PTP1B-IN-20
PTP1B-IN-20 is a selective inhibitor of protein tyrosine phosphatase 1B (PTP1B; IC50=1.05 μM) over the highly homologous T-cell protein tyrosine phosphatase (TCPTP; IC50=78.0 μM), which is a key target for type 2 diabetes inhibition.
For research use only. We do not sell to patients.
- CAS No.: 3001295-81-1
- Formula: C26H28O15
- Molecular Weight:580.49
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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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: 1.05 μM (PTP1B); 78.0 μM (TCPTP)[1]
In Vitro
PTP1B-IN-20 (compound 4) (0-100 μM; 15 min; 37 °C) with 5,6-dihydroxyl groups is more potent than the positive control Na3VO4 (IC50= 2.94 μM)[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 3001295-81-1
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Molecular Weight 580.49
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Formula C26H28O15
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SMILES
OC1=C(C2=C(C(C3=C(C2=O)C=C(C(C)=C3O)O[C@H]4[C@H](O)[C@H]([C@@H]([C@H](O4)CO[C@@H]5OC[C@@H](O)[C@H](O)[C@H]5O)O)O)=O)C=C1)O
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Structure Classification
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Initial Source
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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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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)
PTP1B-IN-20 Related Classifications
HY-N10648 Related Classifications
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