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Inr antidote4/30/2023 ![]() Patients who have contraindications to anticoagulant therapy should avoid using argatroban because it is metabolized by the liver. Argatroban is not excreted by the kidneys, so dose adjustment with renal impairment is unnecessary. For patients with HIT, argatroban at 2 µg/kg/min is adjusted to maintain the aPTT at 1.5 to 3 times the baseline value for a mean of 5 to 7 days. In individuals with unstable angina, argatroban (0.5 to 5.0 µg/kg/min for 4 hours) is administered. In HIT patients, argatroban therapy improves outcomes compared with historic controls, particularly relative to new thrombosis and death caused by thrombosis. For patients with HIT who are administered IV argatroban, benefit is noted as compared with historic controls. The half-life of the anticoagulant effect is approximately 25 minutes when argatroban is used alone. Argatroban causes a dose-dependent increase in aPTT and TT. 279,280 Data with argatroban are limited thus it is approved only for use in HIT. Studies with argatroban primarily have assessed its use as adjunctive therapy with fibrinolytics, in the treatment of HIT, and in patients undergoing coronary angioplasty. Argatroban has a predictable dose response that correlates with changes in anticoagulant parameters. ![]() ![]() Its reversible binding allows for rapid restoration of normal hemostasis on cessation of therapy. Argatroban is metabolized via the CYP 3A4 pathway in the liver with a half-life of 45 minutes. It binds rapidly and reversibly to both clot-bound and soluble thrombin. ![]() 393 This compound is a synthetic N2-substituted arginine derivative that binds to the catalytic site of thrombin with high affinity. Scirica, in Cardiovascular Therapeutics: A Companion to Braunwald's Heart Disease (Fourth Edition), 2013 Argatroban Mechanisms of ActionĪrgatroban is a synthetic direct thrombin inhibitor derived from L-arginine.
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