NSAIDs as a class all work in a similar manner - they inhibit the activity of cyclooxygenase (COX) enzymes and thereby block the formation of prostaglandins (PGs). The induction of NSAID-induced GI ulcers is proposed to follow a 2-step process: direct NSAID exposure causing topical irritation followed by exacerbation of the deleterious effect by inhibition of PG synthesis.
LT-NS001 is unique among NSAIDs as it is the only NSAID that is pharmacologically inactive as a COX inhibitor in the GI tract, but once absorbed into the bloodstream, it is converted rapidly and quantitatively to naproxen.
Inside the GI tract, LT-NS001 is lipophilic and neutral (rather than hydrophilic and acidic as is naproxen); As a result, treatment of patients with LT-NS001 is associated with less GI toxicity including fewer gastric ulcers, than treatment with equivalent doses of naproxen.
Currently, NSAID-induced ulcers are treated by combining NSAID therapy with a proton pump inhibitor (PPI) or a histamine-2 receptor antagonist (H2). The chronic administration of PPI's has been associated with serious side effects such as interference with anti-platelet treatments, increased susceptibility to infections and increased risk of bone fracture. LT-NS001 utilizes a proprietary technology which has demonstrated improved GI safety without the need for concomitant alkalinizing agents and their associated risks. LT-NS001 is a single agent, non-substitutable NSAID with a unique, patented bio-activated technology.
LT-NS001 is an investigational drug product candidate undergoing clinical evaluation and has not been approved by the U.S. Food and Drug Administration.