AT1R-agonist-1
AT1R-agonist-1 is an angiotensin II type 1 receptor (AT1R) agonist with a Ki value of 1.4 nM. AT1R-agonist-1 exhibits low Gαq activity, retains β-arrestin recruitment function, and accesses the deep allosteric pocket inside AT1R via its flexible side chain. AT1R-agonist-1 possesses positive inotropic effects (enhancing cardiac contractile function) and causes almost no increase in blood pressure. AT1R-agonist-1 can be used for research on conditions such as refractory cardiogenic shock.
For research use only. We do not sell to patients.
- CAS No.: 3124030-35-6
- Formula: C57H77N13O13
- Molecular Weight:1152.30
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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
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
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Angiotensin II Type 1 1.4 nM (Ki) |
AT1R-agonist-1 (Compound 12) (10 μM; 10 min) acts as a highly weak partial agonist of Gαq signaling in AT1R-expressing HEK293 cells, with an EC50 > 10,000 nM and 11% relative efficacy to AngII[1].
AT1R-agonist-1 (dose-response concentrations, 10 μM; 10 min) potently recruits β-arrestin2 to AT1R in HEK293 cells, with an EC50 of 2.5 nM and 89% relative efficacy to AngII[1].
AT1R-agonist-1 (dose-response concentrations, 10 μM; 10 min) acts as a partial agonist of PKC signaling in AT1R-expressing HEK293 cells, with an EC50 of 4.8 nM and 51% relative efficacy to AngII[1].
AT1R-agonist-1 (dose-response concentrations, 10 μM; 3 min) acts as a partial agonist of Rho signaling in Gα12/13-knockout, AT1R-expressing HEK293 cells, with an EC50 of 21 nM and 47% relative efficacy to AngII[1].
AT1R-agonist-1 (10 μM; 1 min) shows negligible PKC activation in rat primary VSMCs, with an EC50 >10,000 nM and 13% relative efficacy to AngII[1].
AT1R-agonist-1 (10 μM; 1 min 30 s) shows negligible Rho activation in rat primary VSMCs, with an EC50 >10,000 nM and 12% relative efficacy to AngII[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Sprague-Dawley (male, 230-350 g, 7-9 weeks of age)[1]
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Dosage:0.96 and 9.6 nmol/kg/min
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Administration:i.v.; continuous infusion; 10 minutes
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Result:Induced negligible increases in mean arterial blood pressure, significantly increased left ventricular ejection fraction, and showed a positive area under the curve (AUC) for ejection fraction change relative to vehicle controls at 0.96 nmol/kg/min.
Caused only a marginal, transient increase in mean arterial blood pressure that returned to baseline within 10 minutes; increased left ventricular ejection fraction via a reduction in left ventricular end-systolic volume (with no change in end-diastolic volume), leading to a corresponding increase in stroke volume at 9.6 nmol/kg/min.
Was significantly reduced in inotropic response and abolished in mild pressor effect by pretreatment with losartan (3 mg/kg, i.v. 10 minutes before perfusion), confirming AT1R-dependent activity.
Chemical Information
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CAS No. 3124030-35-6
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Molecular Weight 1152.30
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Formula C57H77N13O13
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Sequence
Asp-Arg-Val-Tyr-Ile-His-Pro-{Tyr(Bzl)}
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Sequence Shortening
DRVYIHP-{Tyr(Bzl)}
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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.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
AT1R-agonist-1 Related Classifications
HY-P11847 Related Classifications
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