Anatomical Therapeutic Chemical Classification System
Aceclofenac is a non-steroidal agent with marked anti-inflammatory and analgesic properties. The mode of action of aceclofenac is largely based on the inhibition to prostaglandin synthesis. Aceclofenac is a potent inhibitor of the enzyme cyclo-oxygenase, which is involved in the production of prostaglandins.
Acemetacin is a glycolic acid ester of indomethacin and the pharmacological activity resulting from acemetacin administration in man is derived from the presence of both acemetacin and indomethacin. The precise pharmacological mode of action of acemetacin is not known. However, unlike other NSAIDs, acemetacin is only a relatively weak inhibitor of prostaglandin synthetase.
Benzydamine exerts an anti-inflammatory and analgesic action by stabilising the cellular membrane and inhibiting prostaglandin synthesis.
Celecoxib is an oral, selective, cyclooxygenase-2 (COX-2) inhibitor within the clinical dose range (200-400 mg daily). No statistically significant inhibition of COX-1 (assessed as ex vivo inhibition of thromboxane B2 [TxB2] formation) was observed in this dose range in healthy volunteers.
Chondroitin sulfate belongs to the polysaccharide subgroup of glycosaminoglycans. Chondroitin sulfate is one of the main elements of the cartilage, which joins a central protein, forming what we know as proteoglycan, which is what gives the cartilage its mechanical and elastic properties.
Dexibuprofen (= S(+)-ibuprofen) is considered to be the pharmacologically active enantiomer of racemic ibuprofen. Racemic ibuprofen is a non-steroidal substance with antiinflammatory and analgesic effects. Its mechanism of action is thought to be due to inhibition of prostaglandin synthesis.
Dexketoprofen belongs to the non-steroidal anti-inflammatory group of drugs. The mechanism of action of Dexketoprofen is related to the reduction of prostaglandin synthesis by the inhibition of cyclooxygenase pathway. Furthermore, the inhibition of the synthesis of prostaglandins could affect other inflammation mediators such as kinins, causing an indirect action which would be additional to the direct action.
Diacerein is an anthraquinone derivative which has moderate anti-inflammatory activity. It is anti-inflammatory at high doses and devoid of any irritant effect on the stomach.
Diclofenac is a non-steroidal anti-inflammatory drug. The mechanism of action of diclofenac in AK may be related to the inhibition of the cycloxygenase pathway leading to reduced prostaglandin E2 (PGE2) synthesis. In addition, immunohistochemistry (IHC) from skin biopsies ac revealed that the clinical effects of diclofenac in AK are primarily due to anti-inflammatory, anti-angiogenic and possibly anti-proliferative effects and apoptosis-inducing mechanisms.
Etoricoxib is an oral, selective cyclo-oxygenase-2 (COX-2) inhibitor within the clinical dose range. Cyclooxygenase is responsible for generation of prostaglandins. Two isoforms, COX-1 and COX-2, have been identified. COX-2 is the isoform of the enzyme that has been shown to be induced by pro-inflammatory stimuli and has been postulated to be primarily responsible for the synthesis of prostanoid mediators of pain, inflammation, and fever. COX-2 is also involved in ovulation, implantation and closure of the ductus arteriosus, regulation of renal function, and central nervous system functions (fever induction, pain perception and cognitive function). It may also play a role in ulcer healing. COX-2 has been identified in tissue around gastric ulcers in man but its relevance to ulcer healing has not been established.
Flurbiprofen is a propionic acid derivative NSAID which acts through inhibition of prostaglandin synthesis. In humans flurbiprofen has potent analgesic, antipyretic and anti-inflammatory properties.
Glucosamine is an endogenous substance, a normal constituent of the polysaccharide chains of cartilage matrix and synovial fluid glucosaminoglycans. In vitro and in vivo studies have shown glucosamine stimulates the synthesis of physiological glycosaminoglycans and proteoglycans by chondrocytes and of hyaluronic acid by synoviocytes.
