2. Metabolic Enzyme/Protease Membrane Transporter/Ion Channel
  3. Xanthine Oxidase BCRP GLUT
  4. Xanthine oxidase-IN-23

Xanthine oxidase-IN-23 (Compound BPF) is an orally active, reversible, mixed-type Xanthine oxidase inhibitor with an IC50 of 3.33 μM. Xanthine oxidase-IN-23 directly binds to XOD in a reversible mixed-type manner to inhibit its catalytic activity. Xanthine oxidase-IN-23 upregulates ABCG2 and downregulates GLUT9 to promote renal urate excretion. Xanthine oxidase-IN-23 reduces serum urate levels and improves renal function in hyperuricemic mice. Xanthine oxidase-IN-23 can be used in the research of hyperuricemia.

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Xanthine oxidase-IN-23

Xanthine oxidase-IN-23 Chemical Structure

CAS No. : 3055112-52-9

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Xanthine oxidase-IN-23 Related Antibodies

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Description

Xanthine oxidase-IN-23 (Compound BPF) is an orally active, reversible, mixed-type Xanthine oxidase inhibitor with an IC50 of 3.33 μM. Xanthine oxidase-IN-23 directly binds to XOD in a reversible mixed-type manner to inhibit its catalytic activity. Xanthine oxidase-IN-23 upregulates ABCG2 and downregulates GLUT9 to promote renal urate excretion. Xanthine oxidase-IN-23 reduces serum urate levels and improves renal function in hyperuricemic mice. Xanthine oxidase-IN-23 can be used in the research of hyperuricemia[1].

IC50 & Target[1]

GLUT9

 

In Vitro

Xanthine oxidase-IN-23 (15 min) potently inhibits purified xanthine oxidase via a reversible mixed-type inhibition mode, with an IC50 of 3.33 μM[1].
Xanthine oxidase-IN-23 (0.5-8 μM) exhibits potent DPPH free radical scavenging activity, with a scavenging rate of over 50% at 2 μM[1].

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

Xanthine oxidase-IN-23 Related Antibodies
In Vivo

Xanthine oxidase-IN-23 (100-200 mg/kg; p.o.) dose-dependently reduces serum uric acid levels in hyperuricemic mice by inhibiting hepatic XOD activity and modulating renal uric acid transporters, while also protecting against hyperuricemia-induced renal damage without causing liver injury[1].

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

Animal Model: Kunming mice (male, 5 weeks old, 39.4 g)[1]
Dosage: 100 mg/kg; 200 mg/kg
Administration: p.o.; single dose
Result: Significantly reduced serum uric acid (SUA) levels compared to the hyperuricemia model group.
Significantly reduced hepatic uric acid levels and hepatic xanthine oxidase (XOD) activity compared to the model group (200 mg/kg dose).
Completely reversed the downregulation of renal uric acid secretion transporter ABCG2 while significantly downregulating renal uric acid reabsorption transporter GLUT9 (200 mg/kg dose).
Significantly restored elevated serum creatinine (CRE) levels to near normal and mitigated hyperuricemia-induced mild renal tubular dilation and eosinophilic material accumulation.
Increased urinary uric acid levels at early time points after modeling compared to the model group (200 mg/kg dose).
Caused no significant changes in hepatic index, serum alanine aminotransferase (ALT), or aspartate aminotransferase (AST) levels, indicating no liver injury.
Molecular Weight

456.08

Formula

C17H12Br2O5
CAS No.
SMILES

O=C(/C=C/C1=CC(O)=C(O)C=C1Br)/C=C/C2=CC(O)=C(O)C=C2Br
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Purity & Documentation
References
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Xanthine oxidase-IN-23 Related Classifications

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    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Xanthine oxidase-IN-233055112-52-9Xanthine OxidaseBCRPGLUTXOBreast cancer resistance proteinABCG2Glucose transporterrenal functionuric acidGLUT9molybdenum centeramino acid residueshyperuricemic micehyperuricemiaxanthine oxidaseDPPH free radicalInhibitorinhibitorinhibit

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