MDL-19744A
MDL-19744A is an orally active and selective α1-adrenergic receptor antagonist, with rat α1-adrenergic receptor IC50 of 8 nM. MDL-19744A increases renal blood flow, dose-related decreases mean arterial blood pressure, increases urinary sodium excretion, and mediates renal vasodilation. MDL-19744A can be used for the research of hypertension.
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- CAS No.: 97233-26-6
- 화학식: C21H25NO3S
- 분자량:371.49
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보관:
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
- Protocol
- 순도&문서
- References
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Help & FAQs
All Adrenergic Receptor Isoforms
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Biological Activity
제품 설명
IC50 & Target
[1]|
α1-adrenergic receptor |
In Vitro
MDL-19744A (Compound 1) potently and selectively inhibits α1-adrenergic receptor binding in rat cerebrocortex tissue, with an IC50 of 8 nM for α1 receptors[1].
MDL-19744A (30 min) potently antagonizes α1-adrenergic receptor-mediated vasoconstriction in isolated rabbit aortic strips, with a pA2 of 8.13[1].
MDL-19744A (3 μM) is inactive as a β-adrenergic receptor blocker in isolated guinea pig ventricles[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MDL-19744A (0.03-3 mg/kg; i.v.; single dose) produces decreases in mean arterial blood pressure in anesthetized normotensive dogs, with an ED15 for hypotension of 0.08 mg/kg and a maximal mean arterial blood pressure reduction of -47 mmHg at 1 mg/kg i.v[1].
MDL-19744A (0.01-1 mg/kg; i.v.; cumulative dose) produces dose-dependent increases in renal blood flow and increases in urinary sodium excretion in anesthetized normotensive dogs[1].
MDL-19744A (0.1-3 mg/kg; i.v.; single dose) selectively antagonizes α1-adrenergic receptors in pithed rats, shifting Phenylephrine (HY-B0769)-induced pressor responses at 0.1-1.0 mg/kg i.v. while only weakly affecting α2-mediated responses at 3.0 mg/kg i.v[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:spontaneously hypertensive rats (SHR) (conscious)[1]
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Dosage:30 mg/kg
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Administration:p.o.; single dose
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Result:Produced a maximal decrease in mean arterial blood pressure of -70 mmHg.
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Animal Model:normotensive dogs (anesthetized)[1]
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Dosage:0.01 mg/kg; 0.03 mg/kg; 0.1 mg/kg; 0.3 mg/kg; 1.0 mg/kg
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Administration:i.v.; cumulative dose
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Result:Produced a 9% increase in renal blood flow and a -5% change in mean arterial blood pressure at 0.01 mg/kg cumulative dose.
Produced a 17% increase in renal blood flow and a -9% change in mean arterial blood pressure at 0.03 mg/kg cumulative dose.
Produced a 27% increase in renal blood flow and a -15% change in mean arterial blood pressure at 0.1 mg/kg cumulative dose.
Produced a 34% increase in renal blood flow, a -23% change in mean arterial blood pressure, and increased urinary sodium excretion from a baseline of 42 to 104 µequiv/min at 0.3 mg/kg cumulative dose.
Produced a 42% increase in renal blood flow and a -32% change in mean arterial blood pressure at 1.0 mg/kg cumulative dose.
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Animal Model:rats[1]
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Dosage:0.1 mg/kg; 0.3 mg/kg; 1.0 mg/kg; 3 mg/kg
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Administration:i.v.; single dose
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Result:Shifted the Phenylephrine-induced diastolic blood pressure dose-response curve (DR2 = 0.07, 0.02 mg/kg) at doses of 0.1-1.0 mg/kg.
Weakly affected α2-mediated responses at 3.0 mg/kg i.v.
Chemical Information
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CAS No. 97233-26-6
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분자량 371.49
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화학식 C21H25NO3S
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SMILES
O=C1C2=C(SC(C)=C2)CC[C@H]1CN[C@@H]3[C@@H]([C@H](CC3)OC4=CC=CC=C4)O
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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.
순도&문서
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
MDL-19744A Related Classifications
HY-183954 Related Classifications
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