Aprotinin 蛋白酶抑制剂（抑肽酶）
| EC | EINECS 232-994-9 |
| MDL | MFCD00130541 |
| CAS | 9087-70-1 |
| 分子式 | C284H432N84O79S7 |
| 分子量 | 6511.44 |
| 纯度 | ≥98% |
| 单位 | 瓶 |
| 生物活性 | Aprotinin是丝氨酸蛋白酶 (BPTI) 抑制剂，对胰蛋白酶和胰凝乳蛋白酶胰凝乳蛋白酶的 Ki 值分别为0.06 pM和9 nM。[1-6] |
| In Vitro | 抑肽酶是一种从牛肺中分离出的丝氨酸蛋白酶抑制剂, 是一种复合蛋白酶抑制剂, 具有抗纤维蛋白溶解作用, 可抑制接触激活, 并可降低对体外循环的炎症反应[2]。抑肽酶抑制胰蛋白酶 (牛, Ki = 0.06 pM) , 胰凝乳蛋白酶 (牛, Ki = 9 nM) , 纤溶酶 (人, 0.23 nM) [1]。抑肽酶也是NOS活性的竞争蛋白抑制剂。它抑制NOS-I和NOS-II, Ki值分别为50μM和78μM[3]。抑肽酶显着抑制纤维蛋白溶解, IC50为0.16±0.05μM[4]。 |
| In Vivo | 高剂量抑肽酶可以减少与原发性心脏手术相关的失血和输血要求, 如冠状动脉旁路移植术 (CABG) 或心脏瓣膜置换手术[5]。抑肽酶以剂量依赖性方式抑制血栓形成。以1.5mg kg-1 (推注) 和3mg kg-1h-1输注 (维持输注) 的剂量的抑肽酶导致出血时间减少的趋势。从3mg kg-1推注剂量加6mg kg-1h-1开始, 抑肽酶显着减少出血时间, 显示减少约84％±2.9％。在最高剂量为5 mg kg-1和10 mg kg-1 h-1时, 观察到最强的效果[4]。抑肽酶可能影响肿瘤坏死因子-α (TNF) 水平。在抑肽酶处理的野生型小鼠中I / R后可溶性TNFRI水平显着增加, 并且在所有TNFRInull小鼠中均未检测到[6]。 |
| SMILES | [RPDFCLEPPYTGPCKARIIRYFYNAKAGLCQTFVYGGCRAKRNNFKSAEDCMRTCGGA] |
| 靶点 | Serine Protease |
| 动物实验 | 大鼠：在研究中使用雄性Wistar大鼠 (180-220g) 。将抑肽酶溶解在生理盐水中。通过推注注射然后维持输注来施用抑肽酶。给予的剂量是1.5mg kg-1和3mg kg-1h-1, 3mg kg-1和6mg kg-1h-1至5mg kg-1和10mg kg-1h-1。通过大鼠的药代动力学研究评估两种药物的血浆浓度[4]。小鼠：使用缺血/再灌注的完整小鼠模型 (30分钟-I / 60分钟-R) 并且在野生型小鼠 (WT, C57BL / 6; n = 10) , WT中测量左心室峰值+ dP / dt。具有抑肽酶 (4mL / kg; n = 10) 的小鼠, 缺乏TNFRI的转基因小鼠 (TNFRInull; n = 10) 和含有抑肽酶的TNFRInull (n = 10) [6]。 |
| 数据来源文献 | [1]. Fritz H, et al. Biochemistry and applications of aprotinin, the kallikrein inhibitor from bovine organs. Arzneimittelforschung. 1983; 33 (4) :479-94.
[2]. Levy JH, et al. Efficacy and safety of aprotinin in cardiac surgery. Orthopedics. 2004 Jun; 27 (6 Suppl) :s659-62. [3]. Venturini G, et al. Aprotinin, the first competitive protein inhibitor of NOS activity.Biochem Biophys Res Commun. 1998 Aug 10; 249 (1) :263-5 [4]. Sperzel M, et al. Evaluation of aprotinin and tranexamic acid in different in vitro and in vivo models of fibrinolysis, coagulation and thrombus formation. J Thromb Haemost. 2007 Oct; 5 (10) :2113-8. Epub 2007 Jul 31. [5]. Davis R, et al. Aprotinin. A review of its pharmacology and therapeutic efficacy in reducing blood loss associated withcardiac surgery. Drugs. 1995 Jun; 49 (6) :954-83. [6]. Sabbagh MJ, et al. Aprotinin exacerbates left ventricular dysfunction after ischemia/reperfusion in mice lacking tumor necrosis factor receptor I. J Cardiovasc Pharmacol. 2008 Oct; 52 (4) :355-62. |
| 备注 | 以上数据均来自公开文献, Jinpan暂未进行独立验证, 仅供参考。These protocols are for reference only. Jinpan does not independently validate these methods. |
| 规格 | 10mg 50mg 100mg |
是一种丝氨酸蛋白酶 (BPTI) 抑制剂。
使用本产品的应用案例（仅供参考）
In Vitro
Western blotting. （0.3 µM Aprotinin）
MCF-7 cells were treated with the aforementioned CoCl2 concentrations for 24 h and cells were lysed with ice-cold radioimmunoprecipitation assay buffer (150 mM NaCl, 1.0% NP-40, 0.1% Triton X-100, 0.5% sodium deoxycholate, 0.1% SDS and 50 mM Tris-HCl, pH 8.0) and protease inhibitors (AEBSF at 2 mM, Aprotinin at 0.3 µM, Bestatin at 116 µM, E-64 at 14 µM, Leupeptin at 1 µM and EDTA at 1 mM; Beijing Jinpan Science & Technology Co., Ltd., Beijing, China).
来源文献：Li Q, Ma R, Zhang M. CoCl2 increases the expression of hypoxic markers HIF-1α, VEGF and CXCR4 in breast cancer MCF-7 cells. Oncol Lett. 2018 Jan;15(1):1119-1124. doi: 10.3892/ol.2017.7369. Epub 2017 Nov 8. PMID: 29391899; PMCID: PMC5769392.