xanthine oxidase-in-1

Xanthine oxidase-IN-1 is an effective inhibitor of xanthine oxidase with an IC50 value of 6.5 nM. It plays a central role in purine catabolism through the degradation of bioactive nucleotides facilitated by nucleic acid and nucleotide intermediates.

Xanthine Oxidase-IN-11, an analog of XO8, is an inhibitor of xanthine oxidase (XO) [1].

Xanthine oxidase-IN-12 (Compound 11), an inhibitor of xanthine oxidase (XO), has an IC50 value of 91 nM and exhibits antioxidant properties, also reducing intracellular reactive oxygen species (ROS) [1].

Xanthine oxidase-IN-16 is an effective orally active inhibitor of xanthine oxidase (XO), demonstrating significant therapeutic efficacy in rats with hyperuricemia and an IC50 of 102 nM.

Xanthine oxidase-IN-10 (XO8 analog) is an inhibitor of xanthine oxidase (XO) used in gout research.

Nicotinamide N-oxide (Nicotinamide 1-oxide) is recognized as an in vivo metabolite of nicotinamide which is a precurser of nicotinamide-adenine dinucleotide (NAD+) in animals. The enzyme that catalyzes the reduction of nicotinamide N-oxide to nicotinamide in the liver is xanthine oxidase.

CYPMPO is a free radical spin trap with excellent trapping capabilities toward hydroxyl and superoxide radicals in biological and chemical systems. Decay of the superoxide adduct of CYPMPO proceeds in an apparent first order fashion with half-lives of 15 and 51 minutes in a UV-illuminated hydrogen peroxide solution and a hypoxanthine/xanthine oxidase system, respectively. CYPMPO traps superoxide radicals generated by bovine neutrophils as effectively as DEPMPO.[1] The high melting point (126°C), low hygroscopic properties, and long shelf-life in aqueous solutions offer significant practical advantages for use of CYPMPO over DEPMPO and DMPO.

Xanthine oxidase-IN-7 (compound 1h) is a potent, orally active xanthine oxidase (XO) inhibitor with an IC50 of 0.36 μM, effectively reducing serum uric acid levels and showing potential for hyperuricemia and gout research [1].

Xanthine oxidase-IN-4 (compound 19a) is an orally active and potent xanthine oxidase (XO) inhibitor with an IC50 of 0.039 μM, suitable for research in hyperuricemia and gout. Xanthine oxidase-IN-4 demonstrates hypouricemic potency in potassium oxonate-induced hyperuricemia rats. [1].

Febuxostat (TEI 6720) sodium has the potential in gout and hyperuricemia research which is a potent, selective and non-purine inhibitor of xanthine oxidase (XO) with a Ki value of 0.6 nM [1] [2] [3].

Xanthine oxidase-IN-5, a powerful and orally active inhibitor of xanthine oxidase (XO), exhibits an IC50 value of 0.70 μM. It possesses favorable drug-like characteristics, with ligand efficiency (LE) and lipophilic ligand efficiency (LLE) values of 0.33 and 3.41, respectively. Moreover, Xanthine oxidase-IN-5 showcases significant hypouricemic effects in a hyperuricemic rat model [1].

XO COX LOX-IN-1 is a potent inhibitor of xanthine oxidase cyclooxygenase lipoxygenase XO COX LOX. XO COX LOX-IN-1 can be used in the study of inflammatory, cancer and metabolic diseases.

Febuxostat 67M-1 is an inhibitor of xanthine oxidase. It reduces uric acid production in the body and reduces the risk of gout or kidney stone formation.

Febuxostat 67M-4 is a derivative compound of Febuxostat 67M-1 which is an inhibitor of xanthine oxidase. It reduces uric acid production in the body and reduces the risk of gout or kidney stone formation.

Febuxostat 67M-2 is a derivative compound of Febuxostat 67M-1 which is an inhibitor of xanthine oxidase. It reduces uric acid production in the body and also used to reduce the risk of gout or kidney stone formation.

6-Methoxypurine-9-β-D-5'(R)-C-methylriboside, an analog of hypoxanthine—a purine base predominantly found in muscle tissue and a metabolite generated when purine oxidase acts on xanthine—displays anti-inflammatory properties and functions as a potential endogenous poly(ADP-ribose) polymerase (PARP) inhibitor. Its cytoprotective role is underscored by its ability to inhibit PARP activity, thus preventing peroxynitrite-induced mitochondrial depolarization and subsequent superoxide production. Furthermore, hypoxanthine serves as a biomarker for hypoxia [1] [2].

Xanthine oxidase-IN-8 (Icarisids J) (Compound 7) acts as an inhibitor of xanthine oxidase with an inhibitory concentration (IC50) of 29.71 μM [1].

Xanthine Oxidase-IN-9 (also known as Icarisids E or Compound 2) effectively inhibits xanthine oxidase (XOD) with an IC50 value of 31.81 μM [1].

NoxA1ds TFA is a potent and selective inhibitor of NADPH oxidase 1 (NOX1) with an inhibition concentration (IC50) of 20 nM, showing selectivity over NOX2, NOX4, NOX5, and xanthine oxidase. It effectively inhibits NOX1-derived O2- production in HT-29 human colon cancer cells and attenuates VEGF-induced migration of human pulmonary artery endothelial cells under hypoxic conditions in vitro.

URAT1&XO Inhibitor 1 (compound 29) serves as a dual inhibitor with IC50 values of approximately 10 μM for URAT1 and 1.01 μM for Xanthine Oxidase. It induces a hypouricemic effect in the potassium oxonate-induced hyperuricemic rat model and is utilized in research pertaining to hyperuricemia [1].

Compound BDEO (URAT1&XO inhibitor 2) serves as a dual-action inhibitor targeting both xanthine oxidase (XO) and URAT1, demonstrating an IC50 value of 3.3 μM for XO inhibition. It effectively impedes uric acid uptake in HEK293 cells with URAT1 expression, evidenced by a Ki of 0.145 μM. In hyperuricemic mice models, the compound has been shown to reduce serum urate levels and uric acid excretion, indicating potential utility for hyperuricemia research [1].

Potent and selective NADPH oxidase 1 (NOX1) inhibitor (IC50 = 20 nM). Exhibits selectivity for NOX1 over NOX2, NOX4, NOX5 and xanthine oxidase. Inhibits NOX1-derived O2- production in HT-29 human colon cancer cells. Attenuates VEGF-induced human pulmonary

NoxA1ds acetate is a potent and selective NADPH oxidase 1 (NOX1) inhibitor (IC50 : 20 nM). Exhibits selectivity for NOX1 over NOX2, NOX4, NOX5 and xanthine oxidase. Inhibits NOX1-derived O2- production in HT-29 human colon cancer cells. Attenuates VEGF-induced human pulmonary artery endothelial cell migration under hypoxic conditions in vitro.