Dapivirine, an anti-retroviral (ARV)-based microbicide, is a substituted diaminopyrimidine (DAPY) derivative and a potent non-nucleoside reverse-transcriptase inhibitor (NNRTI) with antiviral activity against HIV-1. Dapivirine showed high activity against wild-type and mutant HIV in in virto HIV models inhibiting a broad panel of HIV-1 isolates from different classes, including a wide range of NNRTI-resistant isolates. Developed by Janssen Sciences (formerly Tibotec Pharmaceuticals), dapivirine was initially tested as an oral treatment for HIV in a number of Phase I/II clinical trials. In 2014 the International Partnership for Microbicides (IPM) began its work on the monthly dapivirine ring. Phase I/II clinical trials in Africa, Europe and the United States proved that dapivirine is safe and well-tolerated. Phase III long-term safety and efficacy studies of the monthly dapivirine ring as part of IPM's Dapivirine Ring Licensure Program confirmed that the monthly dapivirine ring can safely help prevent HIV infection in women. In 2016 the ASPIRE Study reported a 27 percent reduction in HIV-1 acquisition with a trend toward greater protection in women over age 21 and no significant protection for women under age 21.

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.

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.

Clonixin is a nonsteroidal agent. It is an anilino-nicotinic acid derivative. It is a drug of anti-inflammatory antipyretic and analgesic activity that produces minor digestive side-effects. At high concentrations, clonixin inhibited PGE2 formed by COX-2 and partly by COX-1 activity. The drug is indicated for the relief of headaches, muscle aches, joint, dental, ear, dysmenorrhea, post-traumatic, post-surgical, gynecological. Adverse effects are occasionally nausea, dizziness, and somnolence, were mild and transient. On rare occasions, and administering high doses, it is possible the appearance of dry mouth or constipation. Concomitant use of anticholinergic drugs to be avoided by the possibility that they enhance their effects atropine.

Pizotifen (INN) or pizotyline (USAN), trade name Sandomigran, is a benzocycloheptene-based drug used as a medicine, primarily as a preventative to reduce the frequency of recurrent migraine headaches. Pizotifen is a serotonin antagonist acting mainly at the 5-HT2A and 5HT2C receptors. It also has some activity as an antihistamine as well as some anticholinergic activity. The main medical use for pizotifen is for the prevention of vascular headache including migraine and cluster headache. Pizotifen is one of a range of medications used for this purpose, other options include propranolol, topiramate, valproic acid and amitriptyline. While pizotifen is reasonably effective, its use is limited by side effects, principally drowsiness and weight gain, and it is usually not the first choice medicine for preventing migraines, instead being used as an alternative when other drugs have failed to be effective. It is not effective in relieving migraine attacks once in progress. Pizotifen has also been reported as highly effective in a severe case of erythromelalgia, a rare neurovascular disease that is sometimes refractory to the other drugs named above. Side effects include sedation, dry mouth, drowsiness, increased appetite and weight gain. Occasionally it may cause nausea, headaches, or dizziness. In rare cases, anxiety, aggression and depression may also occur. Pizotifen is well absorbed from the gastro-intestinal tract, peak plasma concentrations occurring approximately 5 hours after oral administration. The absorption of pizotifen is fast (absorption half life 0.5 to 0.8 hours) and nearly complete (80%). Over 90% is bound to plasma proteins. Pizotifen undergoes extensive metabolism. Over half of a dose is excreted in the urine, chiefly as metabolites; a significant proportion is excreted in the faeces. The primary metabolite of pizotifen (N-glucuronide conjugate) has a long elimination half-life of about 23 hours.

Hymecromone (4-methylumbelliferone) is already approved drug in Europe and Asia where it is used to treat biliary spasm. It is used as choleretic and antispasmodic drugs and as a standard for the fluorometric determination of enzyme activity. The concomitant administration of Hymecromone with products, containing metoclopramide, leads to mutual decrease of their action. Due to a danger of diarrhea with subsequent hypokalemia, Hymecromone should be applied with caution to patients on cardiac glycosides therapy (in these cases the sensitivity to them is increased). Hymecromone can be administered simultaneously with otherspasmolytics and analgesics. Very rare allergic reactions, itching, erythema, rashes; diarrhea which normally disappears by reduction of dose or discontinuance of therapy.

Hydroxytamoxifen (Afimoxifene) is an active metabolite of tamoxifen exerting estrogen receptor modulatory function. In addition, hydroxytamoxifen binds to regulates transcriptional activity of the estrogen-related receptor gamma. ASCEND Therapeutics, Inc. was developing TamoGel (4-hydroxytamoxifen gel) for a variety of estrogen-dependent conditions, including breast cancer, cyclic breast pain and gynecomastia.

Strychnine is an indole alkaloid obtained from the seeds of the Indian tree Strychnos nux-vomica. It gets its scientific name “strychnos” from Carl Linnaeus, who classified it back in 1753, but it was known to the population of India way before then. Nux vomica originates in India. Strychnine-containing baits are currently labelled for below-ground use and are intended for the control of pocket gophers. Their use as indoor pesticides has been eliminated since 1989. In the past, strychnine has been used as a pesticide to control rats, moles, gophers, and coyotes. Strychnine is highly toxic to most domestic animals. Strychnine is a competitive antagonist at glycine receptors and thus a convulsant. It has been used as an analeptic, in the treatment of nonketotic hyperglycinemia and sleep apnea.

Diclofenac is a nonsteroidal anti-inflammatory drug (NSAID) of the phenylacetic acid class with anti-inflammatory, analgesic, and antipyretic properties. Contrary to the action of many traditional NSAIDs, diclofenac inhibits cyclooxygenase (COX)-2 enzyme with greater potency than it does COX-1. In addition diclofenac can inhibit the thromboxane-prostanoid receptor, affect arachidonic acid release and uptake, inhibit lipoxygenase enzymes, and activate the nitric oxide-cGMP antinociceptive pathway. Other novel mechanisms of action may include the inhibition of substrate P, inhibition of peroxisome proliferator activated receptor gamma (PPARgamma), blockage of acid-sensing ion channels, alteration of interleukin-6 production, and inhibition of N-methyl-D-aspartate (NMDA) receptor hyperalgesia. Similar to other NSAIDs, diclofenac is associated with serious dose-dependent gastrointestinal, cardiovascular, and renal adverse effects. Since its introduction in 1973, a number of different diclofenac-containing drug products have been developed with the goal of improving efficacy, tolerability, and patient convenience. Delayed- and extended-release forms of diclofenac sodium were initially developed with the goal of improving the safety profile of diclofenac and providing convenient, once-daily dosing for the treatment of patients with chronic pain. New drug products consisting of diclofenac potassium salt were associated with faster absorption and rapid onset of pain relief. These include diclofenac potassium immediate-release tablets, diclofenac potassium liquid-filled soft gel capsules, and diclofenac potassium powder for oral solution. The advent of topical formulations of diclofenac enabled local treatment of pain and inflammation while minimizing systemic absorption of diclofenac. SoluMatrix diclofenac, consisting of submicron particles of diclofenac free acid and a proprietary combination of excipients, was developed to provide analgesic efficacy at reduced doses associated with lower systemic absorption. The drug's likely impact on the Asian vulture population was widely reported. The dramatic mortality was attributed largely to renal failure caused by exposure to diclofenac in livestock carcasses on which the birds fed. Although not the most endearing species, vultures are important environmental scavengers and, since veterinary use of diclofenac was stopped in the region in 2006, the decline in vulture numbers has slowed.