Nitidine (chloride)

Nitidine chloride, a potential anti-malarial lead compound derived from Zanthoxylum nitidum (Roxb) DC, exerts potent anticancer activity through diverse pathways, including inducing apoptosis, inhibiting STAT3 signaling cascade, DNA topoisomerase 1 and 2A, ERK and c-Src/FAK associated signaling pathway, also has anti-inflammatory activity. Nitidine chloride inhibits LPS-induced inflammatory cytokines production via MAPK and NF-kB pathway^{[1][2][3][4][5]}. In Vitro:Nitidine chloride (0-32 μM, 24-48 h) inhibits the proliferation of A498 and 768-O cells^[1].
Nitidine chloride (8-16 μM, 24 h) induces apoptosis in A498 and 768-O cells^[1].
Nitidine chloride (0-16 μM, 48 h) induces apoptosis in A498 cells, causes cell cycle arrest, and inhibits the ERK pathway^[1].
Nitidine chloride (0-10 μM, 24 h) induces apoptosis in HSC3 and HSC4 cells, inducing apoptosis in OSCC cells through dephosphorylation of STAT3^[2]. In Vivo:Nitidine chloride (5 mg/kg, intraperitoneal injection, once daily, 5 weeks) inhibits tumor growth in mice and induces apoptosis in renal cancer cells in vivo^[1].
Nitidine chloride (0.375-10 mg/kg, intraperitoneal injection, once daily, 3 weeks) downregulates hypertrophy in mouse myocardium through AGT4B-mediated autophagy^[3].
Nitidine chloride (5-10 mg/kg, intraperitoneal injection, single dose) exerts anti-inflammatory effects in endotoxin-treated mice through Akt-mediated IL-10 production^[4].