HYJ-2
HYJ-2 is a URAT1 inhibitor and urate-lowering agent. HYJ-2 inhibits URAT1-mediated urate transport and interacts with key residues within the URAT1 binding pocket. HYJ-2 reduces serum urate levels in hyperuricemic mice without inducing liver or kidney injury. HYJ-2 shows low cytotoxicity to hepatocytes and renal cells. HYJ-2 does not significantly induce hepatocyte apoptosis or mitochondrial dysfunction. HYJ-2 can be used in studies related to hyperuricemia and gout.
For research use only. We do not sell to patients.
- Formula: C14H9Cl2N3O2
- Molecular Weight:322.15
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
HYJ-2 (10-10000 nM) potently inhibits URAT1-mediated urate uptake in HEK293 cells overexpressing URAT1, with an IC50 of 368 nM[1].
HYJ-2 exhibits low cytotoxicity against HEK293T cells, with an IC50 of 353.1 μM[1].
HYJ-2 exhibits low cytotoxicity against HepG2 cells, with an IC50 value of 287.3 μM[1].
HYJ-2 (100 μM; 24 h) does not significantly promote apoptosis in HepG2 cells[1].
HYJ-2 (100 μM; 24 h) exerts weak effects on mitochondrial function in HepG2 cells, with 73.7% of cells retaining high mitochondrial membrane potential[1].
HYJ-2 exhibits excellent metabolic stability in human liver microsomes, with a half-life of 990 min, and 97.3% of the parent drug remains after 60 min of incubation[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:human hepatocellular carcinoma HepG2 cells
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Concentration:100 μM
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Incubation Time:24 h
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Result:Induced an apoptotic rate of 5.6% in HepG2 cells, which was comparable to the control group.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Kunming mice with Hyperuricemia (male, 19-21 g)[1]
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Dosage:2 mg/kg
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Administration:19 days
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Result:Reduced mean serum uric acid levels from 1042.3 μM to 683.3 μM, corresponding to a 36.7% decrease rate.
Alleviated renal pathological injury associated with long-term hyperuricemia, with better preservation of renal tubular architecture and a more pronounced reduction in interstitial inflammatory cell infiltration than the reference drug group.
Showed no apparent hepatic pathological abnormalities.
Chemical Information
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Molecular Weight 322.15
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Formula C14H9Cl2N3O2
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SMILES
CC1=CC=CC2=C(C(C3=CC(Cl)=C(O)C(Cl)=C3)=O)N=NN21
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)