TMA-IN-1
TMA-IN-1 (Compound 7) is a highly potent, orally active and selective TMA Lyase inhibitor with an estimated Kd value of 3.2 μM. TMA-IN-1 reduces Trimethylamine oxide (TMAO) levels. TMA-IN-1 can be used for the research of heart failure.
For research use only. We do not sell to patients.
- CAS No.: 160172-20-3
- Formula: C9H13NO
- Molecular Weight:151.21
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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
All Endogenous Metabolite Isoforms
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Biological Activity
Description
IC50 & Target
[1]|
Microbial Metabolite |
In Vitro
TMA-IN-1 (100 μM) binds to recombinant TMA lyase, with an estimated Kd value of 3.2 μM[1].
TMA-IN-1 (5 μM) shows low binding rate to rodent plasma proteins (the unbound fraction is 85% in mice and 90% in rats)[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
TMA-IN-1 (10-80 mg/kg; p.o.; single dose) significantly reduces circulating TMAO levels in fecal microbiota-transplanted mice[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
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CAS No. 160172-20-3
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Molecular Weight 151.21
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Formula C9H13NO
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SMILES
O[C@]1(C#C)CN2CCC1CC2
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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)
TMA-IN-1 Related Classifications
HY-W589560 Related Classifications
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