Silodosin (KAD 3213; KMD 3213) is a potent, selective and orally active α1A-adrenergic receptor (α1A-AR) blocker. Silodosin exhibits high affinity for α1A-AR (K_i=0.036 nM), over 162-fold and 50-fold than for α1B-AR and α1D-AR with K_i values of 21 nM and 2.0 nM, respectively. Silodosin is an effective and well-tolerated agent, it can be used for the investigation of LUTS/BPH^[1][3].

Ki: 0.036 nM (α1A-AR); 21 nM (α1B-AR); 2 nM (α1D-AR)^[1]

Silodosin (KAD 3213; KMD 3213) inhibits norepinephrine-induced increases in intracellular Ca²⁺ concentrations in alpha 1a-AR-expressing Chinese hamster ovary cells with an IC₅₀ of 0.32 nM but had a much weaker inhibitory effect on the alpha 1b- and alpha 1d-ARs^[1].
Silodosin potently inhibits 2-[2-(4-hydroxy-3-[125I]iodophenyl)ethylaminomethyl]-alpha-tetralone binding to the cloned human alpha 1a-AR, with a K_i value of 0.036 nM, but has 583- and 56-fold lower potency at the alpha 1b- and alpha 1d-ARs, respectively^[2].
Silodosin (0-10 µM; 24 hours) decreases ELK1 gene expression as a dose-dependent manner in all the bladder cancer cell lines^[4].
Silodosin (0-10 µM; 24 hours) decreases ELK1 protein expression as a as a dose-dependent manner^[4].
Silodosin (0-10 µM; 96 hours) insignificantly changes cell viability of AR-positive UMUC3 or TCCSUP cultured in an androgen-depleted condition or that of AR-negative 647V. In contrast, silodosin reduced the growth of UMUC3 cells cultured with normal FBS containing androgens (58% decrease at 10 µM)^[4].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

Silodosin (intravenous injection; 0.1-0.3mg/kg) reduces the obstruction-induced increases in MinP by 27.7 % (0.1 mg/kg) and 20.8 %(0.3 mg/kg). It improves detrusor overactivity and reduces the grade of obstruction, and thus may be effective for both storage and voiding dysfunction for the treatment of LUTS/BPH^[2].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

495.53

C₂₅H₃₂F₃N₃O₄

160970-54-7

西洛多辛；西罗多辛

Room temperature in continental US; may vary elsewhere.

DMSO : ≥ 50 mg/mL (100.90 mM)

* “≥” means soluble, but saturation unknown.

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：

——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

• 1.

  请依序添加每种溶剂： 10% DMSO    40% PEG300    5% Tween-80    45% saline

  Solubility: ≥ 2.5 mg/mL (5.05 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (5.05 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

  将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液

• 2.

  请依序添加每种溶剂： 10% DMSO    90% (20% SBE-β-CD in saline)

  Solubility: ≥ 2.5 mg/mL (5.05 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (5.05 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。

  将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
• 3.

  请依序添加每种溶剂： 10% DMSO    90% corn oil

  Solubility: ≥ 2.5 mg/mL (5.05 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (5.05 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

  以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

• [1]. Maxime Rossi , Silodosin in the treatment of benign prostatic hyperplasia. Drug Des Devel Ther. 2010; 4: 291–297.

  [2]. Villa L, et al. Effects by silodosin on the partially obstructed rat ureter in vivo and on human and rat isolated ureters.Br J Pharmacol. 2013 May;169(1):230-8.

  [3]. Osman NI, et al.Silodosin : a new subtype selective alpha-1 antagonist for the treatment of lower urinary tract symptoms in patients with benign prostatic hyperplasia.Expert Opin Pharmacother. 2012 Oct;13(14):2085-96.

  [4]. Kawahara T, et al. Silodosin inhibits the growth of bladder cancer cells and enhances the cytotoxic activity of cisplatin via ELK1 inactivation.Am J Cancer Res. 2015 Sep 15;5(10):2959-68. eCollection 2015.