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Detail of > 12786-39-9

  • CAS Number:
  • 12786-39-9
  • Name:
  • Trypsin inhibitor(soybean Kunitz) (9CI)

  • Synonyms:
  • 1H,28H-Pyrrolo[2,1-b1][1,2,5,8,11,14,17,20,23,26,29]dithianonaazacyclodotriacontine,cyclic peptide deriv.; 67H,72H-Tripyrrolo[2,1-t1:2',1'-d3:2'',1''-l5][1,2,5,8,11,14,17,20,23,26,29,32,35,38,41,44,47,50,53,56,59,62,65,68,71,74,77,80,83,86,89,92,95,98,101,104,107,110,113,116,119,122,125,128,131,134,137,140,143]dithiaheptatetracontaazacyclohexatetracontahectine,cyclic peptide deriv.; Trypsin inhibitor (soybean Kunitz reduced), cyclic (39®86),(136®145)-bis(disulfide)
  • Molecular Weight:
  • 0
  • EINECS:
  • 232-906-9
  • Solubility:
  • H2O: >10 mg/mL
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CAS No. 

12786-39-9 TRYPSIN INHIBITOR

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CAS No. 

12786-39-9 TRYPSIN INHIBITOR

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United States  
  • Tel:(815) 968-0747
  • Address:PO Box 117, Rockford, IL 61105 USA

CAS No. 

12786-39-9 TRYPSIN INHIBITOR

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  • Address:Archway House,77 Ty-Glas Avenue, Llanishen,Cardiff CF14 5DX, UK
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    Reference

    Effect of organic kallikrein on blood coagulation, complement and esterolytic activity of plasma
    Effect of organic kallikrein on blood coagulation, complement and esterolytic activity of plasma. Denk, S.; Eisen, V.; Bluemel, G. (Inst. Exp. Chir., Tech. Univ. Munchen, Munich, Ger.). Kininogenases, Symp. Physiol. Prop. Pharmacol. Ration., Proliferation, Repar., Funct., 3rd, 41-53. Edited by: Haberland, G. L.; Rohen, J. W.; Bluemel, G. Schattauer: Stuttgart, Ger. 9004-04-0 and 12786-39-9 are also in the experiment. (English) 1975. CODEN: 34UUAR. DOCUMENT TYPE: Conference CA Section: 1 (Pharmacodynamics) Org. (pancreatic) kallikrein [9001-01-8] increased esterolytic activity of rat blood plasma which was inhibited by soybean-trypsin inhibitor (SBTI) [12786-39-9] and Trasylol (aprotinin) [9004-04-0] as well. The blood coagulation and CH50 (serum concn. causing 50% coagulation) were not significantly influenced by high doses of pancreatic kallikrein. After incubation of human plasma with high doses of pancreatic kallikrein the esterolytic activity was effectively inhibited by aprotinin, whereas the esterolytic activity due to an activation of plasma kallikrein was reduced by SBTI. Org. kallikrein did not influence the activity of clotting factor XI and XII in vitro. Only excessively high doses of org. kallikrein produced decreases in total complement and C4 in human sera, whereas lower doses had the same effect in rat sera. Only a slight effect of pancreatic kallikrein on the activation of Cls to Cl was to be seen in studies with HAO serum. .

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