Fiduxosin is a selective and potent α1-adrenoceptor antagonist with inhibitory effects on α1a-adrenoceptor, α1b-adrenoceptor and α1d-adrenoceptor, with Ki values of 0.160 nM, 24.9 nM and 0.920 nM, respectively. Fiduxosin can be used for the treatment of benign prostatic hyperplasia.

α1D-adrenoceptor:0.92 nM (Ki), α2A-adrenoceptor:92 nM (Ki,Human), α1A-adrenoceptor:0.16 nM (Ki), 5-HT1A receptor:29 nM (Ki,Rat), α1B-adrenoceptor:24.9 nM (Ki), α2b-adrenoceptor:21 nM (Ki,Rat), α2C-adrenoceptor:22 nM (Ki,Human)

Fiduxosin, in addition to β-adrenoceptors (2-5 μM), exhibits low affinity for other adrenoceptors, including cloned human α2a-adrenoceptors (92 nM), α2c-adrenoceptors (22 nM), and rat neonatal lung α2b-adrenoceptors (21 nM). Moreover, Fiduxosin shows low affinity for 5HT1A receptors in rat cortex (29 nM) compared to its affinity at α1a-adrenoceptors (0.16 nM). In the rabbit urethra, Fiduxosin competitively antagonizes PE-induced responses with a pA2 value of 7.58[2].

In anesthetized dogs, Fiduxosin (i.v.) at doses of 30, 100, and 300 μg/kg antagonizes intraurethral pressure (IUP) responses to intravenous epinephrine (EPI). Transient effects on blood pressure are observed with Fiduxosin at doses of 178, 592, and 1780 μg/kg (i.v.) in spontaneously hypertensive rats (SHR), with the lowest dose having no effect on mean arterial pressure (MAP).In SHR, Fiduxosin at a dose of 3 μmol/kg or 1780 μg/kg (i.v.) causes a slight reduction in MAP. However, head-up tilt results in a further diminution of MAP at the 15-minute observation point, with minimal additional changes observed at times ≥30 minutes postdosing.When administered orally at doses of 0.1, 0.3, 1.0, and 3.0 mg/kg, Fiduxosin blocks prostatic intraurethral pressure (IUP) responses to a greater extent than MAP responses. The effective dose (ED50) for IUP is calculated to be 0.24 mg/kg[1].