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DOSAGE FORM: Liquid Injection, 5000 IU/vial, 25000 IU/vial


Heparin, a highly sulfated glycosaminoglycan is widely used as an injectable anticoagulant and has the highest negative charge density of any known biological molecule. It can also be used to form an inner anticoagulant surface on various experimental and medical devices such as test tubes and renal dialysis machines. Pharmaceutical grade heparin is commonly derived from mucosal tissues of slaughtered meat animals such as porcine intestine or bovine lung.

Heparin is usually stored within the secretory granules of mast cells and only released into the vasculature at sites of tissue injury. It has been proposed that rather than anticoagulation the main purpose of heparin is in a defensive mechanism at sites of tissue injury against invading bacteria and other foreign materials.


Heparin is a naturally occurring anticoagulant produced by basophils and mast cells. Heparin acts as an anticoagulant, preventing the formation of clots and extension of existing clots within the blood. While heparin does not break down clots that have already formed (tissue plasminogen activator will), it allows the body's natural clot lysis mechanisms to work normally to break down clots that have already formed. Heparin is used for anticoagulation for the following conditions:

Acute coronary syndrome, e.g., myocardial infarction
Atrial fibrillation
Deep-vein thrombosis and pulmonary embolism
Cardiopulmonary bypass for heart surgery


Heparin binds to the enzyme inhibitor antithrombin III (AT-III) causing a conformational change which results in its active site being exposed. The activated AT-III then inactivates thrombin and other proteases involved in blood clotting, most notably factor Xa. The rate of inactivation of these proteases by AT-III increases 1000-fold due to the binding of heparin.

AT-III binds to a specific pentasaccharide sulfation sequence contained within the heparin polymer GlcNAc/NS (6S)-GlcA-GlcNS (3S, 6S)-IdoA (2S)-GlcNS (6S).

The conformational change in AT-III on heparin binding mediates its inhibition of factor Xa. For thrombin inhibition however, thrombin must also bind to the heparin polymer at a site proximal to the pentasaccharide. The highly negative charge density of heparin contributes to its very strong electrostatic interaction with thrombin. The formation of a ternary complex between AT-III, thrombin and heparin results in the inactivation of thrombin. For this reason heparin's activity against thrombin is size dependent, the ternary complex requiring at least 18 saccharide units for efficient formation. In contrast


Assay NLT 90% - NMT 110%  of labelled Heparin.
Identification Delays the clotting of freshly shed blood
PH 5.5 – 8.0
Sterility Complies to IP
BET NMT 0.03 EU per mg of heparin