Lycopodine

Lycopodine, a pharmacologically important bioactive component derived from Lycopodium clavatumspores, triggers apoptosis by modulating 5-lipoxygenase, and depolarizing mitochondrial membrane potential in refractory prostate cancer cells without modulating p53 activity^[1]. Lycopodine inhibits proliferation of HeLa cells through induction of apoptosis via caspase-3 activation^[2]. IC50 & Target: 5-lipoxygenase^[1] and caspase-3^[2] In Vitro: Lycopodine (5.22-78.3 μg/mL; 12 hours) has 50% viability at 57.62±0.086 μg/mL and 51.46±1.43 μg/mL for PC3 and LnCaP, respectively^[1].
Treated with Lycopodine (74-222 mM; 12 hours), the apoptotic index is with respect to the gradual increase in doses for the PC3 and LnCaP cells^[1].
Lycopodine (74-222 mM; 12 hours) induces cell cycle arrest at G0/G1 phase in PC3 and LnCaP cells^[1].
Lycopodine (0-200 µg/mL; 48 hours) shows cytotoxicity to HeLa cells in a dose and time dependent manner. However, Lycopodine shows minimal cytotoxic effects in normal peripheral blood mononuclear cells (PBMC) even at the highest dose (200 µg/mL)^[2].
Lycopodine (100, 200 µg/mL; 24 hours) increases level of Bax and decreases the mitochondrial cytochrome c. This is followed by an increase in expression of cytochrome c in cytosolic fraction. Lycopodine also cleaves the caspase-3 in the total cell lysate, while the expression of Bcl-2 is down regulated^[2].