SSTR5/TGR5-modulator-1
SSTR5/TGR5-modulator-1 is an orally active and dual-target small molecule, balanced in vitro activity at human TGR5 and human SSTR5. SSTR5/TGR5-modulator-1 activates human TGR5 to promote cAMP accumulation. SSTR5/TGR5-modulator-1 blocks human SSTR5 to inhibit agonist-induced calcium mobilization. SSTR5/TGR5-modulator-1 improves glucose tolerance in mice. SSTR5/TGR5-modulator-1 alleviates gallbladder filling in mice at pharmacologically relevant doses. SSTR5/TGR5-modulator-1 has suboptimal physicochemical and metabolic properties.SSTR5/TGR5-modulator-1 can be used for the research of type 2 diabetes mellitus.
For research use only. We do not sell to patients.
- CAS No.: 3069267-46-2
- Formula: C39H45N5O7S
- Molecular Weight:727.87
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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
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SSTR5 4.37 nM (IC50) |
In Vitro
SSTR5/TGR5-modulator-1 (Compound 19) (30 min (cAMP assay); 10 min (calcium assay pre-incubation)) potently activates human TGR5 (EC50=5.91 nM) and antagonizes human SSTR5 (IC50=4.37 nM) in vitro[1].
SSTR5/TGR5-modulator-1 (30 min (cAMP assay); 10 min (calcium assay pre-incubation)) exhibits comparable cross-species potency, activating mouse TGR5 (EC50=3.40-5.30 nM) and antagonizing mouse SSTR5 (IC50=2.97-19.6 nM) in vitro[1].
SSTR5/TGR5-modulator-1 (1 μM; up to 60 min) shows rapid metabolic turnover in in vitro, with a T1/2 of 2.2 min in human liver microsomes and 2.8 min in mouse liver microsomes[1].
SSTR5/TGR5-modulator-1 (30-100 μM; 24 h) is non-toxic to primary hepatocytes at 30 μM but induces significant cytotoxicity at 100 μM after 24 h incubation[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:primary hepatocytes
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Concentration:30 μM; 100 μM
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Incubation Time:24 h
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Result:Induced significant cytotoxicity at 100 μM.
Showed no significant toxicity observed at 30 μM.
Parmacokinetics
In Vivo
SSTR5/TGR5-modulator-1 (100 mg/kg; p.o.; single dose) attenuates TGR5-mediated gallbladder filling in male C57BL/6 mice compared to the TGR5 agonist monotherapy control[1].
SSTR5/TGR5-modulator-1 (100 mg/kg; p.o.; single dose) enhances the GLP-1-insulin axis in male C57BL/6 mice, supporting its glucose-lowering mechanism of action[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6 (8-week-old male, ~25 g)[1]
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Dosage:10 mg/kg; 30 mg/kg; 100 mg/kg
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Administration:p.o.; single dose
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Result:Demonstrated dose-dependent suppression of blood glucose levels.
Elicited a greater glucose-lowering effect at 100 mg/kg than positive control compound 2 at 50 mg/kg.
Significantly reduced the area under the plasma glucose curve (AUC0-90 min) at all tested doses compared to vehicle control.
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Animal Model:C57BL/6 (8-week-old male)[1]
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Dosage:100 mg/kg
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Administration:p.o.; single dose
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Result:Reduced gallbladder size compared to both vehicle control subgroup without egg yolk stimulation and compound 2 (50 mg/kg)-treated group, indicating a weaker effect on gallbladder filling.
Chemical Information
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CAS No. 3069267-46-2
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Molecular Weight 727.87
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Formula C39H45N5O7S
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SMILES
O=C([C@H]1N(CSC1)CC2=C(C=C(C(OC)=C2)CN3CCC4(CC3)OC(N(C4)C5=CC=C(C=C5)C(O)=O)=O)OC)N6CCN(C7=C6C=CC=C7)C8CC8
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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)
SSTR5/TGR5-modulator-1 Related Classifications
HY-182905 Related Classifications
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