BAPTA-AM is a calcium chelator that is cell-permeable and selective, blocking hERG, hKv1.3, and hKv1.5 channels (IC50=1.3/1.45/1.23 μM). BAPTA-AM has a 105-fold higher affinity for Ca2+ than for Mg2+, and can be used for the role of calcium in cell signaling.

ERG channel (human, HEK293 cells):1.3 μM (IC50), Kv1.3 (human, HEK293 cells):1.45 μM (IC50), Kv1.5 (human, HEK293 cells):1.23 μM (IC50)

METHODS: Chondrocytes were treated with BAPTA-AM (10 μM) and FAC (100 μM) for 24 h. Intracellular ROS levels were measured using the Reactive Oxygen Species Assay kit.
RESULTS: FAC promoted ROS production and this effect was inhibited by the calcium chelator BAPTA-AM. [1]
METHODS: Rat fibroblast RAT2 and Xenopus cells were treated with BAPTA-AM (50 μM) for 1 h, and microtubule depolymerization was detected by Immunostaining.
RESULTS: BAPTA AM treatment for 30 min resulted in almost complete disassembly in most cells, and microtubules were uniformly depolymerized in cells within 60 min. [2]

METHODS: To investigate the effect on ethanol-induced locomotor activity, BAPTA-AM (0-10 mg/kg, Cremophor EL 1.25% (v/v) in distilled water) was injected intraperitoneally into Swiss (RjOrl) mice, followed by ethanol (0-4 g/kg) 30 min later.
RESULTS: Pretreatment with BAPTA-AM blocked the locomotor stimulus produced by ethanol without altering basal locomotion. On the contrary, BAPTA-AM reversed the ethanol-induced hypnosis. [3]
METHODS: To investigate the effect on LPS-induced blood-brain barrier leakage, BAPTA-AM (12 mg/kg, 0.01% pluronic acid in sterile saline) was injected intravenously into FVB mice, followed 30 min later by intraperitoneal injection of LPS (25 mg/kg).
RESULTS: BAPTA-AM reduced LPS-induced blood-brain barrier leakage. [4]