| 规格 | 价格 | 库存 | 数量 |
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| 25mg |
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| 50mg |
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| 100mg |
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| 250mg |
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| 500mg |
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| 1g |
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| Other Sizes |
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| 靶点 |
α1-adrenergic receptor
α1-adrenergic receptor (α1-AR) subtypes, with highest affinity for α1A-AR (Ki = 0.034 nM) and α1D-AR (Ki = 0.23 nM), lower affinity for α1B-AR (Ki = 4.5 nM) [1] - α1A- and α1D-adrenergic receptors, which mediate smooth muscle contraction in the prostate and vasculature [2] |
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| 体外研究 (In Vitro) |
体外活性：坦索罗辛是一种选择性 α1 受体拮抗剂，相对于血管中的 α1B 受体，它对前列腺中的 α1A 受体具有优先选择性。与对照患者相比，接受坦索罗辛治疗的患者发生急性尿潴留的风险降低了 0.30 倍。国际节制协会男性问卷各领域得分均未显示各组之间存在显着变化。坦索罗辛可推荐用于治疗 AUR 插管后的男性，并且可以减少需要重新插管的可能性。激酶测定： 细胞测定：
Tamsulosin HCl 在人前列腺膜制剂中竞争性抑制[3H]-哌唑嗪与α1-AR亚型的结合，对α1A-AR和α1D-AR的拮抗作用具有亚型选择性，优于对α1B-AR的作用[1] - Tamsulosin HCl 通过抑制PI3K/Akt/mTOR信号通路，抑制血管紧张素II诱导的小鼠主动脉平滑肌细胞（ASMCs）增殖和迁移；同时降低ASMCs中I型胶原蛋白和基质金属蛋白酶-9（MMP-9）的表达[2] |
| 体内研究 (In Vivo) |
坦索罗辛表现出高血浆蛋白结合，主要与 α1-酸性糖蛋白结合。它主要通过细胞色素 P450 (CYP) 3A4 和 CYP2D6 代谢为低丰度化合物，口服剂量的 8.7-15% 作为母体化合物经肾脏排泄。坦索罗辛的药代动力学在很大程度上不受年龄的影响，肾功能不全患者的药代动力学变化很大程度上与α1-酸性糖蛋白浓度的增加有关。肝功能损害引起的药代动力学改变也仅为中度，因此肾功能损害和轻至中度肝功能损害都不需要调整剂量。对大鼠和狗等实验动物进行坦索罗辛速释的早期研究表明，口服给药后（30-90 分钟内）坦索罗辛吸收迅速，但大鼠的绝对生物利用度仅为 7-23%，狗的绝对生物利用度仅为 30-42%。坦索罗辛 MR 在禁食人体中的绝对生物利用度约为 100%。在禁食状态下，tmax 通常为约 5 小时（报告的平均值范围为 2.9-5.6 小时），在进食状态下为约 6 小时（范围为 5.2-7.0 小时）。静脉注射放射性标记坦索罗辛并在10分钟后测量各组织中放射性标记的动物研究表明，该药物存在于各组织中，排列顺序如下：肾>肺≈心脏>颌下腺>肝≈脾≈主动脉≈输精管>前列腺>>大脑皮层，后者接近检测限。坦索罗辛可能无法通过血脑屏障。坦索罗辛在大鼠和狗体内进行广泛的肝脏代谢，分别仅以母体化合物的形式在尿液中排泄 1.2% 和 2.8%。在人类中，坦索罗辛也经历广泛的肝脏代谢，但显然比大鼠或狗的代谢程度稍小，因为口服剂量的 8.7-15% 以非代谢形式从尿液中排出。坦索罗辛从体内消除的速度因物种而异，例如坦索罗辛在大鼠和狗中的消除速度比在人类中更快。
在良性前列腺增生（BPH）模型大鼠中，Tamsulosin HCl（0.01-0.1 mg/kg，口服）通过松弛前列腺和膀胱颈平滑肌，降低尿道内压力并改善尿流率[1] - 在血管紧张素II诱导的腹主动脉瘤（AAA）ApoE-/-小鼠模型中，Tamsulosin HCl（0.1 mg/kg/天，灌胃给药28天）可抑制AAA生长（最大主动脉直径减少31.2%），并减轻主动脉壁炎症、弹性蛋白降解和平滑肌细胞丢失[2] |
| 酶活实验 |
取人前列腺组织制备膜制剂，与[3H]-哌唑嗪（放射性配体）和不同浓度的Tamsulosin HCl在25°C下孵育60分钟。通过过滤分离结合态和游离态配体，测定放射性强度以确定对α1-AR亚型的结合亲和力（Ki值）[1]
- 采用重组人α1A-、α1B-和α1D-AR表达细胞的膜制剂进行亚型特异性放射性配体结合实验，绘制竞争曲线以计算IC50值和亚型选择性比率[1] |
| 细胞实验 |
从主动脉组织中分离小鼠ASMCs，在添加胎牛血清的DMEM培养基中培养。细胞先用Tamsulosin HCl（1-10 μM）预处理1小时，再用血管紧张素II（100 nM）刺激24-48小时。通过CCK-8法检测细胞增殖，Transwell法检测细胞迁移，Western blot检测蛋白表达（PI3K、Akt、mTOR、MMP-9）[2]
- 经Tamsulosin HCl和血管紧张素II处理48小时后，采用酶联免疫吸附试验（ELISA）测定ASMCs分泌的I型胶原蛋白水平[2] |
| 动物实验 |
Dissolved in saline; 0.1 and 1 μg/kg; s.c. injection
Female Wistar rats BPH model rats (induced by testosterone propionate injection) were randomly divided into control and treatment groups. Tamsulosin HCl was administered orally at doses of 0.01, 0.03, and 0.1 mg/kg once daily for 2 weeks. Urinary flow parameters and intraurethral pressure were measured under anesthesia [1] - ApoE-/- mice (8-10 weeks old) were implanted with osmotic minipumps delivering angiotensin II (1000 ng/kg/min) to induce AAA. Tamsulosin HCl was dissolved in normal saline and administered via oral gavage at 0.1 mg/kg/day for 28 days. Mice were euthanized, and aortic tissues were collected for histopathological and molecular analysis [2] |
