1-MNA anticoagulant activity and the release of prostacyclin (PGI2)

In vivo studies demonstrate the anticoagulant activity of 1-MNA (Chlopicki et al., 2007 – Literature  >>). During these studies, 1-MNA resulted in dose-dependent thrombolysis which was maintained over time (anticoagulant effect) (Diagrams A – D).

The anticoagulant activity of 1-MNA has also been shown in studies focusing on the level of 6-keto-PGF (stable PGI2 metabolite) and thromboxane B2 (TXB2) in arterial blood. These studies show that the anticoagulant response to 1-MNA  correlates with the concentration of 6-keto-PGF, reflecting the level of PGI2 being released into the bloodstream. The concentration of TXB2 increased over time, but only to a slight degree (Diagram C).

Diagram C. The influence of 1-MNA on the release of PGl2. The level of 6-keto-PGF and other prostanoids measured after administering 1-MNA (30 mg/kg). (Chlopicki et al., 2007Literature  >>).

The anticoagulant features of 1-MNA have also been tested in a model of arterial thrombosis in animals with hypertension (Chlopicki et al., 2007– Literature  >>). These studies revealed that, depending on the dose (3-30 mg/kg), 1-MNA reduced the created thrombus (Diagram D).

Diagram D. Anticoagulant activity of 1-MNA in a model of arterial thrombosis in laboratory animals with hypertension. (Chlopicki et al., 2007Literature  >>).

These studies suggest that 1-MNA is an endogenous prostacyclin activator and may regulate thrombotic and inflammatory processes occurring within the cardiovascular system.

The anticoagulant properties of 1-MNA result from its capacity to stimulate endothelial cells. This mechanism is connected with PGI2 release along the cyclooxygenase 2 (COX-2) pathway. Endogenous prostacyclin has anticoagulant and anti-atherosclerotic activity. Its deficiency results in increased aggregation of blood platelets and in the creation of arterial blood clots.