Molecular Formula | C25H32F3N3O4 |
Molar Mass | 495.53 |
Density | 1.249±0.06 g/cm3(Predicted) |
Melting Point | >104°C (dec.) |
Boling Point | 601.4±55.0 °C(Predicted) |
Specific Rotation(α) | D25 -14.0° (c = 1.01 in methanol) |
Flash Point | 317.5°C |
Solubility | DMSO 99 mg/mL Water <1 mg/mL Ethanol 99 mg/mL |
Vapor Presure | 2.58E-15mmHg at 25°C |
Appearance | Solid |
Color | White to Off-White |
pKa | 14.85±0.10(Predicted) |
Storage Condition | under inert gas (nitrogen or Argon) at 2–8 °C |
Refractive Index | 1.552 |
In vitro study | Silodosin has a higher selectivity for the α(1A)-AR subtype than tamsulosin hydrochloride, naftopidil or prazosin hydrochloride (affinity tamsulosin hydrochloride is highest, followed by silodosin, prazosin hydrochloride or naftopidil). In human and rat isolated prostates, Silodosin and tadalafil have a synergistic inhibition of rat neuro-mediated contractile effects. |
In vivo study | In the lower urinary tract tissues of rabbits, Silodosin strongly antagonized norepinephrine-induced contractions (including prostate, urethra and bladder triangle, with PA(2) or pK B values of 9.60, respectively, 8.71 and 9.35). In rats, Silodosin was administered at 12 hours, 18 hours and 24 hours after oral administration. The phenylephrine-induced increase in intraurethral pressure (relative to the control treatment group) was significantly inhibited. Silodosin(0.1-0.3 mg/kg) or Prazosin(0.03-0.1 mg/kg) reduced the barrier-induced intraluminal ureteral pressure by 21-37% or 18-40%, respectively. Silodosin inhibits isolated rat and human ureteral contractions and has excellent functional selectivity to relieve pressure on obstructed ureters in loaded rats. In young and old dogs with benign prostatic hyperplasia, Silodosin(0.3-300 mg/kg) dose-dependently inhibited the increase in Urethral pressure induced by hypogastric nerve stimulation (no significant hypotensive effect). |
HS Code | 29339900 |