Antipyretic Analgesics

Etoricoxib is a member of the class of bipyridines that is 2,3'-bipyridine which is substituted at the 3, 5, and 6' positions by 4-(methylsulfonyl)phenyl, chlorine, and methyl groups, respectively. It has a role as a cyclooxygenase 2 inhibitor and a non-steroidal anti-inflammatory drug. It is a sulfone, a member of bipyridines and an organochlorine compound.

Naproxen is a non steroidal anti-inflammatory drug. It is a PG synthetase inhibitor and can inhibit prostate synthetase. It has significant analgesic and antipyretic effects. It is absorbed completely and rapidly by oral administration. The plasma concentration reaches the peak 2-4 hours after a single administration. More than 99% of naproxen is bound to plasma protein in the blood. The T1 / 2 ratio is 13-14 hours. About 95% of naproxen is excreted in the urine as its original form and metabolites. Clinically, it is used to treat rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, gout, arthritis and tenosynovitis. It can also be used to relieve the pain caused by musculoskeletal sprain, contusion, injury and dysmenorrhea. However, it should be noted that, like other NSAIDs, severe gastrointestinal adverse reactions may occur at any time during naproxen treatment. Therefore, patients with active gastroduodenal ulcer should not use naproxen. Patients with other gastrointestinal diseases should take naproxen under strict medical supervision.

Used as antipyretic and analgesic

Isopropylaminopyrine is a pyrazole derivative as a non steroidal anti-inflammatory reagent. Isopropylaminopyrine has analgesic, antipyretic, anti-inflammatory and antibacterial activities.

Codeine Phosphate is the phosphate salt of codeine, a naturally occurring phenanthrene alkaloid and opioid agonist with analgesic, antidiarrheal and antitussive activities. Codeine mimics the actions of endogenous opioids by binding to the opioid receptors at many sites within the central nervous system (CNS). Stimulation of mu-subtype opioid receptors results in a decrease in the release of nociceptive neurotransmitters such as substance P, GABA, dopamine, acetylcholine and noradrenaline; in addition, the codeine metabolite morphine induces opening of G-protein-coupled inwardly rectifying potassium (GIRK) channels and blocks the opening of N-type voltage-gated calcium channels, resulting in hyperpolarization and reduced neuronal excitability. Stimulation of gut mu-subtype opioid receptors results in a reduction in intestinal motility and delayed intestinal transit times. Antitussive activity is mediated through codeine's action on the cough center in the medulla.