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.
Biological Activity
Description
IC50 & Target
[1]|
Angiotensin II Type 1 1.4 nM (Ki) |
In Vitro
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. .
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 (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)