GSK3395879
GSK3395879 is a TRPV4 antagonist that acts on hTRPV4 with an IC50 of 1 nM. GSK3395879 blocks agonist-induced TRPV4-mediated Ca2+ mobilization. GSK3395879 inhibits rat pulmonary edema induced by the TRPV4 agonist GSK1016790A (HY-19608). GSK3395879 can be used in research related to heart failure.
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- CAS No.: 2215852-91-6
- 화학식: C20H15F4N3O5S
- 분자량:485.41
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
제품 설명
IC50 & Target
[1]|
hTRPV4 1 nM (IC50) |
In Vitro
GSK3395879 is a highly potent hTRPV4 antagonist with an IC50 of 1 nM[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Sprague-Dawley rats (Male)[1]
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Dosage:0.03, 0.08, and 0.23 mg/kg (i.v. bolus loading dose); 0.6, 1.7, and 5.1 μg/kg/min (continuous i.v. infusion)
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Administration:i.v. bolus followed by continuous i.v. infusion; 60 min
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Result:Inhibited the GSK1016790A-induced decrease in MAP and increase in LW/BW ratio in a dose-dependent manner.
Achieved full inhibition of the GSK1016790A-induced decrease in MAP and increase in LW/BW at an infusion dose of 5.1 μg/kg/min.
Chemical Information
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CAS No. 2215852-91-6
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분자량 485.41
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화학식 C20H15F4N3O5S
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SMILES
FC1=C(C#N)C=CC(O[C@@H]2[C@@](CO)(O)CN(S(C3=C(C#N)C=C(C(F)(F)F)C=C3)(=O)=O)C2)=C1
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocol
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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 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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Ca2+ Staining Technique
Ca2+ staining is an experimental technique that utilizes specific fluorescent probes (such as Fluo-4 AM, Fura-2, etc.) to qualitatively or quantitatively detect dynamic changes in intracellular Ca2+ concentrations; this is achieved by monitoring the changes in fluorescent signals generated when these probes bind to free intracellular calcium ions. The underlying principle relies primarily on the presence of chelating groups within the probe's molecular structure that possess high affinity for calcium ions.
순도&문서
References
[1]. Brnardic EJ, et al. Discovery of Pyrrolidine Sulfonamides as Selective and Orally Bioavailable Antagonists of Transient Receptor Potential Vanilloid-4 (TRPV4). Journal of medicinal chemistry. 2018 Nov 08;61(21):9738-9755. [Content Brief]
[2]. Nilsson M, et al. TRPV4: A Promising Therapeutic Target Ion Channel─Discovery of Ultrapotent Selective Antagonists. Journal of medicinal chemistry. 2026 Jul 23;69(14):16926-16948. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)