S-4048
S-4048 is a glucose-6-phosphate translocase modulator and hypoglycemic agent. S-4048 is taken up by hepatocytes via OATP-1 and is rapidly eliminated via the hepatobiliary system in rats. S-4048 blocks glucose-6-phosphate translocase, prevents glucose-6-phosphate from entering the endoplasmic reticulum, and thereby interferes with the glucose-6-phosphatase system (i.e., the final step of hepatic gluconeogenesis and glycogenolysis) to regulate hepatic glucose production. S-4048 completely inhibits glucose production from pyruvate in GLUT2-deficient hepatocytes without affecting the release of cytoplasmic glucose. S-4048 effectively reduces blood glucose levels in rats and has been used in studies related to type 2 diabetes.
For research use only. We do not sell to patients.
- CAS No.: 173534-37-7
- Formula: C32H30ClN3O7
- Molecular Weight:604.05
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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
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
IC50：9.4 nM for rat microsomes.
In Vitro
S-4048 (10 μM; 30-60 min) does not inhibit the release of cytosolic glucose from GLUT2-/- mouse hepatocytes, indicating this minor glucose release pathway does not require glucose re-entry into the endoplasmic reticulum via glucose-6-phosphate translocase[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
S-4048 (10 mg/kg; i.v. bolus injection) undergoes rapid hepatobiliary elimination in male Wistar rats, with 57% of the 10 mg/kg i.v. bolus dose excreted as parent compound in bile within 30 minutes, driving a high plasma clearance[2].
S-4048 (10-50 mg/kg; i.v. bolus injection) exhibits a short blood glucose lowering effect and comparable hepatobiliary elimination in male mrp-2 deficient GY/TR3 rats relative to Wistar rats[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Wistar (male, 280-360 g, starved for 24 hours prior to experiments)[2]
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Dosage:50 mg/kg (blood glucose reduction); 30 mg/kg/h (sustained blood glucose reduction)
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Administration:i.v. bolus injection; i.v. infusion
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Result:Reduced blood glucose to maximum at 45 minutes, with levels returning to control values within 60 minutes after 50 mg/kg i.v. bolus injection.
Stabilized blood glucose levels at approximately 50% of the control group level after 60 minutes during constant 30 mg/kg/h i.v. infusion.
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Animal Model:Wistar (male, 280-360 g, starved for 24 hours prior to experiments)[2]
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Dosage:10 mg/kg
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Administration:i.v. bolus injection
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Result:Recovered 57% of the total administered dose as parent compound in bile within the first 30 minutes after administration.
Reached initial plasma concentrations of approximately 14 μmol/l, with a plasma clearance of about 80 mL/min/kg and an estimated half-life of about 10 minutes.
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Animal Model:GY/TR3 (male, 280-360 g, mrp-2 deficient mutant Wistar strain, starved for 24 hours prior to experiments)[2]
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Dosage:50 mg/kg (blood glucose study); 10 mg/kg (hepatobiliary elimination study)
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Administration:i.v. bolus injection
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Result:Lowered blood glucose with effect lasting as short as in Wistar rats, with levels returning to control values within 60-90 minutes after 50 mg/kg i.v. bolus injection.
Exhibited hepatobiliary elimination profile similar to that in Wistar rats after 10 mg/kg i.v. bolus injection.
Chemical Information
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CAS No. 173534-37-7
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Molecular Weight 604.05
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Formula C32H30ClN3O7
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SMILES
O=C([C@]1(OC[C@H]2[C@@H](C3=CC=C(Cl)C=C3)C2)C[C@@H](O)[C@@H](O)[C@H](OC(/C=C(N4C=NC5=NC=CC=C54)/C6=CC=CC=C6)=O)C1)O
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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.
Protocols
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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
S-4048 Related Classifications
HY-16443 Related Classifications
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