NADPH tetrasodium salt (Synonyms: Nicotinamide adenine dinucleotide phosphate)

NADPH tetrasodium salt is a sodium salt form of reduced nicotinamide adenine dinucleotide phosphate (NADPH), which is an essential cofactor in cells and acts as an electron donor^[1]. NADPH is a reduced coenzyme II that participates in many biosynthetic metabolic pathways, such as fatty acid synthesis, cholesterol synthesis, oxalic acid cycle, etc.^[1]. NADPH tetrasodium salt is a metabolite produced in Escherichia coli (strain K12, MG 1655)^[2].

In vitro, NADPH tetrasodium salt (100µM) treated HUVEC and PIEC cells for 30 minutes, significantly increasing the O²⁻ production of both cells^[3]. Adding NADPH tetrasodium salt (100µM) to re-concentrated pulmonary artery homogenate significantly increased the activity of soluble guanylate cyclase (sGC), increasing the basal activity by 2.2±1.0 times^[4]. Treatment with NADPH tetrasodium salt (0-300µM) induces rodent β-cells and dose-dependently induces Ca²⁺-dependent exocytosis^[5].

In vivo, intravenous injection of NADPH tetrasodium salt (16 mg/kg) in male SD rats resulted in a significant increase in +dp/dt and a significant decrease in -dp/dt within 60 minutes after administration, which enhanced the cardiac function in rats ^[2]. Intravenous injection of NADPH tetrasodium salt (2.5 mg/kg) treated rat and mouse stroke models, significantly reducing cerebral infarction volume, improving neurological function, and increasing survival rate ^[6].

References:

[1]Qian K, Tang J, Ling Y J, et al. Exogenous NADPH exerts a positive inotropic effect and enhances energy metabolism via SIRT3 in pathological cardiac hypertrophy and heart failure[J]. EBioMedicine, 2023, 98.

[2]Chou H H, Marx C J, Sauer U. Transhydrogenase promotes the robustness and evolvability of E. coli deficient in NADPH production[J]. PLoS genetics, 2015, 11(2): e1005007.

[3] Li,J. Differential NADPH-versus NADH-dependent superoxide production by phagocyte-type endothelial cell NADPH oxidase[J].Cardiovascular Research, 2001, 52(3):477.

[4] Gupte S A, Rupawalla T, Phillibert D, et al. NADPH and heme redox modulate pulmonary artery relaxation and guanylate cyclase activation by NO[J]. Am J Physiol, 1999, 277:1124-32.

[5] Ivarsson R, Quintens R, Dejonghe S, et al. Redox control of exocytosis: regulatory role of NADPH, thioredoxin, and glutaredoxin[J]. Diabetes, 2005, 54(7): 2132-2142.

[6]Mei,Li,Zhi-Peng,et al.Reduced Nicotinamide Adenine Dinucleotide Phosphate, a Pentose Phosphate Pathway Product, Might Be a Novel Drug Candidate for Ischemic Stroke.[J].Stroke A Journal of Cerebral Circulation, 2016.