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Verapress 240 mg /7 (25) 0.03 3.3 mg/1 mg BK-4, 10 mg/8 (25) 8 µg/100 mL BK-8, 200 mg/5 (25) 0.01 5.5 µg/100 mL BK-10, 50 mg/6 (25) 0.04 5.8 µg/100 mL BK-15, 0 mg/4 (10) 0.09 5 to 7.5 µg/100 mL BK-22 (5 µg/1 µg BK-15), 1 µg/10 (10) 10 mg/100 µg/100 mL BK-35, 1 mg/7 (10) 2 µg/100 mL BK-46, 5 mg/7 (12) 9 µg/100 mL BK-62, 0.5 mg/4 (5) 9 µg/100 mL BK-78, 400 mg/6 (50) 0.04 10.2 µg/100 BK-93, 0.3 µg/4 (8) 5 to 60 mg/100 2.04 13 µg/100 mg BK-94, 200 mg/5 (10) 3,000 µg/100 mL BK-100, 0.7 mg/6 (10) 6 µg/100 mL BK-300, 25 mg/8 (20) 7.4 to 10.1 µg/100 mL BK-600, 500 mg/12, 100 µg/100 mL
Pregnancy Category C: Drug interaction data not available.
Use in Specific Populations
Elimination or distribution of drug concentrations during the periconception period has not been studied in pregnant women or neonates. Neonates receiving subcutaneous injection of B. monnieri in a dose of 0.3 to 0.5 mg/kg/dose have an approximate survival rate of approximately 90% to 96%.
B. monnieri is metabolized into monohydroquinoline which excreted to the urine with a half-life of 3 days, and into 4-hydroxymethoxydibenzodioxin which is excreted with a half-life of 4 -6 h.
Clinical Pharmacology
Mechanism of Action
The primary pharmacologic activity of B. monnieri involves inhibition platelet aggregation, including coagulation. The effects on hemoglobin are mediated by the inhibition of 5' hydroxysteroid hydroxylating enzyme 4,5-dialkyltrans-4,5 dihydroxyphenylalanine-5-carboxylic acid methyltransferase (GSHPx), which is a protein kinase substrate. The activity of GSHPx is decreased when plasma concentrations of B. monnieri increase.
Pharmacodynamic Actions
In vitro and animal studies have demonstrated that the drug (BK-4) exerts its antithrombotic effect through inhibition of GSHPx activity by binding directly to the 5' Gylcosidase generic pharmacy drug list (GSSG). It was also shown that the inhibitory effects of BK-4 are also mediated by binding to the GSHPx gene promoter and BK-4 BK-8 are co-expressed on different chromosomes and thus share molecular characteristics of their primary target, thereby providing a pharmacological basis for the inhibitory action of active constituents on the GSHPx enzyme. Other pharmacologic effects were reported in vitro and animal studies, such as anticoagulation, antirheumatic, antiarrhythmias, and an antiarrhythmic effect in the perifusion model of cerebral ischemia/reperfusion.
In vitro studies have demonstrated that BK-4 is a potent inhibitor of platelet aggregation.
B. monnieri was shown to induce a dose-dependent decrease in the amount of thromboxane A2 formed by platelet endothelial cells from sheep, and to induce a further dose-dependent inhibition through GSHPx mediated inhibition. These effects were thought to be mediated through inhibition of prothrombin biosynthesis.
Although the antithrombemic properties of B. monnieri are well known and documented, there is currently not adequate evidence in vitro for their clinical use in the treatment of patients suffering from thrombocytopenic purpura. The therapeutic effectiveness of BK-4 during the period platelet damage induced by heparin administration has been demonstrated in the peripartum period. B. monnieri had a minimal (minimally detectable) and predictable effect at the lowest administered effective doses of BK-4 when used in
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