cadpr

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-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.

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 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 diammonium (cADPR diammonium) serves as a potent calcium mobilization second messenger, synthesized from NAD+ by ADP-ribosyl cyclase. It primarily enhances cytosolic calcium levels by triggering release from the endoplasmic reticulum via Ryanodine receptors, and by facilitating extracellular influx through TRPM2 channels.

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-cADPR is an effective antagonist of cADPR. It helps mitigate kidney damage and reduces 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].

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.

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.

trans-Ned 19 is a nicotinic acid adenine dinucleotide phosphate (NAADP) antagonist and two-pore channel (TPC) blocker. It binds with high affinity to the NAADP receptor to inhibit NAADP-dependent lysosomal/endolysosomal calcium release without affecting IP3 or cADPR-mediated calcium signaling pathways. Functionally, trans-Ned 19 inhibits glucose-induced calcium oscillations in pancreatic islets and low histamine concentration-induced endothelium-dependent vasodilation, and reduces Ebola virus infection of host cells. In immunomodulation, NAADP signaling blockade by trans-Ned 19 promotes the conversion of mouse Th17 cells to regulatory T cells (Tregs) and shows protective effects in intestinal inflammation models.

8-MA-NAD+ (sodium) (8-Methylamino-NAD+ (sodium)) is a derivative of the signaling molecule and enzyme cofactor NAD+. It is utilized for screening analog-sensitive gatekeeper mutations in poly (ADP-ribose) polymerase 1 (PARP1) and for synthesizing cyclic ADP-ribose (cADPR) derivatives.

Erzotabart is an IgG1-kappa monoclonal antibody that targets human CD38 (also known as ADP-ribosyl cyclase 1 or cyclic ADP-ribose hydrolase 1) and displays pronounced antineoplastic activity. Erzotabart acts by modulating CD38-mediated signaling pathways involved in tumor cell metabolism, proliferation, and immune evasion, making it a significant investigational candidate in oncology research.

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.

8-PIP-NAD+ (sodium) (8-Piperidino-NAD+ (sodium)) is a derivative of the signaling molecule and enzyme cofactor NAD+. It is utilized for the detection of Poly(ADP-ribose) Polymerase (PARP) target proteins. Additionally, 8-PIP-NAD+ (sodium) serves as a synthetic intermediate for cyclic ADP-ribose (cADPR) derivatives.