Glafenine is a non-steroidal anti-inflammatory drug (NSAID). Glafenine was withdrawn due to the risk of anaphylaxis and acute kidney failure.

Guacetisal (Broncaspin) is a bronchomucotropic synthesized by the Bayer Italia S.p.A. Research Laboratories. It is obtained from the esterification of acetylsalicylic acid with guaiacol. Guacetisal was used for the treatment of chronic bronchitis and other inflammatory diseases of the respiratory tract. Guacetisal, used rectally, proved to be a valuable instrument for anti-inflammatory and anti-cough treatment in acute diseases of the airways in infancy.

Lisuride (DOPERGIN®), a highly active dopaminergic ergot derivative with prolactin-lowering properties, has a pronounced affinity for dopamine receptors. It may also act as an agonist at some serotonin receptors. Lisuride (DOPERGIN®) is concentrated within the pituitary where it acts on dopamine receptors which inhibit prolactin release. It can be used in the clinical conditions where a dopaminergic or prolactin-lowering effect is needed.

Piritramide is a synthetic opioid that has been used formore than 30 years in parts of Europe as the analgesic of choice for the management of postoperative pain. Piritramide was discovered at Janssen Pharmaceutica in 1960 and is currently manufactured and distributed within continental Europe and some other places by Janssen-Cilag. Piritramide is not available in all countries. It is marketed under the brand name Dipidolor in Germany, Lithuania, Slovenia, Austria. Piritramide is most commonly prescribed i.m. or i.v. for postoperative analgesia. It is used successfully for patient-controlled analgesia in adults 14 and more recently in chil-dren. Piritramide has potency 0.65 to 0.75 times that of morphine. Upon administration, piritramide binds to and activates mu-opioid receptors in the central nervous system (CNS), thereby mimicking the effects of endogenous opioids and producing analgesic relief. The most common side effect of piritramide appears tobe a dose-related incidence of sedation. It is reported in many studies, but rarely accurately quantified. Diaphoresis, urinary retention, flushing, focal myopathy and thrombophlebitis have all been reported. Piritramide is a strong opioid and therefore is regulated much the same as morphine in all known jurisdictions. It was never introduced in the United States and is therefore a Schedule I/Narcotic controlled substance. It is listed under international treaties and other laws such as the German Betabungsmittelgesetz, the Austrian Suchtgiftmittelgesetz, the Opium Laws of various other European countries, Canadian controlled substances act, UK Misuse of Drugs Act of 1971, and equivalents elsewhere.

TILIDINE is a low to medium potency opioid analgesic. It is metabolized to its active metabolites, nortilidine and bisnortilidine. Its analgesic activity is largely exerted through nortilidine which is a potent agonist at Mu opioid receptors.

Benorilate is an aspirin-paracetamol ester with analgesic, antiinflammatory, and antipyretic properties. After absorption, it is rapidly metabolised to salicylate and paracetamol. It has been used orally in the treatment of mild to moderate pain and fever. It has also been used in osteoarthritis, rheumatoid arthritis, and soft-tissue rheumatism. Associated adverse reactions: nausea, diarrhea or constipation, digestive disorders or heartburn, occasionally - a transient skin rash, and sleepiness. Benoral should not be administered concomitantly with probenecid or any other uricosuric agents that decrease tubular reabsorption as any form of salicylate antagonises this effect when given in doses of less than 5 gm per day.

Ziconotide (PRIALT; SNX-111) is a neuroactive peptide, which was approved by FDA in 2004 for the management of severe chronic pain in adult patients for whom intrathecal therapy is warranted, and who are intolerant of or refractory to other treatment, such as systemic analgesics, adjunctive therapies, or intrathecal morphine. Ziconotide acts as a selective N-type voltage-gated calcium channel blocker, which leads to a blockade of excitatory neurotransmitter release from the primary afferent nerve terminals.