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Detail of "105857-23-6"

  • CAS Number:
  • 105857-23-6
  • Name:
  • Plasminogen activator (human tissue-type protein moiety) (9CI)

  • Deleted CAS:
  • 93928-26-8

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CAS No.105857-23-6 Plasminogen activator (human tissue-type protein moiety) (9CI)

Supplier:LGM Pharma [ United States]

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Reference

Effect of Pexelizumab, an Anti-C5 Complement Antibody, as Adjunctive Therapy to Fibrinolysis in Acute Myocardial Infarction
Effect of Pexelizumab, an Anti-C5 Complement Antibody, as Adjunctive Therapy to Fibrinolysis in Acute Myocardial Infarction. Mahaffey, Kenneth W.; Granger, Christopher B.; Nicolau, Jose C.; Ruzyllo, Witold; Weaver, W. Douglas; Theroux, Pierre; Hochman, Judith S.; Filloon, Thomas G.; Mojcik, Christopher F.; Todaro, Thomas G.; Armstrong, Paul W. 105857-23-6 and 219685-93-5 are cas registry numbers. These chemicals are also mentioned in this article. (Duke Clinical Research Institute, Durham, NC, USA). Circulation, 108(10), 1176-1183 (English) 2003 Lippincott Williams & Wilkins. CODEN: CIRCAZ. ISSN: 0009-7322. DOCUMENT TYPE: Journal CA Section: 15 (Immunochemistry) Complement activation mediates myocardial damage that occurs during ischemia and reperfusion through multiple pathways. We performed 2 sep., parallel, double-blind, placebo-controlled trials to det. the effects of pexelizumab (a novel C5 complement monoclonal antibody fragment) on infarct size in patients receiving reperfusion therapy: COMPlement inhibition in myocardial infarction treated with thrombolytics (COMPLY) and complement inhibition in Myocardial infarction treated with Angioplasty (COMMA). The COMPLY trial is reported here. Overall, 943 patients with acute ST-segment elevation myocardial infarction (MI) (20% with isolated inferior MI) receiving fibrinolysis were randomly assigned <6 h after symptom onset to placebo, pexelizumab 2.0-mg/kg bolus, or pexelizumab 2.0-mg/kg bolus plus 0.05 mg/kg per h for 20 h. Infarct size detd. by creatine kinase-MB area under the curve was the primary anal., which included patients who received at least some study drug and fibrinolysis (n=920). The median infarct size did not differ by treatment (placebo, 5230; bolus, 4952; bolus plus infusion, 5557 [ng/mL] × h; bolus vs. placebo, P=0.85; bolus plus infusion vs. placebo, P=0.81), nor did the 90-day composite incidence of death, new or worsening congestive heart failure, shock, or stroke (placebo, 18.6%; bolus, 18.4%; bolus plus infusion, 19.7%). Pexelizumab inhibited complement for 4 h with bolus-only dosing and for 20 to 24 h with bolus-plus-infusion dosing, with no increase in infections. When used adjunctively with fibrinolysis, pexelizumab blocked complement activity but reduced neither infarct size by creatine kinase-MB assessment nor adverse clin. outcomes. .
Tissue-type plasminogen activator: helping patients with acute myocardial infarction
Some chemicals with cas registry numbers like 105857-23-6 and 99149-95-8 are also used. Tissue-type plasminogen activator: helping patients with acute myocardial infarction. Collen, Desire; Lijnen, H. Roger (Center for Transgene Technology and Gene Therapy, Flanders Interuniversity Institute for Biotechnology, Louvain, Belg.). Recombinant Protein Drugs, 107-126. Edited by: Buckel, Peter. Birkhaeuser Verlag: Basel, Switz. ISBN: 3-7643-5904-8(English) 2001. CODEN: 69EWGR. DOCUMENT TYPE: Conference; General Review CA Section: 1 (Pharmacology) A review. The review discusses the use of tissue-type plasminogen activator in myocardial infarction with particular emphasis on protein structure, synthesis regulation, mechanism of action, inhibition, and mutant forms. Urokinase-type plasminogen activator and staphylokinase are also reviewed. .
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