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Formula | C24H25NO4.HCl |
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Molecular Weight | 427.92 | CAS No. | 3717-88-2 | ||||
Solubility (25°C)* | In vitro | Water | 10 mg/mL (23.36 mM) | ||||
DMSO | 3 mg/mL (7.01 mM) | ||||||
Ethanol | Insoluble | ||||||
In vivo (Add solvents to the product individually and in order) |
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* <1 mg/ml means slightly soluble or insoluble. * 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. * Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.) |
Description | Flavoxate (NSC-114649) is a muscarinic AChR antagonist with IC50 of 12.2 μM. | ||
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Targets |
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In vitro | Flavoxate displaces [3H]nitrendipine on the Ca2+ channels binding sites with IC50 of 254 μM. [1] Flavoxate (>10 μM) suppresses carbachol-induced contractions in isolated rat detrusor strips with pD value of 4.55. Flavoxate (>10 μM) suppresses Ca2+-induced contractions in isolated rat detrusor strips with pIC50 value of 4.92. [2] Flavoxate (0.01 μM −10 μM) inhibits CAMP formation in a concentration-dependent manner in membranes from the rat striatum and cerebral cortex, an action which is completely abolished by pretreating the membranes with pertussis toxin (PTX). [3] Flavoxate causes a concentration-dependent reduction of the K+-induced contraction of human urinary bladder. Flavoxate inhibits the peak amplitude of voltage-dependent nifedipine-sensitive inward Ba2+ currents in a voltage- and concentration-dependent manner with Ki value of 10 μM in human detrusor myocytes. [4] Flavoxate inhibits voltage-dependent nifedipine-sensitive inward Ba2+ currents in human detrusor myocytes at both 30 degrees C (Ki = 5.1 mM) and 37 degrees C (Ki = 4.6 mM). [5] | ||
In vivo | Flavoxate (10mg/kg) suppresses both the an initial, rapidly rising phasic contraction (phase 1) and the tonic contraction (phase 2) contractions to the same extent in rats. Flavoxate (10mg/kg) abolishes the bladder contractions without causing any change in the amplitude of the contractions in rats. Flavoxate (3 mg/kg) abolishes the efferent neural activity and the associated bladder contractions for about 10 minutes without changing the baseline vesical pressure in rats. ICV-injected (50 to 200 μg/rat) or IT-injected (100 to 200 μg/rat) Flavoxate abolishes rhythmic bladder contractions during and after injection for five to 15 minutes in a dose-dependent manner in rats. [2] Flavoxate (3 mg/kg, i.v.) abolishes rhythmic bladder contractions and the maximal intervals of voiding contractions is 7.20 min. [3] |
Animal Study: |
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