Flufenamic acid is a member of the anthranilic acid derivatives class of NSAID drugs. Like other members of the class, it is a COX inhibitor and prevents the formation of prostaglandins. Flufenamic acid is known to bind to and reduce the activity of prostaglandin F synthase and activate TRPC6.

Indobufen is an inhibitor of platelet aggregation which acts by reversibly inhibiting the platelet cyclo-oxygenase enzyme. Indobufen under brand name Ibustrin is used for the following conditions: cerebrovascular insufficiency, atherosclerosis of peripheral and cerebral vessels, thrombophlebitis, deep vein thrombosis, and diabetes mellitus. In addition, this drug has been investigated in the phase II clinical trial for the prevention of thromboembolic events in patients with nonrheumatic atrial fibrillation. Racemic indobufen caused a dose-dependent inhibition of TXB2 and PGE2 production (IC50: 0.53 /- 0.06 and 0.34 /- 0.02 ug/ml, respectively). S-Indobufen was approximately 2-fold more potent than the racemate in inhibiting the synthesis of cyclooxygenase products. R-Indobufen affected the same enzyme but only at considerably higher concentrations (IC50: 53 /- 8 ug/ml). Serum LTB4 concentrations were significantly reduced only at indobufen concentrations greater than 50 ug/ml. In conclusion, indobufen is a selective inhibitor of the cyclooxygenase activity of platelet PGG/H synthase in a concentration range corresponding to the therapeutic plasma levels in man. This inhibitory effect is largely due to the S isomer of the drug.

Aluminum flufenamate is an anthranilic acid derivative with analgesic, anti-inflammatory, and antipyretic properties. It is used in musculoskeletal and joint disorders and administered by mouth and topically. Antiphlogistic pain reliever Opyrin (Aluminum flufenamate) was launched in Japan by Taisho Pharmaceutical in 1967.

Ufenamate is a topical analgesic. It is indicated for pain and inflammation associated with musculoskeletal and joint disorders. It is a COX inhibitor. Ufenamate is freely soluble in oil and is poorly soluble in water. It is used in the form of ointments or creams. It is manufactured under the brand name Combec in Japan. It is also an ingredient of Fenazol Ointment 5%, used in Japan for the treatment of eczema, dermatitis and herpes zoster.

Eltenac is a compound with a structural similarity to diclofenac with one benzol ring substituted by a tiophene ring. This modification has been shown to improve the absorption after topical application. Eltenac is an inhibitor of both cyclo-oxygenase-1 and -2. Eltenac had been in phase II clinical trial for the treatment of osteoarthritis of the knee. Eltenac is used in the alleviation of inflammation associated with musculoskeletal disorders and control of post-operative swelling, oedema and endotoxaemia in horses. The local skin reactions reported in humans were erythema, eczema, itching, rash and dry skin.

Mavacoxib (trade name Trocoxil) is a veterinary drug used to treat pain and inflammation in dogs with the degenerative joint disease. Mavacoxib is a non-steroidal anti-inflammatory drug (NSAID) of the coxib class. Mavacoxib acts by preferential inhibition of COX-2-mediated prostaglandin synthesis. It, therefore, possesses analgesic and anti-inflammatory properties. The products of COX-2 metabolism are also involved in ovulation, implantation, and closure of the ductus arteriosus. Mavacoxib is well absorbed after oral administration; bioavailability was 87% in fed dogs and 46 % in fasted conditions and the recommended dose is based on administration with food. Therapeutic concentrations in fed dogs are reached rapidly and peak concentrations are obtained in less than 24 hours after administering a dose. Mavacoxib is approximately 98% bound to plasma proteins. It is extensively distributed throughout the body and almost all the mavacoxib-related residues in plasma comprise parent drug. The rate of body clearance of mavacoxib is slow and the major route of elimination is by biliary excretion of the parent drug. Adverse reactions of the digestive tract such as vomiting and diarrhea were commonly reported, loss of appetite, hemorrhagic diarrhea, and melaena have been reported in uncommon cases. Gastrointestinal ulceration was reported in rare cases. Apathy, degradation of renal biochemistry parameters and impaired renal function have been reported in uncommon cases. In rare cases, these adverse reactions may be fatal.

