For research use only.
CAS No. 168626-94-6
Conivaptan HCl is an orally active, non-peptide, vasopressin V1A and V2 receptor antagonist, used in the treatment of euvolemic and hypervolemic hyponatremia.
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Select hit drugs from each class identified from the Selleck screen were assayed at 0.25X, 0.5X, and 1X MIC for their ability to prevent biofilm formation in vitro. Data were normalized to DMSO control. * p<0.05 (Student’s t-Test; two-tailed).
Antimicrob Agents Chemother, 2017, AAC.01674-17. Conivaptan HCl purchased from Selleck.
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|Description||Conivaptan HCl is an orally active, non-peptide, vasopressin V1A and V2 receptor antagonist, used in the treatment of euvolemic and hypervolemic hyponatremia.|
|In vivo||Conivaptan (0.03, 0.1 and 0.3 mg/kg i.v.) dose-dependently increases urine volume and reduces urine osmolality in both myocardial infarction and sham-operated rats. Conivaptan (0.3 mg/kg i.v.) significantly reduces right ventricular systolic pressure, left ventricular end-diastolic pressure, lung/body weight and right atrial pressure in myocardial infarction rats. Conivaptan (0.3 mg/kg i.v.) significantly increases dP/dt(max)/left ventricular pressure in myocardial infarction rats.  Conivaptan produces an acute increase in urine volume (UV), a reduction in osmolality (UOsm) and, at the end of the investigation, cirrhotic rats receiving the V(1a)/V(2)-AVP receptor antagonist does not show hyponatremia or hypoosmolality. Conivaptan also normalizes U(Na)V without affecting creatinine clearance and arterial pressure.  Conivaptan (0.01 to 0.1 mg/kg i.v.) exerts a dose-dependent diuretic effect in dogs without an increase in the urinary excretion of electrolytes, inhibits the pressor effect of exogenous vasopressin in a dose-dependent manner (0.003 to 0.1 mg/kg i.v.) and, at the highest dose (0.1 mg/kg i.v.), almost completely blocks vasoconstriction caused by exogenous vasopressin. Conivaptan (0.1 mg/kg i.v.) improves cardiac function, as evidenced by significant increases in left ventricular dP/dtmax, cardiac output and stroke volume, and reduces preload and afterload, as evidenced by significant decreases in left ventricular end-diastolic pressure and total peripheral vascular resistance in dogs with congestive heart failure. |
|In vitro||DMSO||107 mg/mL (199.98 mM)|
|Ethanol||7 mg/mL (13.08 mM)|
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
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|Step 1: Enter information below (Recommended: An additional animal making an allowance for loss during the experiment)|
|Dosage||mg/kg||Average weight of animals||g||Dosing volume per animal||ul||Number of animals|
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|% DMSO % % Tween 80 % ddH2O|
Working concentration： mg/ml；
Method for preparing DMSO master liquid: ： mg drug pre-dissolved in μL DMSO (Master liquid concentration mg/mL，)
Method for preparing in vivo formulation：Take DMSO master liquid, next addμL PEG300， mix and clarify, next addμL Tween 80，mix and clarify, next add μL ddH2O，mix and clarify.
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