oxidoreductase enzyme

EPI-589, a quinone derivative and oxidoreductase enzyme inhibitor, is considered safe and well tolerated, showing promise for the treatment of amyotrophic lateral sclerosis (ALS).

1,4-D-Gulonolactone (D-Gulonic acid γ-lactone) (also known as reduced ascorbic acid, RAA) is the substrate of the enzyme L-gulono-1,4-lactone oxidoreductase (EC 1.1.3.8), which catalyzes the last step of the biosynthesis of L-ascorbic acid (vitamin C) in plants and animals. The enzyme L-Gulono-1,4-lactone oxidase is missing in scurvy-prone, vitamin C-deficient animals, such as humans. 1,4-D-Gulonolactone is present in human blood and has been used as one of the markers to compare changes in exercise-induced oxidative stress.

2,5-Furandicarboxylic acid (Dehydromucic Acid) is a normal urinary metabolite in humans. 2,5-Furandicarboxylic acid is also a microbial metabolite, a product of the oxidation of hydroxymethylfurfural (HMF) by the enzyme furfural/HMF oxidoreductase which is found in the bacterium Cupriavidus basilensis.

VPC162134 is an antibacterial agent that inhibits H. pylori, C. jejuni, MRSA, and S. epidermidis with minimum inhibitory concentrations (MIC) of 2.9, 17.5, 93.3, and 93.3 μM, respectively. Additionally, VPC162134 acts as an inhibitor of the enzyme pyruvate ferredoxin oxidoreductase (PFOR).

CB1954(Tretazicar (NSC-115829)), an anticancer prodrug, is activated by NAD(P)H quinone oxidoreductase 2. It is converted in the presence of the enzyme NQO2 and co-substrate caricotamide ( EP-0152R) (EP) into a potent cytotoxic bifunctional alkylating agent.

Caricotamide is a synthetic co-substrate that activates the human endogenous enzyme NRH:quinone oxidoreductase 2 (NQO2) with potential chemoadjuvant activity. When caricotamide is administered simultaneously with the prodrug tretazicar, NQO2 converts tretazicar to the bifunctional alkylating agent dinitrobenzamide, which is capable of forming a high degree of DNA interstrand cross-links, resulting in the inhibition of DNA replication and the induction of apoptosis. NQO2 has been found to be over-expressed in cancers such as hepatocellular carcinoma (HCC), colorectal and ovarian cancers.

L-Lactate dehydrogenase (LAD) is an oxidoreductase enzyme in the anaerobic metabolic pathway and the gluconeogenic pathway, and is found in a wide range of tissues in the body.

Glucose dehydrogenase (GDH) is an oxidoreductase enzyme that facilitates the oxidation of β-D-glucose into β-D-glucono-1,5-lactone, while concurrently reducing cofactor NADP+ to NADPH, and to a lesser degree, NAD+ to NADH. It can utilize both NAD+ and NADP+ as cofactors and serves in the regeneration of NADH and NADPH [1] [2].

Fructosyl-peptide oxidase (FPOX-CE) (Fructosyl-peptide: oxygen oxidoreductase) is an enzyme that catalyzes the oxidation of glycosylated peptides. It exhibits high activity towards small glycosylated peptides; however, it does not show detectable activity with the glycosylated hexapeptide standard fVHLTPE (used in HbA1c measurement). Fructosyl-peptide oxidase (FPOX-CE) is utilized in research for diabetes monitoring.

Pronqodine A is a quinone isolated from Streptomyces, known for its enzyme inhibitory and anti-inflammatory properties. It targets NAD(P)H:quinone acceptor oxidoreductase 1 (NQO1; IC50 = 131.5 nM). In SW 982 human synovial sarcoma cells, it suppresses bradykinin-induced production of prostaglandin E2 (PGE2), 6-keto PGF1α, and PGD2, with IC50 values of 9, 19, and 7 nM, respectively, and it also promotes the generation of reactive oxygen species (ROS) in these cells.

Sorbitol dehydrogenase is a type of oxidoreductase enzyme. Sorbitol dehydrogenase can be used as a marker for liver damage in pharmaceuticals.