Flavoxate hydrochloride

Flavoxate hydrochloride (100 nM-30 μM) causes concentration-dependent relaxation of K⁺-precontracted human detrusor muscle strips, with an IC₅₀ of 2 μM^[1].
Flavoxate hydrochloride (10-30 μM; 5 minutes) inhibits voltage-dependent, nifedipine-sensitive Ba²⁺ currents (L-type Ca²⁺ channel currents) in freshly isolated human detrusor myocytes in a voltage- and concentration-dependent manner, with a K_i value of 10 μM at a holding potential of -60 mV and 56 μM at a holding potential of -90 mV^[1].
Flavoxate hydrochloride (1-30 μM; 22°C, 30°C, 37°C) inhibits voltage-dependent inward Ba²⁺ currents through L-type Ca²⁺ channels in human detrusor muscle cells in a concentration-dependent and temperature-sensitive manner, with enhanced efficacy at higher temperatures (K_i=10.3 μM at 22°C, K_i=5.1 μM at 30°C, K_i=4.6 μM at 37°C), and shifts the steady-state inactivation curve leftward at 30°C^[2].
Flavoxate hydrochloride (10^-8-10^-5 M; 15 min) concentration-dependently inhibits cAMP production in membrane preparations from rat striatum and cerebral cortex via pertussis toxin-sensitive G₁-coupled receptors; its inhibitory effect at 10^-6 M is completely reversed by combined treatment with any two of adenosine A₁, dopamine D₂, or adrenergic α₂ receptor antagonists^[3].
Flavoxate hydrochloride (10^-8-10^-4 M) binds to rat adenosine A₁, adrenergic α₂, dopamine D₂, and muscarinic M₂ receptors with K_i values in the micromolar to submicromolar range, but shows negligible affinity for many other neurotransmitter receptors^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.