| Size | Price | Stock | Qty |
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| 10mg |
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| 25mg |
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| 50mg |
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| 100mg |
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| 250mg |
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Purity: ≥98%
BAPTA-AM is a selective, membrane-permeable and intracellular calcium chelator. In the human leukemia cell lines HL-60 and U937, BAPTA/AM (10 μM) induced internucleosomal DNA cleavage and classic apoptotic morphology. Also, BAPTA/AM increased Ca2+ in intracellular and downregulated c-jun. In bovine chromaffin cells, APTA-AM (50 μM) rapidly and reversibly inhibited Ca2+-activated K+ (I(KCa)) and voltage-gated K+ (I(K)) by 50%. In HEK 293 cells, BAPTA-AM inhibited hERG (Kv11.1), hKv1.3 and hKv1.5 channels with IC50 values of 1.3, 1.45 and 1.23 μM respectively in a concentration dependent way.
| Targets |
Ca2+ chelator; hERG channel
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| ln Vitro |
By chelating intracellular Ca2+, BAPTA-AM upregulates the reduced cardiac sodium current (INa) density and inhibits neuronal Ca2+-activated K+ channel currents[1]. In mouse cortical cultures, lipoxygenase-mediated free radicals cause delayed necrosis, which is induced by the intracellular calcium chelator BAPTA-AM (BAPTA/AM). BAPTA-AM shields neurons from ischemia damage, preventing free radical-mediated toxicity and promoting death in non-neuronal cells while also having a positive effect on neuronal cells. Furthermore, it has been proposed that BAPTA-AM causes an increase in intracellular calcium in I-IL-60 neoplastic cells at a later time rather than an earlier one. Increased release of lactate dehydrogenase (LDH) into the bathing medium after 24 or 48 hours indicates a moderate (45-70%) neuronal damage in mixed cortical cell cultures (DIV 13-16) subjected to 10 μM BAPTA-AM. 48 hours of exposure to 3–10 μM BAPTA–AM causes dose-dependent neuronal damage in cortical cultures[2].
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| ln Vivo |
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| Enzyme Assay |
BAPTA-AM is a well-known membrane permeable Ca2+ chelator. The present study found that BAPTA-AM rapidly and reversibly suppressed human ether a-go-go-related gene (hERG or Kv11.1) K+ current, human Kv1.3 and human Kv1.5 channel currents stably expressed in HEK 293 cells, and the effects were not related to Ca2+ chelation. The externally applied BAPTA-AM inhibited hERG channels in a concentration-dependent manner (IC50: 1.3 μM). Blockade of hERG channels was dependent on channel opening, and tonic block was minimal. Steady-state activation V0.5 of hERG channels was negatively shifted by 8.5 mV (from −3.7 ± 2.8 of control to −12.2 ± 3.1 mV, P < 0.01), while inactivation V0.5 was negatively shifted by 6.1 mV (from −37.9 ± 2.0 mV of control to −44.0 ± 1.6 mV, P < 0.05) with application of 3 μM BAPTA-AM. The S6 mutant Y652A and the pore helix mutant S631A significantly attenuated blockade by BAPTA-AM at 10 μM causing profound blockade of wild-type hERG channels. In addition, BAPTA-AM inhibited hKv1.3 and hKv1.5 channels in a concentration-dependent manner (IC50: 1.45 and 1.23 μM, respectively), and the blockade of these two types of channels was also dependent on channel opening. Moreover, EGTA-AM was found to be an open channel blocker of hERG, hKv1.3, hKv1.5 channels, though its efficacy is weaker than that of BAPTA-AM. These results indicate that the membrane permeable Ca2+ chelator BAPTA-AM (also EGTA-AM) exerts an open channel blocking effect on hERG, hKv1.3 and hKv1.5 channels.[1]
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| Cell Assay |
1. Disruption of calcium homeostasis during neurodegenerative diseases is known to trigger apoptotic or necrotic death in neuronal cells. Recently, the authors reported that intracellular calcium restriction by NMDA receptor antagonists induces apoptosis in cortical cultures. To evaluate whether further restriction of intracellular free calcium can induce apoptosis or necrosis, we examined the neurotoxic characterization of BAPTA/AM, a permeable free calcium chelator, in mouse cortical cultures. 2. Exposure of mixed (glia and neuron) cortical cultures (DIV 13-16) to 3-10 microM BAPTA/AM (non-toxic concentration for glial cells) for 24-48 hr resulted in delayed and necrotic neuronal death. The necrotic findings included swelling and loss of mitochondria and endoplasmic reticulum (ER) with neuronal membrane rupture 24 hr after treatment with BAPTA/AM. Simultaneously, we observed a few TUNEL-positive cells in the neuronal subpopulation of the same cultures. 