cadpr

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.

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 an endogenous metabolite of NAD+ that mobilizes the release of stored Ca2+ in the endoplasmic reticulum via ryanodine receptors in various cell types.[1],[2],[3],[4],[5] This second messenger is generated via the cADP-ribose synthases CD38 and CD157.[6],[5],[7] cADP-Ribose may also trigger the cell surface Ca2+ influx channel TRPM2 in a temperature-dependent manner.[8] In vitro, cADP-ribose modulates Ca2+ signaling in rat and mouse cardiomyocytes treated with isoproterenol , and treatment with this metabolite at 100 μM under heat stress conditions induces the release of oxytocin from the mouse hypothalamus.[9],[4]

Dehydronitrosonisoldipine is an inhibitor of sterile α and TIR motif-containing 1 and can be used in studies about neurodegenerative disorders. Dehydronitrosonisoldipine inhibits axon degenration and the Vincristine-activated cADPR production in neurons.

Sulfo-ara-F-NMN is an analogue of nicotinamide mononucleotide (NMN) with cellular permeability. Sulfo-ara-F-NMN was selective to activate SARM1 and inhibited CD38 with an IC50 of about 10 μM. Activation by Sulfo-ara-F-NMN to Z-48 or NMN, which has a higher cyclase activity, causes conformational changes in SARM1, resulting in cADPR production, NAD depletion, and non-apoptotic cell death.

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.

Erzotabart, an IgG1-kappa monoclonal antibody targeting CD38 (ADP-ribosyl cyclase 1, cyclic ADP-ribose hydrolase 1, cADPr hydrolase 1, cADPR1) in Homo sapiens, exhibits antineoplastic activity [1].

Isoquinoline, 5-iodo- is a potent and selective inhibitor of SARM1(IC50 = 75 nM) by preventing axonal degeneration and by allowing functional recovery of a metastable pool of damaged, but viable, axons.

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].