Epinastine Hydrochloride

Epinastine hydrochloride inhibited histamine release from isolated human skin mast cells induced by both immunologic (anti-IgE) and non-immunologic (calcium ionophore A23187) stimuli at concentrations greater than 0.1 nmol/L. The drug also significantly suppressed IgE-mediated leukotriene C4 production from human basophils at concentrations above 0.1 nmol/L. However, epinastine did not inhibit histamine release from basophils induced by various secretagogues including anti-IgE, concanavalin A, interleukin-3, interleukin-5, A23187, ionomycin, phorbol ester, C5a, or formyl-methionyl-leucyl-phenylalanine. The compound showed no effect on A23187-induced eosinophil cationic protein release from eosinophils and did not inhibit isolated protein kinase C from rat brain. Epinastine also did not affect substance P-induced activation or stem cell factor priming of mast cells. These results confirmed that epinastine hydrochloride exerts antiallergic effects through stabilization of skin mast cells and suppression of leukotriene production.

Fig. 1 Inhibition of histamine release from human skin mast cells by Epinastine. (Amon U.; et al. 2000)

Epinastine hydrochloride-releasing soft contact lenses were developed by soaking preformed lenses in drug solution for treatment of allergic conjunctivitis. Among lenses with different ionicities, anionic lenses demonstrated the maximum and most linear epinastine release profile in vitro. The amount of drug released was directly proportional to the concentration of the loading solution. In a guinea pig allergic conjunctivitis model, the epinastine-releasing anionic contact lens demonstrated prolonged drug release and significantly greater suppression of vascular permeability compared to epinastine eye drops at 12 hours after treatment. This contact lens-based delivery system offers a sustained-release alternative to conventional eye drops.

Fig. 2 An epinastine hydrochloride-releasing soft contact lens (EH-SCL) for guinea pigs. (Minami T.; et al. 2019)