Lubiprostone (Amitiza)

Utilized for chronic idiopathic constipation, inducing intestinal fluid secretion without change in serum electrolyte levels.

A secretagogue.
A bicyclic fatty acid derivative of prostaglandin E1, it primarily activates the apical type 2 chloride channels, accelerates small intestinal and colonic transit in healthy individuals.

Also approved for the treatment of Opioid-Induced Constipation (OIC) in adults with chronic, non-cancer pain.

Approved for IBS-C in women 18 years or older.

Trade name Amitiza

Oral agent.

Chloride-channel activator.

A member of the class of bicyclic acid fatty acid prostaglandin E1, which activates type 2 chloride channels in the apical membrane of intestinal epithelial cells to increase the secretion of chloride rich fluid.

Selectively stimulates intestinal fluid secretion to increse gut motility without clinically significant changes in serum electrolyte levels.

Results in increased intestinal motility and passage of stool increase.

Targets chloride channel activation to increase intestinal fluid balance.

A member of the class of bicyclic fatty acid prostaglandin E1, which activates type 2 chloride channels in the apical membrane of intestinal epithelial cells to increase the secretion of chloride rich fluid.

Chloride channels are key regulators of the intestinal tract, actively transporting chloride ions into the lumen.

Sodium and fluids passively follow as intestinal motility and passage of stool increase.

By increasing intestinal fluid it increases motility in the intestine, facilitating the passage of stools and alleviating constipation.

Has a low systemic bioavailability, rapid onset of action, and satisfactory safety profile.

57-63% of patients with chronic idiopathic constipation have their first spontaneous bowel movement within 24 hours after treatment.

In a review of 268 trials, a meta-analysis of randomized, placebo controlled trials for

treatment of chronic idopathic constipation or irritable bowel syndrome-constipation it significantly improved the severity of constipation, stool consistency, of abdominal pain, degree of straining, and of abdominal bloating at one week and one month except for abdominal pain at one month, which was similar to that of treatment with placebo (Li F et al).

Enhances gastrointestinal fluid secretion and transit.

May stabilize mucosal membranes, which may decrease mucosal inflammation and sensitization.

May be useful in irritable bowel disease with constipation.

Has a dose response relationship in the treatment of chronic constipation.

Women of childbearing age require a negative pregnancy test prior to use.

24 mcg twice daily po.

Protein binding of 94%

Biological half-life is unknown.

Excretion-renal 60% and fecal 30%.

Used in the management of chronic idiopathic constipation, irritable bowel syndrome-associated constipation in women and opioid-induced constipation.

Most common adverse event is nausea at 31%.

Other adverse events include diarrhea (13%), headache (13%), abdominal distention (5%), abdominal pain (5%), flatulence (6%), sinusitis (5%) vomiting (5%) and fecal incontinence (1%).

Not approved for use in children.

Contraindicated in patients exhibiting chronic diarrhea, bowel obstruction, or diarrhea-predominant Irritable bowel syndrome.

A bicyclic fatty acid derived from prostaglandin E1 that acts by specifically activating ClC-2 chloride channels on the apical aspect of gastrointestinal epithelial cells, producing a chloride-rich fluid secretion.

These secretions soften the stool, increase motility, and promote spontaneous bowel movements.

Symptoms of constipation are usually improved within one week, and spontaneous bowel movements may occur within one day.

Does not show signs of tolerance, dependency, or altered serum electrolyte concentration.

There was no rebound effect following withdrawal of treatment, but a gradual return to pre-treatment bowel movement frequency should be expected.

Minimal distribution of the drug occurs beyond the immediate gastrointestinal tissues.

Rapidly metabolized by reduction/oxidation, mediated by carbonyl reductase, and no metabolic involvement of the hepatic cytochrome P450 system.

The measurable metabolite, M3, exists in very low levels in plasma and makes up less than 10% of the total administered dose.

Available through prescription only.

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