As with other non-selective NSAIDs, naproxen exerts it’s clinical effects by blocking COX-1 and COX-2 enzymes leading to decreased prostaglandin synthesis. Although both enzymes contribute to prostaglandin production, they have unique functional differences. The COX-1 enzymes is constitutively active and can be found in normal tissues such as the stomach lining, while the COX-2 enzyme is inducible and produces prostaglandins that mediate pain, fever and inflammation. The COX-2 enzyme mediates the desired antipyretic, analgesic and anti-inflammatory properties offered by Naproxen, while undesired adverse effects such as gastrointestinal upset and renal toxicities are linked to the COX-1 enzyme.

Metformin is a biguanide type oral antihyperglycemic drug used in the management of type 2 diabetes. It lowers both basal and postprandial plasma glucose. Its mechanism of action is different from those of sulfonylureas and it does not produce hypoglycemia. Metformin decreases hepatic glucose production, decreases intestinal absorption of glucose and improves insulin sensitivity by an increase in peripheral glucose uptake and utilization.

Citicoline is a naturally occurring substance that is an essential intermediate in the synthesis of structural phospholipids of cell membrane. Oral dose of Citicoline is metabolized to choline & cytidine. These then enter into the systemic circulation, cross the blood-brain barrier and recombine to form Citicoline within the central nervous system. Citicoline activates the biosynthesis of structural phospholipids in the neuronal membrane, promotes rapid repair of injured cell surface & mitochondrial membrane & increases the level of various neurotransmitters like acetylcholine & dopamine. Citicoline has neuroprotective effects in situations of hypoxia & ischemia, as well as improved learning & memory performance in animal models for the aging brain. Citicoline inhibits the activation of Phospholipase A2 to prevent apoptotic & necrotic cell death.