NADPH tetrasodium salt functions as an important cofactor in a variety of metabolic and biosynthetic pathways. NADPH tetrasodium salt plays a vital role in the biosynthesis of agents, chiral alcohols, fatty acids and biopolymers, while also being required for lipid biosynthesis, biomass formation, and cell replication. The demand for NADPH tetrasodium salt is particularly high in proliferating cancer cells, where it acts as a cofactor for the synthesis of nucleotides, proteins, and fatty acids. NADPH tetrasodium salt is also essential for the neutralization of the dangerously high levels of reactive oxygen species (ROS) generated by increased metabolic activity. NADPH tetrasodium salt is an endogenous inhibitor of ferroptosis^[1][2][3][4].

NADPH tetrasodium salt de novo synthesis is catalyzed by NAD kinases (NADKs), which catalyze the phosphorylation of NAD⁺ to form NADP⁺. NADPH tetrasodium salt is mainly involved in catabolic reactions, whereas NADPH tetrasodium salt is primarily involved in cellular antioxidative effects and anabolic reactions. NADPH tetrasodium salt is used by glutathione reductase (GR) to reduce oxidized glutathione (GSSG) to GSH^[1].
The regeneration rate of NADPH tetrasodium salt is often the rate-limiting step for the over-production of desired chemicals, while maintaining robust cellular growth^[2].
NADPH tetrasodium salt homeostasis is regulated by varied signaling pathways and several metabolic enzymes that undergo adaptive alteration in cancer cells. The metabolic reprogramming of NADPH tetrasodium salt renders cancer cells both highly dependent on this metabolic network for antioxidant capacity and more susceptible to oxidative stress^[3].
NADPH tetrasodium salt is an essential intracellular reductant needed to eliminate lipid hydroperoxides. Indeed, NADPH tetrasodium salt levels are a biomarker of ferroptosis sensitivity across many cancer cell lines^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

833.35

C₂₁H₂₆N₇Na₄O₁₇P₃

2646-71-1

Solid

White to light yellow

O[C@H]1[C@@H](O)[C@H](N2C=C(C(N)=O)CC=C2)O[C@@H]1COP(OP(OC[C@@H]3[C@@H](O)[C@@H](OP(O[Na])(O[Na])=O)[C@H](N(C4=NC=N5)C=NC4=C5N)O3)(O[Na])=O)(O[Na])=O

Room temperature in continental US; may vary elsewhere.

-20°C, stored under nitrogen, away from moisture

*The compound is unstable in solutions, freshly prepared is recommended.

* Please refer to the solubility information to select the appropriate solvent. The compound is unstable in solutions, freshly prepared is recommended.

* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.

• [1]. Tedeschi PM, et al. NAD+ Kinase as a Therapeutic Target in Cancer. Clin Cancer Res. 2016;22(21):5189-5195.  [Content Brief]

  [2]. Ng CY, F et al. Rational design of a synthetic Entner-Doudoroff pathway for improved and controllable NADPH regeneration. Metab Eng. 2015;29:86-96.  [Content Brief]

  [3]. Ju HQ, Lin JF, et al. NADPH homeostasis in cancer: functions, mechanisms and therapeutic implications. Signal Transduct Target Ther. 2020;5(1):231. Published 2020 Oct 7.  [Content Brief]

  [4]. Stockwell BR, et al. Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease. Cell. 2017;171(2):273-285.  [Content Brief]