Heparin pharmacokinetics and molecular data

Heparin Description & Molecular Data
Heparin is a heterogenous group of straight-chain anionic mucopolysaccharides, called glycosaminoglycans, having anticoagulant properties. Although others may be present, the main sugars occurring in Heparin are:


 * 1) α-L-iduronic acid 2-sulfate,
 * 2) 2-deoxy-2-sulfamino-α-D-glucose 6-sulfate,
 * 3) β-D-glucuronic acid,
 * 4) 2-acetamido-2-deoxy-α-D-glucose, and
 * 5) α-L-iduronic acid.

These sugars are present in decreasing amounts, usually in the order (2)> (1)> (4)> (3)> (5), and are joined by glycosidic linkages, forming polymers of varying sizes. Heparin is strongly acidic because of its content of covalently linked sulfate and carboxylic acid groups. In Heparin sodium, the acidic protons of the sulfate units are partially replaced by sodium ions.

Heparin Sodium Injection, USP is a sterile solution of Heparin sodium derived from porcine intestinal mucosa, standardized for anticoagulant activity. It is to be administered by intravenous or deep subcutaneous routes. The potency is determined by a biological assay using a USP reference standard based on units of Heparin activity per milligram.

Carpuject sterile cartridge unit contains a sterile solution of Heparin Sodium Injection, USP. Each mL contains 2.500 USP or 5,000 USP Heparin units of Heparin sodium and benzyl alcohol 1% as a preservative, in Water for Injection. The pH is adjusted between 5.0 to 7.5 with hydrochloric acid or sodium hydroxide.

Each mL of Preservative-Free Heparin Sodium Injection contains 10.000 USP Heparin units in Water for Injection. The pH is adjusted between 5.0 to 7.5 with hydrochloric acid or sodium hydroxide as required.

Clinical Pharmacology
Heparin inhibits reactions that lead to the clotting of blood and the formation of fibrin clots both in vitro and in vivo. Heparin acts at multiple sites in the normal coagulation system. Small amounts of Heparin in combination with antithrombin III (Heparin cofactor) can inhibit thrombosis by inactivating activated Factor X and inhibiting the conversion of prothrombin to thrombin. Once active thrombosis has developed, larger amounts of Heparin can inhibit further coagulation by inactivating thrombin and preventing the conversion of fibrinogen to fibrin. Heparin also prevents the formation of a stable fibrin clot by inhibiting the activation of the fibrin stabilizing factor.

Bleeding time is usually unaffected by Heparin. Clotting time is prolonged by full therapeutic doses of Heparin; in most cases, it is not measurably affected by low doses of Heparin.

Peak plasma levels of Heparin are achieved 2 to 4 hours following subcutaneous administration, although there are considerable individual variations. Loglinear plots of Heparin plasma concentrations with time, for a wide range of dose levels, are linear which suggest the absence of zero order processes. The liver and reticulo-endothelial system are the sites of biotransformation. The biphasic elimination curve, a rapidly declining alpha phase (t1/2 = 10 min.), and after the age of 40 a slower beta phase, indicates uptake in organs. The absence of a relationship between anticoagulant half-life and concentration half-life may reflect factors such as protein binding of Heparin.

Heparin does not have fibrinolytic activity; therefore, it will not lyse existing clots.