Aprotinin is a bovine pancreatic trypsin inhibitor (BPTI) inhibitor which inhibits trypsin and chymotrypsin with K_is of 0.06 pM and 9 nM, respectively.

Ki: 0.06 pM (Trypsin), 9 nM (Chymotrypsin)^[1]

Aprotinin, a serine protease inhibitor isolated from bovine lung, is a complex protease inhibitor that is an antifibrinolytic, inhibits contact activation, and decreases the inflammatory response to cardiopulmonary bypass^[2]. Aprotinin inhibits trypsin (bovine, K_i= 0.06 pM), chymotrypsin (bovine, K_i= 9 nM), plasmin (human, 0.23 nM)^[1]. Aprotinin is also a competitive protein inhibitor of NOS activity. It inhibits NOS-I and NOS-II with K_i values of 50 μM and 78 μM, respectively^[3]. Aprotinin significantly inhibits fibrinolysis with an IC₅₀ of 0.16±0.05 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.

High dose aprotinin can reduce blood loss and transfusion requirements associated with primary cardiac procedures such as coronary artery bypass graft (CABG) or heart valve replacement surgery^[5]. Aprotinin inhibits thrombus formation in a dose-dependent manner. Aprotinin at a dose of 1.5 mg kg^-1 (bolus) and 3 mg kg^-1 h^-1 infusion (maintenance infusion) causes a tendency towards a reduction in bleeding time. Aprotinin significantly reduces the bleeding time starting at a dose of 3 mg kg^-1 bolus plus 6 mg kg^-1 h^-1 showing a reduction of approximately 84%±2.9%. At the highest dose of 5 mg kg^-1 and 10 mg kg^-1 h^-1, the strongest effects are observed^[4]. Aprotinin may affect tumor necrosis factor-alpha (TNF) levels. Soluble TNFRI levels are significantly increased following I/R in the aprotinin treated wild type mice and not detected in all TNFRInull mice^[6].

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.

6511.44

C₂₈₄H₄₃₂N₈₄O₇₉S₇

9087-70-1

Arg-Pro-Asp-Phe-Cys-Leu-Glu-Pro-Pro-Tyr-Thr-Gly-Pro-Cys-Lys-Ala-Arg-Ile-Ile-Arg-Tyr-Phe-Tyr-Asn-Ala-Lys-Ala-Gly-Leu-Cys-Gln-Thr-Phe-Val-Tyr-Gly-Gly-Cys-Arg-Ala-Lys-Arg-Asn-Asn-Phe-Lys-Ser-Ala-Glu-Asp-Cys-Met-Arg-Thr-Cys-Gly-Gly-Ala(Disulfide bridge: Cys5-Cys55,Cys14-Cys38,Cys30-Cys51)

RPDFCLEPPYTGPCKARIIRYFYNAKAGLCQTFVYGGCRAKRNNFKSAEDCMRTCGGA(Disulfide bridge: Cys5-Cys55,Cys14-Cys38,Cys30-Cys51)

抑肽酶；抑胰肽酶；屈来密多

Room temperature in continental US; may vary elsewhere.

H₂O : 100 mg/mL (15.36 mM; Need ultrasonic)

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。

• [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.

Rats: Male Wistar rats (180-220 g) are used in the study. Aprotinin is dissolved in physiological saline. Aprotinin is administered by bolus injection followed by a maintenance infusion. The doses given are 1.5 mg kg^-1 and 3 mg kg^-1 h^-1, 3mg kg^-1 and 6 mg kg^-1 h^-1 up to 5 mg kg^-1 and 10 mg kg^-1 h^-1. Plasma concentrations for the two agents are assessed by pharmacokinetic studies in rats^[4].

Mice: An intact mouse model of ischemia/reperfusion (30 min-I/60 min-R) is used and left ventricular peak + dP/dt is measured in wild type mice (WT, C57BL/6; n=10), WT mice with aprotinin (4mL/kg; n=10), transgenic mice devoid of the TNFRI (TNFRInull; n=10), and TNFRInull with aprotinin (n=10)^[6].

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.

• [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.