BAPTA-AM is a well-known membrane permeable Ca²⁺ chelator. BAPTA-AM inhibits hERG channels, hKv1.3 and hKv1.5 channels in HEK 293 cells with IC₅₀s of 1.3 μM, 1.45 μM and 1.23 μM, respectively^[1]. IC50 & Target: Ca²⁺ chelator^[1]
IC50: 1.3 μM (hERG channel, in HEK 293 cells), 1.45 μM (hKv1.3, in HEK 293 cells), 1.23 μM (hKv1.5, in HEK 293 cells)^[1] In Vitro: BAPTA-AM inhibits neuronal Ca²⁺-activated K⁺ channel currents, and up-regulates the decreased cardiac sodium current (INa) density by chelating intracellular Ca^2+[1].
BAPTA-AM (BAPTA/AM), an intracellular calcium chelator, induces delayed necrosis by lipoxygenase-mediated free radicals in mouse cortical cultures. BAPTA-AM prevents free radical-mediated toxicity promote apoptosis in non-neuronal cells and produce a beneficial effect in neuronal cells by protecting neurons from ischemic damage. In addition, it has been suggested that BAPTA-AM induces a late, but not early, increase of intracellular calcium in I-IL-60 neoplastic cells. Mixed cortical cell cultures (DIV 13-16) exposed to 10 μM BAPTA-AM for 24- or 48-hr show moderate (45-70%) neuronal injury as evaluated by increased LDH release into the bathing medium after 24-48-hr. Exposure of cortical cultures to 3-10 μM BAPTA-AM for 48-hr evoke dose-dependent neuronal damage^[2].