Dexketoprofen is a nonsteroidal anti-inflammatory drug (NSAID), manufactured by Menarini under the tradename Keral. Dexketoprofen is indicated for short-term treatment of mild to moderate pain, including dysmenorrhoea. Dexketoprofen works by blocking the action of a substance in the body called cyclo-oxygenase, which is involved in the production of chemicals in the body called prostaglandins. Prostaglandins are produced in response to injury or certain diseases and would otherwise go on to cause swelling, inflammation, and pain. By blocking cyclo-oxygenase, dexketoprofen prevents the production of prostaglandins and therefore reduces inflammation and pain. Along with peripheral analgesic action, it possesses central analgesic action. Dexketoprofen may cause dizziness, and patients should not, therefore, drive or operate heavy machinery or vehicles until they are familiar with how dexketoprofen affects them. Concomitant use of alcohol and other sedatives may potentiate this effect. In a small subset of individuals, the dizziness may be intolerable and require the transition to an alternative treatment.

Piroxicam is in a class of drugs called nonsteroidal anti-inflammatory drugs (NSAIDs). It was originally brought to market by Pfizer under the tradename Feldene in 1980, became generic in 1992, and is marketed worldwide under many brandnames. Piroxicam works by reducing hormones that cause inflammation and pain in the body. Piroxicam is used to reduce the pain, inflammation, and stiffness caused by rheumatoid arthritis and osteoarthritis. The antiinflammatory effect of Piroxicam may result from the reversible inhibition of cyclooxygenase, causing the peripheral inhibition of prostaglandin synthesis. The prostaglandins are produced by an enzyme called Cox-1. Piroxicam blocks the Cox-1 enzyme, resulting into the disruption of production of prostaglandins. Piroxicam also inhibits the migration of leukocytes into sites of inflammation and prevents the formation of thromboxane A2, an aggregating agent, by the platelets. Piroxicam is used for treatment of osteoarthritis and rheumatoid arthritis.

Naproxen (naproxen sodium, NAPROSYN®) is a propionic acid derivative related to the arylacetic acid group of nonsteroidal anti-inflammatory drugs (NSAIDs). It is an anti-inflammatory agent with analgesic and antipyretic properties. Both the acid and its sodium salt are used in the treatment of rheumatoid arthritis and other rheumatic or musculoskeletal disorders, dysmenorrhea, and acute gout. The mechanism of action of the naproxen (naproxen sodium, NAPROSYN®), like that of other NSAIDs, is not completely understood but involves inhibition of cyclooxygenase (COX-1 and COX-2).

Tolmetin is a nonsteroidal anti-inflammatory agent. It was marketed as Tolectin in USA. TOLECTIN (tolmetin sodium) is indicated for the relief of signs and symptoms of rheumatoid arthritis and osteoarthritis. TOLECTIN is indicated in the treatment of acute flares and the long-term management of the chronic disease. TOLECTIN is also indicated for treatment of juvenile rheumatoid arthritis. The mode of action of tolmetin is not known. However, studies in laboratory animals and man have demonstrated that the anti-inflammatory action of tolmetin is not due to pituitary-adrenal stimulation. Tolmetin inhibits prostaglandin synthetase in vitro and lowers the plasma level of prostaglandin E in man. This reduction in prostaglandin synthesis may be responsible for the anti-inflammatory action.

Indometacin (INN and BAN) or indomethacin (AAN, USAN, and former BAN) is a nonsteroidal anti-inflammatory drug (NSAID) commonly used as a prescription medication to reduce fever, pain, stiffness, and swelling from inflammation. Indomethacin has analgesic, anti-inflammatory, and antipyretic properties. The mechanism of action of Indometacin, like that of other NSAIDs, is not completely understood but involves inhibition of cyclooxygenase (COX-1 and COX-2). Indomethacin is a potent inhibitor of prostaglandin synthesis in vitro. Indomethacin concentrations reached during therapy have produced in vivo effects. Prostaglandins sensitize afferent nerves and potentiate the action of bradykinin in inducing pain in animal models. Prostaglandins are mediators of inflammation. Because indomethacin is an inhibitor of prostaglandin synthesis, its mode of action may be due to a decrease of prostaglandins in peripheral tissues. Indometacin is indicated for: Moderate to severe rheumatoid arthritis including acute flares of chronic disease, Moderate to severe ankylosing spondylitis, Moderate to severe osteoarthritis, Acute painful shoulder (bursitis and/or tendinitis), Acute gouty arthritis. In general, adverse effects seen with indomethacin are similar to all other NSAIDs. For instance, indometacin inhibits both cyclooxygenase-1 and cyclooxygenase-2, it inhibits the production of prostaglandins in the stomach and intestines, which maintain the mucous lining of the gastrointestinal tract. Indometacin, therefore, like other non-selective COX inhibitors can cause peptic ulcers. These ulcers can result in serious bleeding and/or perforation requiring hospitalization of the patient. To reduce the possibility of peptic ulcers, indomethacin should be prescribed at the lowest dosage needed to achieve a therapeutic effect, usually between 50–200 mg/day. It should always be taken with food. Nearly all patients benefit from an ulcer protective drug (e.g. highly dosed antacids, ranitidine 150 mg at bedtime, or omeprazole 20 mg at bedtime). Other common gastrointestinal complaints, including dyspepsia, heartburn and mild diarrhea are less serious and rarely require discontinuation of indomethacin.

