mouse cd38

CD38 inhibitor 1 is a potent CD38 inhibitor that is effective against human CD38 (IC50 value is 7.3 nM) and mouse CD38 (IC50 value is 1.9 nM).

Anti-Mouse CD38 Antibody (NIMR5) is an IgG2a, κ inhibitor antibody derived from rats, designed to target and inhibit mouse CD38.

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]

MK-0159 is an orally available, highly potent CD38 inhibitor with myocardial injury protection for the study of cardiac ischemia and reperfusion injury.

CD38 Inhibitor 3 (compound 1), with an IC50 of 11 nM, is a potent agent that enhances mitochondrial biogenesis, diminishes lactate levels, and augments both NAD+ content and Nrf2 expression. In a Pus1 -/- mouse model of mitochondrial myopathy, it also elevates muscle function and bolstering exercise capacity [1].

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.