Droxicam is a nonsteroidal anti-inflammatory drug that is a pro-drug of piroxicam. The mechanism of action of droxicam, as well as that of piroxicam, is that of inhibition of prostaglandin biosynthesis. Droxicam acts by inhibition of PGE2. Although it belongs to the oxicam family, it is characterised by being a pro-drug of piroxicam, the molecule undergoing conversion by hydrolysis once dissolved in the digestive tract. Droxicam was used for the relief of pain and inflammation in musculoskeletal disorders such as rheumatoid arthritis and osteoarthritis. Droxicam possesses considerable analgesic activity, of equal magnitude to that of piroxicam and notably greater than that of acetylsalicylic acid, dipyrone, phenylbutazone and isoxicam. The antipyretic activity of droxicam, studied by means of different tests, has shown itself to be clearly superior to that of acetylsalicylic acid, dipyrone and 4-aminoantipyrine. Droxicam acts as an inhibitor of ex vivo platelet aggregation in the dog. However, owing to hepatotoxicity, droxicam was withdrawn in many countries.

PHENOPERIDINE is an opioid analgesic partly metabolized to meperidine in the liver. It is derived from pethidine by replacing the N methyl by a phenyl propanol chain. It is reputed to be a typical morphine-like analgesic characterized by its high potency, rapid onset of action, the intensity of its peak effect and the short duration of its pharmacological effects. It is used in general anesthesia.

3-hydroxy-2-phenylcinchoninic acid (also known as oxycinchophen or earlier as HPC) was known as antidiuretic and has been specially found useful in cases of diabetes insipidus. Clinical studies of HPC revealed that this compound reduces water output in cases of diabetes insipidus, and this was reached not by direct action on the water reabsorbing element in the tubules of the kidney, but rather by the mediation of HPC on the pituitary system in the production of the antidiuretic hormone therein. The effect of HPC upon fever and arthritis on patients with rheumatic fever was dramatic. In addition, HPC cannot be considered as an antipyretic, but rather HPC should be considered as enhancing ins some way the output or activity of adrenal cortical hormones. HPC was shown rather toxic (toxic reaction were presented in 20 % of tested patients). That is why the development of this drug was stopped and is become study its derivatives.

Anirolac is a nonsteroidal anti-inflammatory drug. It is chemically related to ketorolac, and to tolmetin and indomethacin, approved nonsteroidal anti-inflammatory drugs marketed as antiarthritics but not as analgesics. Anirolac has shown both analgesic and anti-inflammatory actions in animal models. Anirolac is absorbed rapidly and completely after oral intake and has a plasma elimination half-life of about 2 hours in humans with normal renal function. Anirolac is a cyclooxygenase inhibitor and also inhibits platelet aggregation in vitro. Drowsiness is the most common side effect associated with anirolac. The pain relief provided by oral anirolac was slower to take effect, safe, and lasted longer than that provided by injectable morphine sulfate. It potentiated the GABA-antagonistic effects of the quinolones (norfloxacin, ciprofloxacin, enoxacin, and pipemidic acid).

Amezepine is a tricyclic antidepressant which was never marketed.

Azapropazone is a non-steroidal anti-inflammatory drug. It is indicated for use in the treatment of rheumatoid arthritis, osteo-arthritis and gout. Gastro-intestinal disturbances, allergic skin rashes and photosensitivity, headache, vertigo, oedema and kidney impairment may occur. Gastro-intestinal bleeding and angioedema have been reported. Pre-treatment with this drug failed to modify plasma concentrations of phenobarbitone. Brain levels of imipramine or desmethyl imipramine were unaffected 60 minutes after oral administration of imipramine.

Mofezolac is an NSAID ) (non-steroidal anti-inflammatory drug), which acts via the cyclooxygenase enzyme, preferentially to COX-1. It also has potent inhibitory activity on the algesic responses induced by the mechanical stimulus of the inflamed tissue. It was introduced for the treatment of postoperative and posttraumatic pain, acute upper respiratory tract pain, osteoarthritis, and lumbago. It marketed only in Japan by Yoshitomi Pharmaceutical Ltd. Japan, was approved in July 1994.

Lumiracoxib is a COX-2 selective inhibitor non-steroidal anti-inflammatory drug. On August 11, 2007, Australia's Therapeutic Goods Administration (TGA, the Australian equivalent of the FDA) cancelled the registration of lumiracoxib in Australia due to concerns that it may cause liver failure. New Zealand and Canada have also followed suit in recalling the drug. It has never been approved for use in the United States. Lumiracoxib has a different structure from the standard COX-2 inhibitors (e.g. celecoxib). It more closely resembles the structure of diclofenac (one chlorine substituted by fluorine, the phenylacetic acid has another methyl group in meta position), making it a member of the arylalkanoic acid family of NSAIDs. It binds to a different site on the COX-2 receptor than the standard COX-2 inhibitors. It displays extremely high COX-2 selectivity. The mechanism of action of lumiracoxib is due to inhibition of prostaglandin synthesis via inhibition of cyclooygenase-2 (COX-2). Lumiracoxib does not inhibit COX-1 at therapeutic concentrations. Lumiracoxib is used for the acute and chronic treatment of the signs and symptoms of osteoarthritis of the knee in adults.

Alfadolone or alphadolone is an oral neurosteroid, which can be useful as an analgesic.

Droxypropine belongs to the cough suppressant.