BAPTA-AMBAPTA-AM
MedChemExpress (MCE)
HY-100545
126150-97-8
99.23%
Powder -20°C 3 years 4°C 2 years In solvent -80°C 2 years -20°C 1 year
Room temperature in continental US
may vary elsewhere.
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.
BAPTA-AM inhibits neuronal Ca2+-activated K+ channel currents, and up-regulates the decreased cardiac sodium current (INa) density by chelating intracellular Ca2+[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].
Neuronal injury is quantitatively estimated by measuring lactate dehydrogenase (LDH) released from damaged cells into the bathing medium 24- or 48-hr after the 10 μM BAPTA/AM treatment. The morphological findings are confirmed by staining with neuron-specific enolase (NSE) antibody and tryphan blue[1].
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 Ca2+[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]. MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. 0 --> BAPTA-AM Related Antibodies
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[1]. Tang Q, et al. The membrane permeable calcium chelator BAPTA-AM directly blocks human ether a-go-go-related gene potassium channels stably expressed in HEK 293 cells. Biochem Pharmacol. 2007 Dec 3
74(11):1596-607. [Content Brief]
[2]. Wie MB, et al. BAPTA/AM, an intracellular calcium chelator, induces delayed necrosis by lipoxygenase-mediated free radicals in mouse cortical cultures. Prog Neuropsychopharmacol Biol Psychiatry. 2001 Nov
25(8):1641-59. [Content Brief]