Commendamide
Commendamide is a GPCR G2A/GPR132 agonist (EC50: 11.8 μM). Commendamide can be used for research of autoimmunity and atherosclerosis.
For research use only. We do not sell to patients.
- CAS No.: 193825-78-4
- Formula: C18H35NO4
- Molecular Weight:329.47
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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
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HY-120965
N-Palmitoyl Taurine -
HY-125920
Lauroylsarcosine sodiumBiochemical Assay Reagent -
HY-120968
Arachidoyl ethanolamideEster Product -
HY-120964
N-Stearoyl Taurine -
HY-119723
Myristoyl ethanolamideN-acylserinol Compound -
HY-134055
Arachidonoyl-N,N-dimethyl amide -
HY-W751418
N-Nervonoyl taurineFAAH Substrate -
HY-W721596
Pentadecanoyl ethanolamideEndogenous Lipid Amide -
HY-145475
Nervonoyl ethanolamideEndocannabinoid -
HY-165082
Tricosanoyl ethanolamideEndocannabinoid -
HY-115358
Lignoceroyl Ethanolamide -
HY-139272
Eicosapentaenoyl 1-propanol-2-amideEPA Derivative
Biological Activity
Description
IC50 & Target
EC50: 11.8 μM (GPR132)[1]
Chemical Information
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CAS No. 193825-78-4
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Molecular Weight 329.47
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Formula C18H35NO4
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SMILES
O=C(CNC(CC(CCCCCCCCCCCCC)O)=O)O
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Structure Classification
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Initial Source
culture broth from the commensal bacterium Bacteroides vulgatus
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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 Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Commendamide Related Classifications
HY-119494 Related Classifications
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