TJN 220
TJN 220 is a synthetic derivative of orally active tetrandrine (HY-13764). TJN 220 has a long-lasting and stable antihypertensive effect in various hypertension models. TJN 220 is suitable for controlling nighttime hypertension and does not cause reflex tachycardia. TJN 220 can be used for research on hypertension.
For research use only. We do not sell to patients.
- CAS No.: 118160-59-1
- Formula: C39H44N2O6
- Molecular Weight:636.78
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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
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| HepG2 | IC50 |
5.52 μM
Compound: 5a
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Antiproliferative activity against human HepG2 cells after 48 hrs by MTT assay
Antiproliferative activity against human HepG2 cells after 48 hrs by MTT assay
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[PMID: 28057423] |
| MCF7 | IC50 |
8.55 μM
Compound: 5a
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Antiproliferative activity against human MCF7 cells after 48 hrs by MTT assay
Antiproliferative activity against human MCF7 cells after 48 hrs by MTT assay
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[PMID: 28057423] |
Chemical Information
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CAS No. 118160-59-1
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Molecular Weight 636.78
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Formula C39H44N2O6
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SMILES
CCOC1=C2C3=C(C=C1OC)CCN(C)[C@@]3([H])CC4=CC=C(OC)C(OC5=CC=C(C[C@@]6([H])C7=CC(O2)=C(C=C7CCN6C)OC)C=C5)=C4
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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)
TJN 220 Related Classifications
HY-105515 Related Classifications
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