Dexchlorpheniramine Other names: Chlorophenylpyridamine Chloroprophenpyridamine Chlorphenamine Chlorprophenpyridamine Chloropheniramine

Dexchlorpheniramine, the d-isomer of the racemic compound chlorpheniramine, is two times more active than chlorpheniramine. Dexchlorpheniramine does not prevent the release of histamine, but rather, competes with free histamine for binding at the H₁receptor sites, and competitively antagonizes the effects of histamine on H₁ receptors in the GI tract, uterus, large blood vessels, and bronchial muscle. Blockade of H₁-receptors also suppresses the formation of oedema, flare, and pruritus that result from histaminic activity.

Since dexchlorpheniramine binds to central and peripheral H₁-receptors, sedative effects are likely to occur. H₁-antagonists are structurally similar to anticholinergic agents and therefore possess the potential to exhibit anticholinergic properties of varying degrees. They also have antipruritic effects. Dexchlorpheniramine has high antihistaminic activity, moderate anticholinergic effects and minimal sedative effects. The medicine does not possess antiemetic properties.

The absorption, distribution, metabolism and elimination of dexchlorpheniramine have not been specifically described. However, since dexchlorpheniramine is the primary active isomer of the racemic compound chlorpheniramine, the pharmacokinetics of dexchlorpheniramine are likely to be similar to that of chlorpheniramine.

Dexchlorpheniramine is administered orally. H1-antagonists are generally well absorbed from the GI tract. The onset of action of immediate release formulations of chlorpheniramine is about 30-60 minutes. The C_max of chlorpheniramine occurs in about 2 hours, the maximum therapeutic effect in about 6 hours, and the duration of action lasts between 4-8 hours. Protein binding is approximately 72%. Chlorpheniramine is widely distributed in body tissues and fluids, and it crosses the placenta and is excreted into breast milk.

The metabolism of chlorpheniramine is extensive and rapid, first occurring in the gastric mucosa and then on first-pass through the liver, which may be saturable. N-dealkylation produces several metabolites, which are excreted in the urine along with the parent compound. The half-life in healthy adults and children is 20-24 hours and 10-13 hours, respectively. Excretion rates are dependent on the pH of urine and urinary flow, with the rate decreasing as the pH rises and urinary flow decreases.