Tepoxalin is a nonsteroidal anti-inflammatory drug approved for veterinary use in the United States and many other countries. Marketed under the brand name Zubrin, Tepoxalin is indicated for the control of pain and inflammation associated with osteoarthritis in dogs. Tepoxalin has an unique property as an NSAIDs that suppresses both cyclooxygenase and lipoxygenase.

Triflusal (trade names Disgren, Grendis, Aflen, Triflux, ets) is a member of the salicylate family with a well-established platelet aggregation inhibitory profile that differs from that of acetylsalicylic acid (ASA) in its pharmacokinetic and pharmacodynamic properties. Triflusal irreversibly inhibits cyclooxygenase-1 through its potency is lower than that of acetylsalicylic acid (ASA). Triflusal shows potent inhibition of vascular prostacyclin synthesis, and weak inhibition of platelet phosphodiesterase. Triflusal also favors the production of NO and increases the concentration of cyclic nucleotides. A number of experimental and clinical studies have shown that triflusal is a potentially useful choice in the treatment and prophylaxis of brain ischemia because of its antithrombogenic as well as neuroprotective effects. Triflusal anti-thrombogenic properties have been demonstrated clinically and experimentally, while its neuroprotective effects have been shown only in animal models. Triflusal is administered orally. It Is absorbed primarily in the small intestines and its bioavailability in humans ranges from 83% to 100%. Once absorbed, 99% of triflusal binds to plasma proteins in experimental animals as well as in humans. Triflusal readily crosses organic barriers, but its blood levels are always higher than tissue levels. Upon passage through the liver, triflusal is deacetylated, forming 2-hydroxy-4-trifluoro-methyl-benzoicacid (HTB) as the main active metabolite. Triflusal inhibits platelet aggregation and interaction of platelets with subendothelium. The antiplatelet effect of triflusal has been documented in experimental animals and in humans, in in vitro and ex vivo studies, and in in vivo models of thrombogenesis in animals. Triflusal inhibited collagen- or arachidonic acid-induced platelet aggregation in platelet-rich plasma more effectively than ADP-induced platelet aggregation. Independently of its antithrombotic effect, triflusal acts directly on the nervous tissue to reduce the damage caused by ischemic or cytotoxic insults. The daily oral intake of 600 mg triflusal led to HTB levels in the cerebrospinal fluid that had neuroprotective effects in experimental animals. Traditionally, antiplatelet drugs have been associated with an increased risk of bleeding complications.

Dexibuprofen, S(+)-ibuprofen, is a non-steroidal anti-inflammatory drug and active dextrorotatory enantiomer of ibuprofen. Pharmacotherapeutic effects of dexibuprofen are more potent with lesser side effects than that of the racemic mixture of both isomers. In the acute and chronic treatment of osteoarthritis, it exhibits equivalent efficacy and tolerability as that of celecoxib. Dexibuprofen is a non-selective inhibitor of cyclooxygenase (COX), which is an enzyme involved in prostaglandin (mediators of pain and fever) and thromboxane (stimulators of blood clotting) synthesis via the arachidonic acid pathway. Dexibuprofen is a non-selective cyclooxygenase inhibitor and hence, it inhibits the activity of both COX-1 and COX-2. The inhibition of COX-2 activity decreases the synthesis of prostaglandins involved in mediating inflammation, pain, fever, and swelling while the inhibition of COX-1 is thought to cause some of the side effects of Dexibuprofen including GI ulceration. The major disadvantage of dexibuprofen is its low bioavailability, the account of its low solubility in physiological media.

Alminoprofen is a nonsteroidal anti-inflammatory drug (NSAID) of the phenylpropionic acid class. It has anti-inflammatory properties different from the classical NSAID. Alminoprofen possesses both antiphospholipase A2 (PLA2) activity and anti-cycloxygenase (COX) activity.