8-Br-cADPR sodium salt
Based on 1 Customer Validation
8-Br-cADPR (8-Bromo-Cyclic ADP-Ribose) sodium salt, a cyclic adenosine diphosphate (ADP)-ribose (cADPR) antagonist, is a TRPM2 ion channel antagonist. 8-Br-cADPR sodium salt reduces renal damage and the expression of caspase-3 and TRPM2.
For research use only. We do not sell to patients.
- Purity : 97%
- Formula: C15H18BrN5Na2O13P2
- Molecular Weight:664.16
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Storage:
-80°C
Biological Activity
Description
Chemical Information
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Appearance Solid
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Molecular Weight 664.16
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Formula C15H18BrN5Na2O13P2
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SMILES
O[C@H]1[C@@H](O)[C@H](N2C(Br)=NC3=C2N=CN([C@H]4[C@H](O)[C@H](O)[C@@H](COP(O5)(O[Na])=O)O4)C3=N)O[C@@H]1COP5(O[Na])=O
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Synonyms
8-Bromo-Cyclic ADP-Ribose sodium salt
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Shipping
Shipping with dry ice.
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Storage
-80°C
Protocols
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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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Two-electrode voltage clamp in Xenopus oocytes
Two-electrode voltage clamp measures whole-oocyte membrane current from Xenopus oocytes expressing exogenous ion channels, receptors, or transporters; one intracellular microelectrode senses membrane voltage, and the second injects current so the amplifier can hold the membrane at command voltages while recording the compensating current as the functional readout. The method is suited to Xenopus oocytes because their large size supports microinjection and intracellular electrode impalement, but the large membrane area can limit voltage-clamp speed and accuracy, especially for large or fast currents.
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
Purity & Documentation
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Data Sheet (273 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)