Save up -80% on C1 Esterase Inhibitor (Human)
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|RX BIN: 015558||RX PCN: HT||Group ID: DDN6600||Card Holder ID: DDN6600|
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2019 Price of Berinert
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What is C1 Esterase Inhibitor (Human)
C1 Esterase Inhibitor (Human) is composed of purified endogenous complement component-1 esterase inhibitor (hC1INH) isolated from human plasma. The primary function of endogenous C1INH is to regulate the activation of the complement and contact system pathways. It does this through inhibition of several target proteases within these pathways including activated C1s, kallikrein, factor XIIa and factor XIa. C1 esterase inhibitor has also been shown to inhibit the action of thrombin within the coagulation pathway, and tPA and plasmin within the fibrinolytic pathway. Deficiency of C1-inhibitor permits plasma kallikrein activation, which leads to the production of the vasoactive peptide bradykinin. Additionally, C4 and C2 cleavage goes unchecked, resulting in auto-activation of the complement system. Down-stream effects of the lack of enzyme inhibition by C1 esterase inhibitor results in swelling due to leakage of fluid from blood vessels into connective tissue and consequently the presentation of hereditary angioedema (HAE). Marketed as the product Cyrinze (FDA), this drug is indicated for routine prophylaxis against angioedema attacks in adolescent and adult patients with Hereditary Angioedema (HAE), a human genetic disorder caused by a shortage of C1 inhibitor activity that results in an overreaction of the immune system. The disease is characterized by acute attacks of painful and in some cases fatal swelling of several soft tissues (edema), which may last up to five days when untreated.
C1 Esterase Inhibitor (Human) mechanism of action
C1 inhibitor is a normal constituent of human blood and is one of the serine proteinase inhibitors (serpins). The primary function of C1 inhibitor is to regulate the activation of the complement and intrinsic coagulation (contact system) pathway. C1 inhibitor also regulates the fibrinolytic system. Regulation of these systems is performed through the formation of complexes between the proteinases and the inhibitor, resulting in inactivation of both and consumption of the C1 inhibitor. HAE patients have low levels of endogenous or functional C1 inhibitor. Although the events that induce attacks of angioedema in HAE patients are not well defined, it is thought by some that increased vascular permeability and the clinical manifestation of HAE attacks are primarily mediated through contact system activation. Suppression of contact system activation by C1 inhibitor through the inactivation of plasma kallikrein and factor XIIa is thought to modulate this vascular permeability by preventing the generation of bradykinin1. Administration of C1 Esterase Inhibitor increases plasma levels of C1 inhibitor activity.
Dosage forms of C1 Esterase Inhibitor (Human)
|Kit; powder for solution||intravenous||1500 unit|
|Kit; powder for solution||intravenous||500 unit|
C1 inhibitor C1 inhibitor (human)
Csl Behring Gmb H
Humans and other mammals
Indication of C1 Esterase Inhibitor (Human)
For routine prophylaxis against angioedema attacks in adolescent and adult patients with Hereditary Angioedema (HAE).
Toxicity of C1 Esterase Inhibitor (Human)
The most common adverse reactions observed were headache, nausea, rash and vomiting. Serious arterial and venous thromboembolic (TE) events have been reported at the recommended dose of C1 Esterase Inhibitor (Human) products following administration in patients with HAE. Risk factors may include presence of an indwelling venous catheter/access device, prior history of thrombosis, underlying atherosclerosis, use of oral contraceptives, certain androgens, morbid obesity, and immobility. Monitor patients with known risk factors for TE events during and after administration. Because this product is made from human blood, it may carry a risk of transmitting infectious agents, e.g. viruses, and, theoretically, the Creutzfeldt-Jakob disease (CJD) agent.
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