Gymnopusin
Gymnopusin is an L-type voltage-dependent calcium channel blocker and vasorelaxant. Gymnopusin inhibits KCl- and Norepinephrine-induced contractility as well as CaCl2-induced contractions. Gymnopusin induces endothelium-independent relaxation involving the opening of ATP-sensitive and calcium-activated potassium channels. Gymnopusin disrupts membranes through tonoplast lysis, leading to electrolyte leakage, chlorophyll loss, and photobleaching in duckweed. Gymnopusin inhibits radicle elongation in Amaranthus hypochondriacus seedlings and exhibits phytotoxicity against duckweed. Gymnopusin shows moderate cytotoxicity against mammalian cell lines. Gymnopusin can be used for research on hypertension.
For research use only. We do not sell to patients.
- CAS No.: 113476-61-2
- Formula: C17H16O5
- Molecular Weight:300.31
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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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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Biological Activity
Description
In Vitro
Gymnopusin induces relaxation of rat aortic rings pre-contracted with Norepinephrine (NE) (HY-13715) in a concentration-dependent and endothelium-independent manner, with an EC50 of 63 μM in endothelium-intact rings[1].
Gymnopusin induces relaxation of endothelium-denuded rat aortic rings pre-contracted with KCl (80 mM), with an EC50 of 119 μM[1].
In endothelium-denuded rat aortic rings, the vasodilatory mechanism of Gymnopusin involves the opening of K+ channels[1].
Gymnopusin (49-63 μM; 15 min) inhibits NE-induced contraction in endothelium-denuded rat aortic rings in a non-parallel manner[1].
Gymnopusin (11-63 μM; 15 min) inhibits CaCl2-induced contraction in endothelium-denuded rat aortic rings, indicating Ca2+ entry blocking activity[1].
Gymnopusin (11-63 μM; 15 min) blocks L-type voltage-gated Ca2+ channels in endothelium-denuded rat aortic rings[1].
Gymnopusin (10-1000 μg/mL) inhibits radicle elongation in Amaranthus hypochondriacus seedlings with an IC50 of 330 μM[2].
Gymnopusin (25-200 μM; 72 h) causes electrolyte leakage, growth inhibition, and chlorophyll reduction in Lemna pausicostata cultures[2].
Gymnopusin (100 μM; 12-72 h) causes membrane rupture in Lemna pausicostata frond tissue, and transmission electron microscopy reveals tonoplast rupture, organelle release, and liposomes[2].
Gymnopusin (100 μM; 72 h) causes root cap loss, increased vacuolization, and the appearance of large starch grains within the chloroplast stroma in root tissues of Lemna pausicostata[2].
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. 113476-61-2
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Molecular Weight 300.31
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Formula C17H16O5
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SMILES
OC(C=CC1=C2C(OC)=C(OC)C(O)=CC2=C3)=CC1=C3OC
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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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Mammalian live/dead viability and cytotoxicity staining
Live/dead viability and cytotoxicity staining assays are based on the simultaneous detection of intracellular esterase activity in metabolically active (viable) cells and membrane integrity loss in non-viable cells. In commonly used dual-staining approaches, membrane-permeant fluorogenic substrates are converted by intracellular esterases into fluorescent products in live cells, while impermeant DNA-binding dyes selectively enter cells with compromised plasma membranes and label nucleic acids in dead or dying cells, enabling discrimination between viable and non-viable populations by fluorescence microscopy or flow cytometry.
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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.
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Cell Viability Determination by MTT Colorimetric Assay
The following protocol uses the MTT colorimetric assay as a classic literature-established method for assessing cell viability/metabolic activity in cultured mammalian cells. MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] is reduced by metabolically active cells to a colored formazan product; the amount of formazan is quantified spectrophotometrically and provides an indirect measure of metabolically active viable cells. Importantly, MTT reduction reflects cellular oxidoreductase/metabolic activity rather than an absolute direct count of living cells, so changes in cellular metabolism can alter the signal independently of cell number.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Gymnopusin Related Classifications
HY-187605 Related Classifications
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Keywords
- Gymnopusin
- 113476-61-2
- Calcium Channel
- L-type voltage-dependent calcium channel blocker
- radicle elongation
- calcium-activated potassium channel opening
- ATP-sensitive
- rat aortic rings
- vasorelaxant
- Amaranthus hypochondriacus
- endothelium-independent relaxation
- Lemna pausicostata
- tonoplast lysis
- Inhibitor
- inhibitor
- inhibit