Fadrozole (CGS 16949A) is a tetrahydroimidazole-pyridine derivative is a non-steroidal inhibitor of aromatase. In the third phase of clinical trials it was shown, that this drug has good therapeutic effect as a second-line treatment in postmenopausal women with metastatic breast cancer.

Clidanac is an anti-inflammatory agent developed in Japan for the treatment of rheumatoid arthritis. The drug is mixture of two isomers, d- and l-, and the d-form is more active than the l-form. Therapeutic effect of clidanac is mediated by the inhibition of prostaglandin biosynthesis.

Fenbufen is a nonsteroidal anti-inflammatory drug, developed for the treatment of symptoms associated with such disease as rheumatoid arthritis. Fenbufen acts through its active metabolite, 4-biphenylacetic acid which is a potent inhibitor of COX1 and COX2 enzymes. Fenbufen was found to cause skin rash and liver toxicity and was withdrawn from the market.

Lornoxicam (Xefo®) is a nonsteroidal anti-inflammatory drug of the oxicam class with analgesic, anti-inflammatory and antipyretic properties. It differs from other oxicam compounds in its potent inhibition of prostaglandin biosynthesis, a property that explains the particularly pronounced efficacy of the drug. The inhibition of the cyclooxygenase enzymes (COX-1 and COX-2) by lornoxicam (Xefo®) leads 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.

Tenoxicam (Mobiflex), an anti-inflammatory agent with analgesic and antipyretic properties, is used to treat osteoarthritis and control acute pain. The anti-inflammatory effects of tenoxicam may result from the inhibition of the enzyme cyclooxygenase and the subsequent peripheral inhibition of prostaglandin synthesis. As prostaglandins sensitize pain receptors, their inhibition accounts for the peripheral analgesic effects of tenoxicam. Antipyresis may occur by central action on the hypothalamus, resulting in peripheral dilation, increased cutaneous blood flow, and subsequent heat loss. Taking tenoxicam with other drugs can increase the chance of side effects or alter the therapeutic effect of tenoxicam or the other drug, depending on the combination. Drug types the tenoxicam may interact with include: other analgesic NSAIDs, salicylates such as aspirin, antacids, anticoagulants, cardiac glycosides, ciclosporin, quinolone antibiotics, lithium therapy, diuretics and anti-hypertensives, methotrexate, oral anti-diabetics, cholestyramine, dextromethorphan, mifepristone, corticosteroids, anti-platelet agents and selective serotonin reuptake inhibitors (SSRIs), tacrolimus, zidovudine, and gold/penicillamine. Tenoxicam is available as a prescription-only drug in the United Kingdom and other countries, but not in the US. Outside of the United Kingdom, tenoxicam is also marketed under brand names including Tilatil, Tilcitin, and Alganex. Tenoxicam belongs to the class of NSAIDs known as oxicams. It is used to relieve inflammation, swelling, stiffness, and pain associated with rheumatoid arthritis, osteoarthritis, ankylosing spondylitis (a type of arthritis involving the spine), tendinitis (inflammation of a tendon), bursitis (inflammation of a bursa, a fluid-filled sac located around joints and near the bones), and peri-arthritis of the shoulders or hips (inflammation of tissues surrounding these joints).

Ibufenac was used as an analgesic and anti-inflammatory agent, but was withdrawn from the market due to hepatotoxicity.

Nintedanib is a receptor tyrosine kinase inhibitor with potential antiangiogenic and antineoplastic activities. It is the only kinase inhibitor drug approved to treat idiopathic pulmonary fibrosis. that targets multiple receptor tyrosine kinases (RTKs) and non-receptor tyrosine kinases (nRTKs). Nintedanib inhibits the following RTKs: platelet-derived growth factor receptor (PDGFR) α and β, fibroblast growth factor receptor (FGFR) 1-3, vascular endothelial growth factor receptor (VEGFR) 1-3, and Fms-like tyrosine kinase-3 (FLT3). Among them, FGFR, PDGFR, and VEGFR have been implicated in IPF pathogenesis. Nintedanib binds competitively to the adenosine triphosphate (ATP) binding pocket of these receptors and blocks the intracellular signaling which is crucial for the proliferation, migration, and transformation of fibroblasts representing essential mechanisms of the IPF pathology.

Nintedanib is a receptor tyrosine kinase inhibitor with potential antiangiogenic and antineoplastic activities. It is the only kinase inhibitor drug approved to treat idiopathic pulmonary fibrosis. that targets multiple receptor tyrosine kinases (RTKs) and non-receptor tyrosine kinases (nRTKs). Nintedanib inhibits the following RTKs: platelet-derived growth factor receptor (PDGFR) α and β, fibroblast growth factor receptor (FGFR) 1-3, vascular endothelial growth factor receptor (VEGFR) 1-3, and Fms-like tyrosine kinase-3 (FLT3). Among them, FGFR, PDGFR, and VEGFR have been implicated in IPF pathogenesis. Nintedanib binds competitively to the adenosine triphosphate (ATP) binding pocket of these receptors and blocks the intracellular signaling which is crucial for the proliferation, migration, and transformation of fibroblasts representing essential mechanisms of the IPF pathology.

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.

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.