Concanavalin A is a natural product, a phytoalexin (glycan-binding protein). Concanavalin A has antitumor activity and can also induce acute liver injury.

Huh7 cells:20 μg/mL, HIV-1:2.2–2.6 μg/mL (EC50), CT-26 cells:10 μg/mL, MCF-7 cells:15 μg/mL, HSV:98 nM, ML-1 cells:10 μg/mL, HepG2 cells:5 μg/mL

METHODS: Human hepatocellular carcinoma cells HuH-7 and Hep G2 were treated with Concanavalin A (1-40 µM) for 3-48 h, and the expression levels of target proteins were detected by Western Blot.
RESULTS: After Concanavalin A stimulation, LC3-II in both human hepatocellular carcinoma cell lines increased in a dose- and time-dependent manner. [1]
METHODS: HUVECs and EA.hy926 cells were treated with Concanavalin A (0.3-1 µg/mL) for 6-24 h. The pro-angiogenic activity was detected by Matrigel tube formation and ELISA assay.
RESULTS: Different concentrations of Concanavalin A, especially at 1 or 3 µg/mL, significantly promoted angiogenesis in HUVEC and Ea.hy926 cells. The total primary fragment length in HUVEC and Ea.hy926 cells was significantly higher in Concanavalin A-treated cells compared to the negative control. [2]

METHODS: To assay antitumor activity in vivo, Concanavalin A (10 mg/kg, intravenously) and ISO-1 (10 mg/kg, intraperitonealy) were administered to BALB/c mice bearing ML-1 liver tumor nodules twice every three days for 30 days.
RESULTS: Concanavalin A treatment significantly reduced the number and size of hepatic tumor nodules and, in the presence of ISO-1, the therapeutic effect of Concanavalin A was abolished. MIF does play an important role in Concanavalin A-induced autophagy and antitumor activity in vivo. [1]