Myristamidopropyl dimethylamine [MAPD] is an amidoamine compound that shows activity against Acanthamoeba as well as a variety of other causal agents of microbial keratitis. MAPD, present in Opti-Free Express Multi-Purpose Disinfecting solution for contact lenses, has been shown to exhibit anti-acanthamoeba activity. Challenge test assays were used to study the efficacy of 50 mg/L MAPD against Pseudomonas aeruginosa, Staphylococcus aureus, Candida albicans, Fusarium solani and Acanthamoeba polyphaga. MAPD gave a 3.7 log kill of P. aeruginosa after 60 min, 5.4 log for S. aureus by 45 min and 5 log for C. albicans and F. solani within 15 min. A. polyphaga cysts were reduced by 4 log within 120 min. MAPD also possesses excellent antifungal and antibacterial activity. MAPD may represent a broad-spectrum therapeutic antimicrobial for keratitis and surgical prophylaxis and deserves further evaluation in these roles. Myristamidopropyl dimethylamine uses and applications also include: surfactant; emulsifier for cosmetics and toiletries; conditioner; viscous builder; softener for textile finishes.

Oxaflozane is non-tricyclic antidepressant with serotoninergic action. In animals, oxaflozane has anti-cataleptic and anti-aggressive action with weak potentiation of stereotypes provoked by amphetamine. Oxaflozane was developed by Solvay Pharma and marketed in France under tradename Conflictan. The drug was discontinued in 2004.

Methylbenzethonium chloride is a quaternary ammonium with antimicrobial activity, which is used in combination with aminoglycoside antibiotic, paromomycin (brand name LESHCUTAN) for the topical treatment of cutaneous leishmaniasis.

Meglumine acetrizoate is a contrast agent used as a component of radiopaque medium in diagnostic procedures such as hysterosalpingography.

Temoporfin is a photosensitizer (based on chlorin) used in photodynamic therapy for the treatment of squamous cell carcinoma of the head and neck. It is marketed in the European Union under the brand name Foscan. It is used in patients in whom other treatments have stopped working, and who are not suitable for radiotherapy (treatment with radiation), surgery or systemic chemotherapy (medicines used to treat cancer; ‘systemic’ means that they are given as treatments throughout the body). When Foscan is injected, temoporfin is distributed within the body, including within the tumour. When it is illuminated with laser light of a specific wavelength, temoporfin is activated and reacts with oxygen in the cells to create a highly reactive and toxic type of oxygen. This kills the cells by reacting with and destroying their components, such as their proteins and DNA. By restricting the illumination to the tumour, cell damage is limited to the tumour cells, leaving other areas of the body unaffected. The U.S. Food and Drug Administration (FDA) declined to approve Foscan in 2000. The EU approved its use in June 2001.

A potent, selective and orally active receptor antagonist of leukotriene D4, verlukast (MK-571), was discovered and developed from a styrylquinoline lead structure based on a hypothetical model of the leukotriene D4 receptor. MK-571 blocks the action of LTD4 in animals and man, and is effective in a number of animal models of antigen-induced bronchoconstriction at plasma concentration at or below 2 ug/mL. MK-571 also blocks antigen-induced asthmatic responses in man. MK-571 is a potent and selective leukotriene D4 (LTD4) antagonist and ABCC multidrug resistance protein 1(MRP1) inhibitor. The cysteinyl leukotrienes (CysLTs), LTC4, LTD4, and LTE4, mediate their actions through two distinct G-protein coupled receptors. LTD4 is the preferred ligand for the CysLT1 receptor, whereas LTC4 and LTD4 bind with approximately equal affinity to the CysLT2 receptor. MK-571 is a selective, orally active CysLT1 receptor antagonist. It blocks the binding of LTD4, but not LTC4, to human and guinea pig lung membranes with Ki values of 0.22 nM and 2.1 nM, respectively. MK-571 effectively blocks LTD4 activation of recombinant human and mouse CysLT1 receptors but is ineffective at blocking LTC4 or LTD4 activation of the recombinant human or murine CysLT2 receptors.

Benidipine is an orally triple L-, T-, and N-type calcium channel blocker for the treatment of hypertension and angina pectoris synthesized and developed by Kyowa Hakko Kogyo Co., Ltd. Benidipine, approved in Japan in November 1991, has become one of the three best selling CCBs and is highly useful as a potent, long-lasting antihypertensive and antianginal agent.

Cinromide possesses antiepileptic activity in various animal models. However, in the experiments for human, this drug had a very limited clinical usefulness and was withdrawn from testing by its manufacturer. The lack of an antiepileptic response may have been due to factors other than species differences but indicates that a positive result of a drug in animal models is not the sole factor necessary to predict beneficial antiepileptic activity in humans. In addition, cinromide was studied for the patients with Lennox-Gastaut Syndrome, as a result, there was no difference between cinromide and placebo in terms of seizure reduction or global evaluations.

Bevantolol (INN) was a drug candidate for angina and hypertension that acted as both a beta blocker and a calcium channel blocker. Animal experiments confirm both agonist and antagonist effects on alpha-receptors, in addition to antagonist activity at beta-1 receptors. By binding and antagonizing beta-1 receptors Bevantolol inhibits the normal normal epinephrine-mediated sympathetic actions such as increased heart rate. This has the effect of decreasing preload and blood pressure. Bevantolol was discovered and developed by Warner-Lambert but in January 1989 the company announced that it had withdrawn the New Drug Application. As of 2016 it wasn't marketed in the US, UK, or Europe.

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.