Sulfasalazine is an anti-inflammatory indicated for the treatment of ulcerative colitis and rheumatoid arthritis. The mode of action of Sulfasalazine or its metabolites, 5-aminosalicylic acid (5-ASA) and sulfapyridine (SP), is still under investigation, but may be related to the anti-inflammatory and/or immunomodulatory properties that have been observed in animal and in vitromodels, to its affinity for connective tissue, and/or to the relatively high concentration it reaches in serous fluids, the liver and intestinal walls, as demonstrated in autoradiographic studies in animals. In ulcerative colitis, clinical studies utilizing rectal administration of Sulfasalazine, SP and 5-ASA have indicated that the major therapeutic action may reside in the 5-ASA moiety. The relative contribution of the parent drug and the major metabolites in rheumatoid arthritis is unknown. Sulfasalazine is used for the treatment of Crohn's disease and rheumatoid arthritis as a second-line agent. Sulfasalazine is marketed under the trade name Azulfidine among others.

Methyl salicylate (or methyl 2-hydroxybenzoate), also known as wintergreen oil, is a natural product and is present in white wine, tea, porcini mushroom Boletus edulis, Bourbon vanilla, clary sage, red sage and fruits including cherry, apple, raspberry, papaya and plum. Methyl salicylate is topically used in combination with methanol and under brand name SALONPAS to temporarily relieves mild to moderate aches and pains of muscles and joints associated with: strains, sprains, simple backache, arthritis, bruises. The precise mechanism of action of methyl salicylate is not known, but there is suggested, that it cause dilation of the capillaries thereby increasing blood flow to the area.

Pamicogrel is a cyclooxygenase inhibitor with platelet anti-aggregatory properties which is under development by Kanebo for chronic arterial occlusion. It also has potential in both prophylaxis and treatment of ischemic brain injury. An NDA was submitted in Japan in April 1997. The effects of the drug on platelet aggregation were originally disclosed in EP-00159677, while the later European patent, EP-00560136, claims its use in brain dysfunction induced by hypoxia arising from disturbance of cerebral circulation, such as cerebral hemorrhage or cerebral infarction.

Transcrocetinate (TSC) is a novel compound that offers promise as a treatment for conditions caused by hypoxia or ischemia. Unlike crocetin, it worked well in the more severe hemorrhagic shock model. Although many of the earlier studies with TSC involved the treatment of the ischemic conditions of hemorrhagic shock in both rats and swine, a few other studies involved treating purely hypoxic situations. One study showed that TSC was capable of promoting survival in rats breathing 10% oxygen. TSC also was able to increase arterial PO2 values in a rat model of acute respiratory distress syndrome (ARDS) caused by injection of oleic acid. The drug acts via a mechanism that has not been previously exploited in a pharmaceutical. TSC increases the rate of oxygen diffusion between the erythrocytes and the tissues by altering the 'structure' of water in blood plasma. It does this by causing additional hydrogen bonds to form among the water molecules. Animal toxicology studies have demonstrated that high levels of TSC are well-tolerated, and a Phase I clinical study has shown that TSC is also safe in humans. Delayed TSC treatment improves outcomes in experimental models of both ischemic and hemorrhagic stroke. TSC may be a safe and beneficial therapeutic modality for early stroke intervention, irrespective of the type of stroke involved. Transcrocetinate is in phase III clinical trial for the treatment of glioblastoma.

NCX-4016, a nitric oxide non-steroidal anti-inflammatory drug (NO-NSAID) which can inhibit cyclooxygenase as well as release nitric oxide, is under development by NicOx as a potential treatment for thrombosis, inflammation and rheumatoid arthritis. NCX-4016 possesses a broad spectrum of antithrombotic and antiinflammatory activities. NCX-4016 has been shown to inhibit platelet activation in vitro more effectively than aspirin, to inhibit smooth muscle cell proliferation, to exert an endothelial cell protective activity and to suppress the function of several inflammatory cells potentially involved in atherothrombosis. In animal models, NCX-4016 protected from platelet thromboembolism, prevented restenosis in atherosclerosis-prone animals, protected the heart from ischemia/reperfusion injury, and induced neoangiogenesis in critically ischemic limbs. Moreover, it displayed little or no gastric toxicity and appeared to protect stomach from noxious stimuli, including aspirin. NCX-4016 has been evaluated in healthy volunteers and found to inhibit platelet cyclo-oxygenase-1 (COX-1) similarly to or slightly less than aspirin, to raise the circulating levels of NO-degradation products, and to have little or no gastric toxicity in short term studies. NCX-4016 was in Phase II clinical trials for the treatment of vascular disorders such as peripheral vascular disease and other cardiovascular diseases including thrombosis, complications of endothelium-related diseases such as diabetes and other. But this research was discontinued.