3. The neurotoxicity evoked by BAPTA/AM (10 microM) was significantly attenuated by the addition of 0.5 microM cycloheximide (a protein synthesis inhibitor), 10 microM actinomycin D (an RNA transcription inhibitor), a high extracellular potassium concentration (total 15 mM KCl), 100 microM t-ACPD (a metabotrophic agonist), 100 microM alpha-tocopherol (a free radical scavenger), 100 microM deferoxamine (a ferric ion chelator), 100 microM L-NAME (a nitric oxide synthase (NOS) inhibitor), 50 microM DNQX (a non-NMDA receptor blocker), and 3-30 microM esculetin (a lipoxygenase inhibitor). However, 0.3-3 mM ASA (a cyclooxygenase inhibitor), 100 ng/ml nerve growth factor (NGF), 10 microM MK-801 (a NMDA receptor antagonist), 20 microM zVAD-fmk (caspase inhibitor) and 50 U/ml catalase failed to inhibit the injury. 4. However, NGF and catalase blocked the neurotoxicity induced by BAPTA/AM in young neuronal cells (DIV 6). BAPTA/AM (10 microM) did not alter the expression of inducible nitric oxide synthase (iNOS) on glial cells. 5. These results suggest that the feature of neuronal death induced by BAPTA/AM exhibits predominantly delayed necrosis mediated by lipoxygenase-dependent free radicals.[2]
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| Animal Protocol |
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| References |
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| Additional Infomation |
2-[N-[2-(acetyloxymethoxy)-2-oxoethyl]-2-[2-[2-[bis[2-(acetyloxymethoxy)-2-oxoethyl]amino]phenoxy]ethoxy]anilino]acetic acid acetyloxymethyl ester is an alpha-amino acid ester.
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| Molecular Formula |
C34H40N2O18
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| Molecular Weight |
764.68
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| Exact Mass |
764.227
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| Elemental Analysis |
C, 53.40; H, 5.27; N, 3.66; O, 37.66
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| CAS # |
126150-97-8
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| Related CAS # |
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| PubChem CID |
2293
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| Appearance |
White to off-white solid powder
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| Density |
1.4±0.1 g/cm3
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| Boiling Point |
796.1±60.0 °C at 760 mmHg
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| Melting Point |
86-90°C
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| Flash Point |
435.3±32.9 °C
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| Vapour Pressure |
0.0±2.8 mmHg at 25°C
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| Index of Refraction |
1.551
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| LogP |
2.28
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| Hydrogen Bond Donor Count |
0
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| Hydrogen Bond Acceptor Count |
20
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| Rotatable Bond Count |
31
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| Heavy Atom Count |
54
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| Complexity |
1100
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| Defined Atom Stereocenter Count |
0
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| InChi Key |
YJIYWYAMZFVECX-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C34H40N2O18/c1-23(37)47-19-51-31(41)15-35(16-32(42)52-20-48-24(2)38)27-9-5-7-11-29(27)45-13-14-46-30-12-8-6-10-28(30)36(17-33(43)53-21-49-25(3)39)18-34(44)54-22-50-26(4)40/h5-12H,13-22H2,1-4H3
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| Chemical Name |
Acetyloxymethyl 2-[N-[2-(acetyloxymethoxy)-2-oxoethyl]-2-[2-[2-[bis[2-(acetyloxymethoxy)-2-oxoethyl]amino]phenoxy]ethoxy]anilino]acetate
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| Synonyms |
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
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| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (3.27 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: 2.5 mg/mL (3.27 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (3.27 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.3077 mL | 6.5387 mL | 13.0774 mL | |
| 5 mM | 0.2615 mL | 1.3077 mL | 2.6155 mL | |
| 10 mM | 0.1308 mL | 0.6539 mL | 1.3077 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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