Description

Baxter Healthcare Corporation 
Deerfield, IL 60015 USA 
For Product Inquiry 1 800 ANA DRUG (1-800-262-3784)
MLT-01119/3.0 

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NDA 17-037/S-158 
Page 13 
HEP-LOCK
 
 (Heparin Lock Flush Solution, USP) 
R
x 
only 
DESCRIPTION 
Heparin is a heterogeneous 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. 
Structural formula of Heparin Sodium (representative sub-units): 
HEP-LOCK (Heparin Lock Flush Solution, USP) is a sterile solution for intravenous flush only. It is 
not to be used for anticoagulant therapy. Each mL contains heparin sodium 10 or 100 USP units, 
derived from porcine intestines and standardized for use as an anticoagulant, sodium chloride 9 mg and 
benzyl alcohol 0.01 mL in Water for Injection. pH 5.0-7.5; sodium hydroxide and/or hydrochloric acid 
used, if needed, for pH adjustment. The potency is determined by biological assay using a USP 
reference standard based on units of heparin activity per milligram. 
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 

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NDA 17-037/S-158 
Page 14 
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. Loglinear plots of 
heparin plasma concentrations with time, for a wide range of dose levels, are linear, which suggests the 
absence of zero order processes. Liver and the reticulo-endothelial system are the sites of 
biotransformation. The biphasic elimination curve, a rapidly declining alpha phase (t
½
= 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. 
Patients over 60 years of age, following similar doses of heparin, may have higher plasma levels of 
heparin and longer activated partial thromboplastin times (APTTs) compared with patients under 60 
years of age. 
Heparin does not have fibrinolytic activity; therefore, it will not lyse existing clots.