JTP-103237
Based on 1 publication(s) in Google Scholar
JTP-103237 is a MGAT2 inhibitor (IC50: 0.019 μM and 6.423 μM for hMGAT2 and hMGAT3 respectively). JTP-103237 modulates fat absorption, decreases plasma glucose levels and prevents diet-induced obesity.
For research use only. We do not sell to patients.
- CAS No.: 1883864-16-1
- Formula: C24H29F3N6O
- Molecular Weight:474.52
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications Citing Use of MedChemExpress (MCE) JTP-103237
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Biological Activity
Description
Chemical Information
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CAS No. 1883864-16-1
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Molecular Weight 474.52
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Formula C24H29F3N6O
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SMILES
FC(F)(F)OC1=CC=C(C2=NN=C3CN(C4=NC(C(C)(C)C)=CC(C(C)(C)C)=N4)CCN32)C=C1
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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.
Publications (1)
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Journal Impact Factor
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Most Recent
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Mol Ther
A CRISPR-based genome-wide loss-of-function screen defines a role of host metabolism in regulating hepatitis B virus infection. [Abstract]2025 Dec 1:S1525-0016(25)01019-6. PMID: 41332134
Protocols
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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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)