8-bromo-cyclic adp-ribose

Cyclic ADP-ribose (cADP-ribose) is a calcium mobilizing nucleotide that is biosynthesized from NAD+ by cADP-ribose synthases, including CD38. cADP-Ribose appears to activate calcium channels in intracellular membranes, which in turn activate ryanodine receptors. 8-bromo-cADP-Ribose is a stable, cell-permeable analog that blocks calcium release evoked by cADP-ribose in sea urchin egg homogenates with an IC50 value of 1.7 μM. It is commonly used to investigate intracellular signaling through cADP-ribose in isolated cells and tissues.

8-Br-cADPR is an effective antagonist of cADPR. It helps mitigate kidney damage and reduces the expression of caspase-3 and TRPM2.

8-Br-7-CH-cADPR disodium (7-Deaza-8-bromo-cADPR) is a potent antagonist of cADPR. It partially inhibits calcium increase induced by sTIR dimerization and significantly reduces axonal degeneration induced by paclitaxel.

8-Br-cADPR (8-Bromo-Cyclic ADP-Ribose) sodium salt is an antagonist of cyclic adenosine diphosphate (ADP)-ribose (cADPR) and the TRPM2 ion channel. It can alleviate kidney injury and reduce the expression of caspase-3 and TRPM2.

8-Br-7-CH-cADPR (7-Deaza-8-bromo-cADPR) is an effective antagonist of cADPR. It can partially inhibit the calcium elevation induced by sTIR dimerization. Moreover, 8-Br-7-CH-cADPR significantly reduces axonal degeneration triggered by paclitaxel.

8-Bromo NAD+ serves as a prodrug for the cyclic ADP-ribose (cADPR) inhibitor, 8-bromo cADPR, undergoing conversion to its active form by the enzyme CD38. At a concentration of 1 mM, it effectively inhibits the rise in intracellular calcium levels and chemotaxis triggered by N-formyl-Met-Leu-Phe (fMLP) in mouse bone marrow-derived neutrophils. Furthermore, when applied at 100 µM, this compound reduces LPS-induced nitrite production and decreases the secretion of TNF-α and IL-2 in mouse primary microglial cells.