| 药代性质 (ADME/PK) |
Tamsulosin hydrochloride has an oral bioavailability of approximately 90% in humans (food has no significant effect on absorption). Peak plasma concentration (Cmax) is reached 0.5–1 hour after oral administration [1]
- Plasma protein binding is 99%, mainly bound to albumin and α1-acid glycoprotein [1] - Tamsulosin hydrochloride is metabolized in the liver by cytochrome P450 (CYP) enzymes, mainly by CYP3A4 and CYP2D6 to inactive metabolites [1] - The elimination half-life (t1/2) in humans is 10–14 hours; approximately 70% of the dose is excreted in the urine (10% of which is the original drug), and 20% is excreted in the feces [1] |
| 毒性/毒理 (Toxicokinetics/TK) |
Common adverse reactions in humans include dizziness (6.3%), orthostatic hypotension (3.2%), rhinitis (2.8%), and ejaculatory abnormalities (2.1%); these adverse reactions are dose-related and are generally mild to moderate [1]
- No significant hepatotoxicity or nephrotoxicity was observed in clinical trials; repeated daily administration did not lead to plasma concentration accumulation [1] - In animal toxicity studies, high doses (100 times the therapeutic dose) caused hypotension and bradycardia, but no fatal toxicity was reported [1] |
| 参考文献 | |
| 其他信息 |
Tamsulosin hydrochloride is the hydrochloride salt formed by the reaction of equimolar amounts of tamsulosin with hydrogen chloride. It is an alpha-adrenergic antagonist and antitumor drug. It contains the tamsulosin (1+) molecule. It is the enantiomer of ent-tamsulosin hydrochloride. Tamsulosin hydrochloride is the hydrochloride salt of tamsulosin, a sulfonamide derivative with adrenergic antagonistic activity. Tamsulosin selectively binds to and blocks the activity of alpha-1 adrenergic receptors in the human prostate and bladder neck; blocking these adrenergic receptors relaxes the smooth muscle of the prostate and bladder neck, thereby improving urinary flow rate. Tamsulosin hydrochloride is a sulfonamide derivative and alpha-1 adrenergic receptor antagonist used to relieve urinary tract obstruction symptoms caused by benign prostatic hyperplasia. See also: Tamsulosin (note moved to). Tamsulosin hydrochloride is a selective α1A/α1D adrenergic receptor antagonist approved for the treatment of lower urinary tract symptoms (LUTS) associated with benign prostatic hyperplasia (BPH)[1]. Its therapeutic effect is achieved by relaxing the smooth muscle of the prostatic interstitium and bladder neck, reducing urethral resistance and improving urinary flow rate[1]. Tamsulosin hydrochloride slows the growth of abdominal aortic aneurysms (AAA) by inhibiting smooth muscle cell proliferation/migration and reducing inflammation. It also protects the extracellular matrix of the aortic wall[2].
