cadp-ribose

Cyclic ADP-Ribose (ammonium salt) (cADPR) is an endogenous NAD⁺ metabolite that triggers Ca²⁺ release from ER stores via ryanodine receptors and is synthesized by CD38 and CD157. It may also activate TRPM2 in a temperature-dependent manner. Showing potential in research related in inflammation and immunology.

Cyclic ADP-ribose (cADPR) is an effective calcium mobilization second messenger synthesized from NAD+ by ADP-ribosyl cyclase. It mainly increases cytosolic calcium through Ryanodine receptor-mediated endoplasmic reticulum release and extracellular influx via the opening of TRPM2 channels.

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-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.

Cyclic ADP-ribose ammonium (cADPR ammonium) is a potent calcium mobilization second messenger synthesized from NAD+ by ADP-ribosyl cyclase. It raises cytosolic calcium levels through Ryanodine receptor-mediated release from the endoplasmic reticulum and facilitates extracellular influx via TRPM2 channels [1][2][3].

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