LIMBREL ACTS ON COX-1, COX-2 AND 5-LOX PATHWAYS. LIMBREL IS NOT SELECTIVE FOR EITHER COX-1 OR COX-2 ENZYMES. LIMBREL ACTS BY RESTORING AND MAINTAINING THE BALANCE OF FATTY ACIDS IN OA. LIMBREL DAMPENS AA METABOLISM AT RELATIVELY EQUAL LEVELS IN THE COX PATHWAY (MEDIATED BY CONVERSION OF AA VIA THE COX-1 & COX-2 ENZYMES), AS WELL AS INHIBITING THE METABOLISM OF AA BY THE 5-LOX ENZYME. THIS BALANCED INHIBITION OF METABOLISM IN THE COX PATHWAY YIELDS RELATIVELY EQUAL LEVELS OF THROMBOXANES, PROSTAGLANDINS, AND PROSTACYCLINS THAT ARE KEY MEDIATORS OF SYSTEMIC ORGAN FUNCTION. INHIBITION OF THESE MEDIATORS IN THE COX PATHWAY, IN CONJUNCTION WITH INHIBITION OF LEUKOTRIENES IN THE LOX PATHWAY, RESULTS IN A βDUAL INHIBITIONβ MECHANISM THAT MANAGES INFLAMMATION WITH MINIMAL EFFECTS ON ORGAN FUNCTION. INHIBITION OF 5-LOX HAS BEEN SHOWN IN CELL-BASED ASSAYS TO REDUCE THE PRODUCTION OF LTB4, AN AGENT THAT FOSTERS WBC CHEMOTAXIS AND THE SUBSEQUENT RELEASE OF HISTAMINES, ROS, AND PRO-INFLAMMATORY CYTOKINES. IN ADDITION, DIRECT INHIBITION OF THE 5-LOX ENZYME HAS BEEN OBSERVED IN ENZYMATIC ASSAYS. THIS BALANCED DOWN-REGULATION OF THESE ENZYMATIC PATHWAYS IS RELATIVELY WEAK WHEN COMPARED TO THE EFFECTS OF TRADITIONAL NSAIDS AND SELECTIVE COX-2 INHIBITORS, THUS ALLOWING THE BODY TO PRODUCE AA METABOLITES AT RELATIVELY EQUAL LEVELS TO MAINTAIN PHYSIOLOGIC FUNCTION.
LIMBREL ALSO ACTS AS A STRONG ANTIOXIDANT TO LIMIT THE OXIDATIVE CONVERSION OF AA BY ROS TO OTHER DAMAGING FATTY ACID PRODUCTS INCLUDING HYDROXYL RADICALS, SUPEROXIDE ANION RADICALS AND HYDROGEN PEROXIDE. LIMBREL HAS DEMONSTRATED AN OXYGEN RADICAL ABSORBANCE CAPACITY