Ecallantide
HAE is caused by a mutation of the C1-inhibitor gene. Defective or missing C1-inhibitor permits activation of kallikrein, a protease that is responsible for liberating bradykinin from its precursor kininogen. An excess of bradykinin leads to fluid leakage from blood vessels, causing swelling of tissues typical of HAE.Ecallantide suppresses this pathogenetic mechanism by selectively and reversibly inhibiting the activity of plasma kallikrein.
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| CAT# | 10-101-160 |
| CAS | 460738-38-9 |
| Synonyms/Alias | DX-88 cpd;EPI-KAL-2;Kalbitor |
| M.F/Formula | C305H442N88O91S8 |
| M.W/Mr. | 7053.83 |
| Sequence | EAMHSFCAFKADDGPCRAAHPRWFFNIFTRQCEEFIYGGCEGNQNRFESLEECKKMCTRD(Disulfide bridge: 7-57; 16-40; 32-53) |
| Labeling Target | Plasma kallikrein |
| Application | Treatment of hereditary angioedema, Reduction of blood loss during cardiothoracic surgery [plasma kallikrein inhibitor] |
| Activity | Inhibitor |
| Biological Activity | Ecallantide is a highly specific recombinant plasma kallikrein inhibitor developed for treatment of hereditary angioedema (HAE). |
| Areas of Interest | Hereditary angioedema |
| Functions | Serine-type endopeptidase activity |
| Disease | Hereditary angioneurotic edema |
| Source# | Synthetic |
Storage | -20°C |
Organism | Human |
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