Dicyclomine 2.5 mg, Dried Aluminum Hydroxide 200 mg, Light Magnesium Oxide 100 mg, Simethicone 20 mg / 5 ml Oral suspension

Dicyclomine relieves smooth muscle spasm of the gastrointestinal tract. Animal studies indicate that this action is achieved via a dual mechanism:

Atropine did not affect responses to these two agonists. In vivo studies in cats and dogs showed dicyclomine to be equally potent against acetylcholine (ACh)- or barium chloride (BaCl2)-induced intestinal spasm while atropine was at least 200 times more potent against effects of ACh than BaCl2. Tests for mydriatic effects in mice showed that dicyclomine was approximately 1/500 as potent as atropine; antisialagogue tests in rabbits showed dicyclomine to be 1/300 as potent as atropine.

Absorption and Distribution — In man, dicyclomine is rapidly absorbed after oral administration, reaching peak values within 60-90 minutes. Mean volume of distribution for a 20 mg oral dose is approximately 3.65 L/kg suggesting extensive distribution in tissues.

Elimination — The metabolism of dicyclomine was not studied. The principal route of excretion is via the urine (79.5% of the dose). Excretion also occurs in the feces, but to a lesser extent (8.4%). Mean half-life of plasma elimination in one study was determined to be approximately 1.8 hours when plasma concentrations were measured for 9 hours after a single dose. In subsequent studies, plasma concentrations were followed for up to 24 hours after a single dose, showing a secondary phase of elimination with a somewhat longer half-life.

Simeticone is a chemically inert defoaming substance. It alters the interfaces of gas bubbles trapped in gastrointestinal mucus, helping bubbles break or combine so that gas can be expelled more easily.

The cited oral reference states that activated dimeticone is not absorbed from the gastrointestinal tract and is excreted unchanged in feces. Its local physical action therefore does not call for an invented systemic bioavailability, plasma peak or elimination half-life.

Aluminium hydroxide acts locally as an antacid.

Most orally administered aluminium hydroxide remains in the gastrointestinal tract as poorly absorbed salts and leaves in feces. These qualitative disposition findings do not demonstrate equal neutralizing capacity or absorption across gel strengths and combinations. The label warns of aluminium accumulation in chronic renal failure.