dosing, with a peak response at 75 minutes. The full duration of the effect was not monitored, and doses smaller than 20 mg were ineffective. Ten milligrams oral cisapride, administered 3 times daily for several days to patients with GERD, resulted in a significant increase in LESP, and an increased esophageal acid clearance.

Stomach: Cisapride (single 10 mg doses or 10 mg given orally 3 times daily up to 6 weeks) significantly accelerated gastric emptying of both liquids and solids. Acceleration of gastric emptying, measured over a 4 hour period following a radio-labeled test meal given at lunch time, was greatest when 10 mg cisapride was given both in the morning and again before the test meal, intermediate when 20 mg was given as a single administration in the morning and least when only 10 mg was given on the morning of the test meal. The increases in gastric emptying were proportional to the plasma levels of cisapride measured in these subjects over the same 4 hours that the gastric emptying test was conducted.


Clinical trials have shown that cisapride can reduce the severity of symptoms of nocturnal heartburn associated with gastroesophageal reflux disease. Two placebo-controlled studies, one using a dose of 10 mg qid, the other both 10 and 20 mg qid, showed effects on nighttime heartburn, although the 10 mg dose in the second study was only marginally effective. There were no consistent effects on daytime heartburn, symptoms of regurgitation, or histopathology of the esophagus. Use of antacids was only infrequently affected and slightly decreased. In a third controlled trial of similar design to the others, neither 10 mg nor 20 mg taken 4 times daily was superior to placebo. In these clinical trials cisapride did not wshow a significant effect on LESP.

In a clinical trial comparing 10 mg cisapride to placebo, pH probe evaluation, in a relatively small number of patients, did not reveal a significant difference in pH.

Last reviewed on RxList: 2/3/2017
This monograph has been modified to include the generic and brand name in many instances.

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