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Some legal experts argue that simply adding a vitamin to an existing drug does not constitute meaningful clinical differentiation
- It is metabolized via: - COX pathway Prostaglandins & Thromboxane - LOX pathway Leukotrienes Why limiting NSAID use matters: NSAIDs inhibit COX enzymes: - COX-1 inhibition gastric protection, platelet aggregation - COX-2 inhibition inflammation, pain, and fever Major Risks: - Gastrointestinal (GIT): ulcers, bleeding - Renal: reduced renal perfusion, risk of kidney injury - Cardiovascular: increased risk of thrombosis and heart events High-risk NSAIDs: - Indomethacin higher GI & CNS side effects - Diclofenac higher cardiovascular risk - Piroxicam high GI toxicity Safer options (relatively): - Ibuprofen moderate safety if used short-term - Celecoxib / Etoricoxib (COX-2 selective) Key Clinical Note: - Indomethacin is commonly used in neonates to treat Patent Ductus Arteriosus (PDA) by closing the ductus after birth
The ESI source conditions were set as following: sheath gas flow rate of 50 arbitrary units (Arb), auxiliary gas flow rate of 15 Arb, capillary temperature of 320 C, full MS resolution of 60,000, MS/MS resolution of 15,000, collision energy of 10/30/60 in normalized collision energy (NCE) mode, and spray voltage of 3.8 kV (positive) or 3.4 kV (negative)
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