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Aspirin produces its anti-thrombotic actions by inhibiting the COX-1 enzyme in platelets. However, aspirin causes significant bleeding and ulcers in the rat stomach.1 In preclinical studies, ATB-340 exhibits equivalent inhibition of COX-1 but without gastrointestinal damage.
As with other NSAIDs, aspirin triggers gastric damage by causing white blood cells (leukocytes) to stick to the inner surface of blood vessels in the stomach, contributing significantly to ulcer formation. Current medical practice is to combine aspirin with an acid reduction drug (e.g., a proton pump inhibitor such as esomeprazole), reducing risk to the stomach but increasing damage to the small intestine. ATB-340 demonstrates markedly reduced leukocyte adherence in rats compared to aspirin.