Chlorprothixene is an antagonist of multiple receptors including 5-HT2 (Ki = 3.4 nM), D1 (Ki = 18 nM), D2 (Ki = 18 nM), D3 (Ki = 4.56 nM), H1 (Ki = 3.75 nM), muscarinic acetylcholine receptors, α1-Adrenergic.
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Chlorprothixene (CPTX) is an antipsychotic drug of the thioxanthene class. Chlorprothixene exerts strong binding affinities to the dopamine and histamine receptors, such as D1, D2, D3, D5 and H1 with Ki values of 18 nM, 2.96 nM, 4.56 nM, 9 nM and 3.75 nM, respectively, but has little affinity to H3 (Ki >1000 nM)[1]. Chlorprothixene inhibited the proton currents in a concentration-dependent manner (IC50 = 1.7 μM). Chlorprothixene at 3 μM slightly shifted the activation voltage toward depolarization. Both the activation and the deactivation kinetics of the proton currents were slowed by chlorprothixene 1.2- and 3.5-fold, respectively. Thus, the inhibition of proton currents may be partly responsible for the antioxidant effects of thioxanthene antipsychotic drugs[3]. Chlorprothixene also shows high affinities for both rat 5-HT6 from stably transfected HEK-293 cells, and rat 5-HT7 receptors from transiently expressed COS-7 cells, with Ki values of 3 nM and 5.6 nM, respectively[4]. Administration of Chlorprothixene restores normal ceramide concentrations in murine bronchial epithelial cells, reduces inflammation in the lungs of mice with cystic fibrosis (CF) and prevents infection with Pseudomonas aeruginosa, by inhibiting acidsphingomyelinase (Asm) and not neutral sphingomyelinase (Nsm)[5].
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