BONNI COUGH

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 H₁-receptor 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. Dexchlorpheniramine has high antihistaminic activity, moderate anticholinergic effects and minimal sedative effects.

Guaifenesin is an expectorant the action of which promotes or facilitates the removal of secretions from the respiratory tract. The precise mechanism of action of guaifenesin is not known; however, it is thought to act as an expectorant by increasing the volume and reducing the viscosity of secretions in the trachea and bronchi. In turn, this may increase the efficiency of the cough reflex and facilitate removal of the secretions. Guaifenesin is over-the-counter drug for the treatment of cough and common cold.

Noscapine is a benzylisoquinoline alkaloid from plants of the poppy family, without painkilling properties. Noscapine is often used as an antitussive medication. Noscapine can increase the effects of centrally sedating substances such as alcohol and hypnotics. Noscapine, and its synthetic derivatives called noscapinoids, are known to interact with microtubules and inhibit cancer cell proliferation. Mechanisms for its antitussive action are unknown, although animal studies have suggested central nervous system as a site of action. Furthermore, noscapine causes apoptosis in many cell types and has potent antitumor activity against solid murine lymphoid tumors (even when the drug was administered orally) and against human breast and bladder tumors implanted in nude mice. Antifibrotic effect of noscapine based on novel mechanism, which it shows through EP2 prostaglandin E2 receptor-mediated activation of protein kinase A.