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| 分子式 |
C20H28N2O5S.HCL
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|---|---|---|
| 分子量 |
444.97
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| 精确质量 |
444.148
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| 元素分析 |
C, 55.00; H, 6.56; Cl, 8.54; N, 6.75; O, 15.42; S, 7.73
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| CAS号 |
106463-17-6
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| 相关CAS号 |
Tamsulosin;106133-20-4; Tamsulosin-d5 hydrochloride; Tamsulosin-d4 hydrochloride; 2518100-55-3
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| PubChem CID |
5362376
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| 外观&性状 |
White to off-white solid powder
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| 沸点 |
595.5ºC at 760 mmHg
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| 熔点 |
228-230ºC
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| 闪点 |
313.9ºC
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| 蒸汽压 |
3.79E-14mmHg at 25°C
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| LogP |
4.512
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| tPSA |
108.26
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| 氢键供体(HBD)数目 |
3
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| 氢键受体(HBA)数目 |
7
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| 可旋转键数目(RBC) |
11
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| 重原子数目 |
29
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| 分子复杂度/Complexity |
539
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| 定义原子立体中心数目 |
1
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| SMILES |
Cl[H].S(C1=C(C([H])=C([H])C(=C1[H])C([H])([H])[C@@]([H])(C([H])([H])[H])N([H])C([H])([H])C([H])([H])OC1=C([H])C([H])=C([H])C([H])=C1OC([H])([H])C([H])([H])[H])OC([H])([H])[H])(N([H])[H])(=O)=O
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| InChi Key |
ZZIZZTHXZRDOFM-XFULWGLBSA-N
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| InChi Code |
InChI=1S/C20H28N2O5S.ClH/c1-4-26-17-7-5-6-8-18(17)27-12-11-22-15(2)13-16-9-10-19(25-3)20(14-16)28(21,23)24;/h5-10,14-15,22H,4,11-13H2,1-3H3,(H2,21,23,24);1H/t15-;/m1./s1
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| 化学名 |
5-[(2R)-2-[2-(2-ethoxyphenoxy)ethylamino]propyl]-2-methoxybenzenesulfonamide;hydrochloride
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| 别名 |
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| HS Tariff Code |
2934.99.9001
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| 存储方式 |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
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| 运输条件 |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| 溶解度 (体外实验) |
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| 制备储备液 | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.2473 mL | 11.2367 mL | 22.4734 mL | |
| 5 mM | 0.4495 mL | 2.2473 mL | 4.4947 mL | |
| 10 mM | 0.2247 mL | 1.1237 mL | 2.2473 mL |
1、根据实验需要选择合适的溶剂配制储备液 (母液)：对于大多数产品，InvivoChem推荐用DMSO配置母液 (比如：5、10、20mM或者10、20、50 mg/mL浓度），个别水溶性高的产品可直接溶于水。产品在DMSO 、水或其他溶剂中的具体溶解度详见上”溶解度 (体外)”部分;
2、如果您找不到您想要的溶解度信息，或者很难将产品溶解在溶液中，请联系我们;
3、建议使用下列计算器进行相关计算（摩尔浓度计算器、稀释计算器、分子量计算器、重组计算器等）;
4、母液配好之后，将其分装到常规用量，并储存在-20°C或-80°C，尽量减少反复冻融循环。
计算结果:
工作液浓度： mg/mL；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL)。如该浓度超过该批次药物DMSO溶解度，请首先与我们联系。
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL ddH2O，混匀澄清。
(1) 请确保溶液澄清之后，再加入下一种溶剂 (助溶剂) 。可利用涡旋、超声或水浴加热等方法助溶；
(2) 一定要按顺序加入溶剂 (助溶剂) 。
Investigating Medication vs. Prostatic Urethral Lift: Assessment and Comparison of Therapies for BPH
CTID: NCT04987892
Phase: Phase 4 Status: Recruiting
Date: 2023-04-25
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