HD202A
HD202A is an orally active, selective dual inhibitor of MNK1/MNK2 (with IC50 values of 6.09 nM and 8.06 nM, and Kd values of 1.913 μM and 5.244 μM, respectively) that inhibits the MNK-eIF4E signaling pathway. By downregulating perilipin 2 and SCD1, while upregulating adipose triglyceride lipase and PPARγ coactivator 1α, HD202A enhances mitochondrial fatty acid oxidation and redox homeostasis. HD202A effectively suppresses body weight gain, hepatic lipid accumulation and elevation of serum lipids, significantly improves glucose tolerance and insulin sensitivity of the organism, and ameliorates inflammatory features. With these comprehensive pharmacological activities, HD202A exhibits great application potential in studies of metabolic dysfunction-associated steatotic liver disease.
For research use only. We do not sell to patients.
- CAS No.: 2930131-74-9
- Formula: C25H24N6OS
- Molecular Weight:456.56
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
|
MNK1 6.09 nM (IC50) |
MNK2 8.06 nM (IC50) |
PPARγ1 |
eIF4E |
MNK1 1.913 μM (Kd) |
MNK2 5.244 μM (Kd) |
HD202A (compound 26) (0.1-1 μM) dose-dependently inhibits MNK-mediated eIF4E phosphorylation in A549 cells[1].
HD202A (1 μM) reduces lipid droplet accumulation and downregulates Plin2 in differentiated 3T3-L1 adipocytes without causing cytotoxicity[1].
HD202A (1 μM; 24-36 h) reduces lipid accumulation, restores lipid homeostasis, and improves mitochondrial function in PA-induced HepG2 cells; at 25 μM, it inhibits HepG2 cell proliferation[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:HepG2 cells
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Concentration:25 μM; with or without 400 μM Palmitate
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Incubation Time:24-36 h
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Result:Inhibited HepG2 cell proliferation by ~40%.
HD202A (25-75 mg/kg; p.o.; single dose) exhibits in vivo MNK inhibitory activity in white adipose tissue, liver, and skeletal muscle of mice when measured 24 hours postdose[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6J (male, 20 weeks old, mean body weight ~48 g, HFD-induced MASLD)[1]
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Dosage:12.5 mg/kg; 25 mg/kg; 50 mg/kg
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Administration:p.o.; daily; 11 weeks
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Result:Attenuated HFD-induced body weight gain dose-dependently without altering food intake.
Reduced fat mass and increased lean mass.
Decreased liver, epididymal fat, and (at 50 mg/kg only) subcutaneous fat indices.
Improved glucose homeostasis dose-dependently, with faster glucose clearance and reduced AUC in ITT and OGTT at 50 mg/kg.
Reduced fasting glucose, serum TG, TC, LDL-C, NEFA, ALT, AST, and TNF-α levels across relevant doses.
Reduced hepatic triglyceride content and macrovesicular steatosis dose-dependently.
Decreased hepatic iNOS H-scores and increased hepatic CD163 H-scores (without changing F4/80 levels) at 50 mg/kg.
Suppressed hepatic P-eIF4E levels.
Downregulated SCD1 and Plin2 expression.
Upregulated ATGL and PGC-1α expression.
Chemical Information
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CAS No. 2930131-74-9
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Molecular Weight 456.56
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Formula C25H24N6OS
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SMILES
O=C(N1CCC(N(C)C)CC1)C2=CC=C(C3=NN4C(S3)=NC=C4C5=CC=C(C#N)C=C5)C=C2
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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)
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