cadpr

DSRM-3716 是选择性的SARM1 NADase 抑制剂，IC50为 75 nM，相较于其他 NAD+加工酶、受体和转运蛋白具有选择性。DSRM-3716显示出强大的轴突保护作用。

Cyclic ADP-ribose (cADPR) is an effective calcium mobilization second messenger, which is synthesized from NAD + by ADP-ribosyl cyclase. Cyclic ADP-ribose mainly increases cytosolic calcium through Ryanodine receptor-mediated endoplasmic reticulum release

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]

8-Br-7-CH-cADPR (7-Deaza-8-bromo-cADPR) 是一种cADPR有效拮抗剂。该化合物能部分抑制sTIR二聚化引发的钙离子升高。此外，8-Br-7-CH-cADPR 对于降低紫杉醇诱导的轴突变性也有显著效果。

8-Br-cADPR为cADPR的高效拮抗剂,能有效减轻肾损伤并降低caspase-3与TRPM2的表达水平.

Cyclic ADP-ribose ammonium (cADPR ammonium) is a powerful calcium mobilization second messenger synthesized from NAD+ by an ADP-ribosyl cyclase. It primarily raises cytosolic calcium levels through Ryanodine receptor-mediated release from the endoplasmic reticulum, while also facilitating extracellular influx through the opening of 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 是一种不育α和含TIR 图案1的抑制剂，可用于有关神经退行性疾病的研究。Dehydronitrosonisoldipine 抑制轴突退化和长春碱激活的神经元中cADPR 的产生。

Sulfo-ara-F-NMN 是一种具有细胞渗透性的烟酰胺单核苷酸 (NMN) 的类似物。Sulfo-ara-F-NMN 对激活 SARM1具有选择性，对 CD38具有抑制作用， IC50 约为 10 μM。Sulfo-ara-F-NMN 对具有更高的环化酶活性 CZ-48或 NMN 的激活会引起 SARM1的构象变化，导致 cADPR 的产生、NAD 的消耗和非凋亡细胞死亡。

Erzotabart为一IgG1-kappa型人源单克隆抗体，针对CD38(ADP-核糖环化酶 1，环 ADP-核糖水解酶 1，cADPr 水解酶 1，cADPR1)。该化合物展现出抗肿瘤活性。

8-bromo NAD+ 作为循环ADP-核糖（cADPR）抑制剂8-bromo cADPR的前药形式，通过CD38转化为8-bromo-cADPR。在1 mM浓度下，8-bromo NAD+ 阻止由N-formyl-Met-Leu-Phe (fMLP) 在分离的小鼠骨髓衍生的中性粒细胞内引起的细胞内钙水平增加和趋化作用。同时，在100 µM浓度下使用，减少了小鼠原代小胶质细胞中LPS诱导的亚硝酸盐产生以及TNF-α和IL-2的分泌。