Tropisetron

Tropisetron is an orally active 5-HT₃R antagonist (K_i = 5.3 nM) as well as being a potent and selective α7 nicotinic partial agonist (EC₅₀ = 1.3 μM). Tropisetron prevents phosphorylation and activation of the p38 MAPK. Tropisetron inhibits both IL-2 gene transcription and IL-2 synthesis in stimulated T cells. Tropisetron inhibits the binding to DNA and the transcriptional activity of NFAT and AP-1. Tropisetron is anti-inflammatory and antiemetic. Tropisetron has antitumor and neuroprotective effects. Tropisetron can be studied in research for diseases including hemorrhagic cystitis, chronic joint inflammation, lung cancer and chronic cerebral hypoperfusion^{[1][2][3][4][5][6]}. In Vitro:ropisetron (10-50 μg/mL; 72 h) inhibits T cell activation in human peripheral T cells^[2].
Tropisetron (10-50 μg/mL; 30 min) inhibits the activation of NFAT, AP-1, NF-κB and IL-2 production in Jurkat cells^[2].
Tropisetron (1-50 μg/mL; 4 h) decreases the phosphorylation level of p38 MAPK in human monocytes treated with LPS (HY-D1056)^[3]. In Vivo:Tropisetron (2.5-7.5mg /kg; Intraperitoneal injection; 5 days) has an improved effect in a rat model of hemorrhagic cystitis induced by cyclophosphamide (HY-17420)^[4].
Tropisetron (5-10 mg/kg; Intraperitoneal injection; 10-22 days) has antitumor effect in lung cancer mouse model^[5].
Tropisetron (1-5 mg/kg; Intraperitoneal injection; 35 days) improves the spatial memory impairment induced by chronic cerebral hypoperfusion in rat models^[6].