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ABT-239 is a novel, highly efficacious, non-imidazole class of H3R antagonist and a transient receptor potential vanilloid type 1 (TRPV1) antagonist.

Perfusion of the TMN with ABT-239 (10 μM) increases histamine release from the TMN, NBM, and cortex, but not from the striatum or NAcc. TMN perfusion with ABT-239 activates c-Fos selectively in the NBM and cortex[4].

ABT-239 (3 mg/kg, i.p.) significantly delays onset of seizure, reduces behavioral seizures elicited by KA, and reduces in the incidence of head bobbing and forelimb clonus in mice. ABT-239 (1 mg/kg, i.p.) in conbination with sub-therapeutic dose of SVP (150 mg/kg, i.p.), significantly decreases the number of immobility, head bobbing and forelimb clonus, where as a higher dose combination of ABT-239 (3 mg/kg, i.p.) causes enhanced reduction in all the stages. ABT-239 (3 mg/kg, i.p.) and TDZD-8 (10 mg/kg, i.p.) have more powerful reduction in the number of pyknotic neurons in mice hippocampi. The high dose combination of ABT-239 and TDZD-8 produces the most pronounced increase in Bcl-2 expression as well as decrease in the level of Bax[1]. ABT-239 (3 mg/kg, i.p.) administration transforms a short-term learning event into a long-term remembered experience in WT but not in histamine-depleted mice[2]. Concomitant administration of either ABT-239 (1 and 3 mg/kg, i.p.) and nicotine (0.035 mg/kg, i.p.), or ABT-239 (0.1 mg/kg, i.p.) and nicotine (0.0175 mg/kg, i.p.) further increases nicotine-induced improvement in both memory acquisition and consolidation[3].

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