Loxoprofen (INN) is a non-steroidal anti-inflammatory drug in the propionic acid derivatives group. It is marketed in Brazil, Mexico and Japan by Sankyo as its sodium salt, loxoprofen sodium, under the trade name Loxonin, Argentina as Oxeno and in India as Loxomac. It is available in these countries for oral administration, and a transdermal preparation was approved for sale in Japan on January 2006. It is usually used to treat rheumatoid arthritis and osteoarthritis. It is also used to reduce pain and inflammation after surgery, wounds and tooth removal, as well as to bring down fever or ease pain induced by acute inflammation of upper respiratory tract Loxoprofen is a prodrug. When administered orally, loxoprofen sodium hydrate is absorbed from the gastrointestinal tract as an unchanged compound with only a modest gastric-mucosal irritation. It is then rapidly biotransformed into the active metabolite trans-OH form (SRS coordination) with a potent inhibitory effect on prostaglandin biosynthesis to exert its pharmacologic effects. Inhibition of prostaglandin biosynthesis constitutes the mechanism of action of this drug, the site of action being cyclooxygenase.

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.

Iguratimod, a methanesulfonanilide, is an anti-inflammatory drug for the treatment of rheumatoid arthritis that has been developed exclusively in Japan and China. It inhibits the production of immunoglobulins and various inflammatory cytokines (interleukin-1, -6 and -8 and TNF), and exerts anabolic effects on bone metabolism by stimulating osteoblastic differentiation and inhibiting osteoclastogenesis. On the molecular level, it inhibits the nuclear transcription factor NF-κB but not its inhibitor, IκBα. In addition to these immunomodulatory and other long-lasting effects, iguratimod inhibits cyclooxygenase-2, which provides a synergistic short-term action against pain and inflammation. Efficacy and tolerability are comparable to salazosulfapyridine, and probably also to methotrexate. Combination with methotrexate is synergistic in patients with insufficient response to methotrexate and does not significantly increase adverse events.

Propacetamol is a bioprecursor of paracetamol. It is rapidly hydrolyzed by plasma esterases and releases its constituent paracetamol by the end of its intravenous or intramuscular administration. Its metabolism is identical to that of paracetamol. It is used in post-operative care and is delivered by I.V. It is given if the patient is unable to take oral or rectally delivered paracetamol and non-steroidal anti-inflammatory drugs are contraindicated. The onset of analgaesia from propacetamol is more rapid than paracetamol given orally. 2 g of propacetamol are equivalent to 1g of paracetamol.

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.

Amygdalin is a naturally occurring cyanogenic glycoside derived from nuts, plants, and the pits of certain fruits, primarily apricots. Bitter almonds containing amygdalin are used in Traditional Chinese Medicine to remove “blood stasis” and to treat abscesses. Amygdalin was first used as a cancer treatment in Russia in 1845, and in the United States in the 1920s. Laetrile is another name for the natural product amygdalin. Hydrogen cyanide is thought to be the main anticancer compound formed from laetrile (Amygdalin) via in situ release. Cyanide from the hydrolysis of amygdalin is believed to be cytotoxic with actions selective against cancerous cells, but results from animal studies were mostly negative. Other animal studies suggest it may help to relieve pain due to its anti-inflammatory and analgesic effects. One study suggested amygdalin can inhibit tumor growth, but subsequent tests were unable to confirm this observation. Laetrile (Amygdalin) has shown little anticancer activity in animal studies and no anticancer activity in human clinical trials. In 1970, an IND application to study laetrile was filed by the McNaughton Foundation (San Ysidro, California). This request was initially approved but later rejected because preclinical evidence in animals showed that laetrile was not likely to be effective as an anticancer agent. The side effects associated with laetrile toxicity mirror the symptoms of cyanide poisoning, including liver damage, difficulty walking (caused by damaged nerves), fever, coma, and death. Laetrile (Amygdalin) is not approved for use in the United States.

Aceclofenac is a non-steroidal anti-inflammatory drug (NSAID) analog of Diclofenac. It is used for the relief of pain and inflammation in rheumatoid arthritis, osteoarthritis and ankylosing spondylitis. The dose is 100 mg twice daily, and should not be given to people with porphyria or breastfeeding mothers and is not recommended for children. Aceclofenac is a cytokine inhibitor. Aceclofenac works by blocking the action of a substance in the body called cyclo-oxygenase. Cyclo-oxygenase is involved in the production of prostaglandins (chemicals in the body which cause pain, swelling and inflammation). Aceclofenac is the glycolic acid ester of diclofenac. The incidence of gastric ulcerogenicity of aceclofenac has been reported to be significantly lower than that of other frequently prescribed NSAIDs: for instance, 2-fold less than naproxen, 4-fold less than diclofenac, and 7-fold less than indomethacin. Aceclofenac is metabolized in human hepatocytes and human microsomes to form [2-(2',6'-dichloro-4'-hydroxy- phenylamino)phenyl] acetoxyacetic acid as the major metabolite, which is then further conjugated.