Ibuprofen is a propionic acid derivative NSAID that has demonstrated its efficacy by inhibition of prostaglandin synthesis. In humans ibuprofen reduces inflammatory pain, swellings and fever. Furthermore, ibuprofen reversibly inhibits platelet aggregation.
Indometacin has anti-inflammatory, antipyretic, and analgesic effects, it is an inhibitor of prostaglandin synthetase.
Ketoprofen is a non-steroidal anti-inflammatory drug. It has anti-inflammatory and analgesic actions.
Ketorolac is a non-steroidal anti-inflammatory agent demonstrating analgesic and anti-inflammatory activity. Ketorolac inhibits the cyclo-oxygenase enzyme essential for biosynthesis of prostaglandins. Ketorolac has been shown to reduce prostaglandin levels in the aqueous humour after topical ophthalmic administration.
Lornoxicam is a non-steroidal anti-inflammatory drug with analgesic properties and belongs to the class of oxicams. Lornoxicams mode of action is mainly related to the inhibition of the prostaglandin synthesis (inhibition of the cyclooxygenase enzyme) leading to desensitisation of peripheral nociceptors and consequently inhibition of inflammation. A central effect on nociception, which seems to be independent of anti-inflammatory effects has also been suggested.
Mefenamic acid is a non-steroidal anti-inflammatory drug (NSAID) with anti-inflammatory, analgesic and antipyretic properties.
Meloxicam is a non-steroidal anti-inflammatory drug (NSAID) of the oxicam family, with anti-inflammatory, analgesic and antipyretic properties. The anti-inflammatory activity of meloxicam has been proven in classical models of inflammation. As with other NSAID, its precise mechanism of action remains unknown. However, there is at least one common mode of action shared by all NSAID (including meloxicam): inhibition of the biosynthesis of prostaglandins, known inflammation mediators.
Nabumetone is a non acidic non steroidal anti-inflammatory agent with weak prostaglandin synthesis properties. Nabumetone undergoes rapid and extensive metabolism in the liver to 6-methoxy-2-naphthylacetic acid (6-MNA), the principal active metabolite which is a potent inhibitor of prostaglandin synthesis.
Naproxen is a non-steroidal anti-inflammatory analgesic compound with antipyretic properties as has been demonstrated in classical animal test systems. Naproxen exhibits its anti-inflammatory effect even in adrenalectomised animals, indicating that its action is not mediated through the pituitary-adrenal axis.
Niflumic acid is an analgesic and anti-inflammatory agent used in the treatment of rheumatoid arthritis.
Nimesulide is a non-steroidal anti-inflammatory drug with analgesic and antipyretic properties which acts as an inhibitor of prostaglandin synthesis enzyme cyclo-oxygenase. Cyclo-oxygenase produces prostaglandins, some of them being implicated in the development and maintenance of inflammation.
Oxaprozin has analgesic, anti-inflammatory, and antipyretic properties. The mechanism of action of oxaprozin, like that of other NSAIDs, is not completely understood but involves inhibition of cyclooxygenase (COX-1 and COX-2).
Parecoxib is a prodrug of valdecoxib. Valdecoxib is a selective COX-2 inhibitor within the clinical dose range. Cyclooxygenase is responsible for generation of prostaglandins.
Piroxicam is a non-steroidal anti-inflammatory agent with analgesic and antipyretic activity.
Rofecoxib is a nonsteroidal anti-inflammatory drug that exhibits anti-inflammatory, analgesic, and antipyretic activities in animal models. The mechanism of action of rofecoxib is believed to be due to inhibition of prostaglandin synthesis, via inhibition of cyclooxygenase-2 (COX-2).
Sulindac is a fluorinated indene with a structural resemblance to indometacin. It has analgesic, anti-inflammatory and antipyretic actions.
Tenoxicam is a non-steroidal anti-inflammatory drug (NSAID) which has anti-inflammatory, analgesic, antipyretic properties and it also inhibits platelet aggregation.
NSAID with anti-inflammatory, analgesic, and antipyretic effects. Tolfenamic acid is a prostaglandin synthesis inhibitor and a leukotriene synthesis inhibitor.