产品
编 号：F101514
分子式：C34H40N2O18
分子量：764.68
分子式：C34H40N2O18
分子量：764.68
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
询价
询价
1mg
询价
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5mg
询价
询价
10mg
询价
询价
50mg
询价
询价
结构图
CAS No: 126150-97-8
产品详情
生物活性：
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.
体外研究：
BAPTA-AM inhibits neuronal Ca2+-activated K+ channel currents, and up-regulates the decreased cardiac sodium current (INa) density by chelating intracellular Ca2+. 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.
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.
体外研究：
BAPTA-AM inhibits neuronal Ca2+-activated K+ channel currents, and up-regulates the decreased cardiac sodium current (INa) density by chelating intracellular Ca2+. 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.
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