Olamufloxacin (HSR-903) is an oral fluoroquinolone antimicrobial agent which has been reported to have a potent activity against respiratory pathogens, such as Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, Klebsiella pneumoniae, Staphylococcus aureus, Chlamydia spp. and Legionella spp., as well. Olamufloxacin inhibits DNA gyrase from the susceptible and resistant bacterial strains. It has been shown that olamufloxacin possesses a more potent antibacterial activity against potential respiratory pathogens compared with other quinolone derivatives. An oral formulation of olamufloxacin was undergoing phase III for Bacterial infections in Japan (Discontinued).

Lenampicillin is a prodrug of ampicillin that inhibits bacterial penicillin binding proteins (transpeptidase) and thus is effective against a wide range of bacterial infections. The drug was developed and marketed in Japan (Takacillin, Varacillin), however its current marketing status is unknown and supposed to be discontinued.

Dexfenfluramine, also marketed under the name Redux, is a serotoninergic anorectic drug. Dexfenfluramine, the dextrorotatory isomer of fenfluramine, is indicated for use in the management of obesity in patients with a body mass index of > or = 30 kg/m2, or > or = 27 kg/m2 in the presence of other risk factors. Unlike fenfluramine, dexfenfluramine is a pure serotonin agonist. Dexfenfluramine increases serotonergic activity by stimulating serotonin (5-hydroxytryptamine; 5-HT) release into brain synapses, inhibiting its reuptake into presynaptic neurons and by directly stimulating postsynaptic serotonin receptors. Dexfenfluramine reduces blood pressure, percent glycosylated hemoglobin, and concentrations of blood glucose and blood lipids, but these benefits may be indirect. Dexfenfluramine may also be of some value in controlling eating habits in diabetic patients, preventing weight gain after smoking cessation, and treating bulimia, seasonal affective disorder, neuroleptic-induced obesity, and premenstrual syndrome. Dexfenfluramine's most frequent adverse effects are insomnia, diarrhea, and headache; it has also been associated with primary pulmonary hypertension. The drug should not be combined with other serotonergic agonists because of the risk of serotonin syndrome. The recommended dosage is 15 mg twice daily. Dexfenfluramine is effective in the treatment of obesity in selected patients. Because its efficacy is lost after six months of continuous treatment, it should be viewed primarily as an adjunct to diet and exercise. Dexfenfluramine was approved by the FDA in 1996 and has been widely used for the treatment of obesity. However, Dexfenfluramine was removed from the U.S. market in 1997 following reports of valvular heart disease and pulmonary hypertension.

Adrenochrome monoaminoguanidine (S-Adchnon) is a hemostatic capillary-stabilizing agent demonstrating pharmacological effects against radiation injury by reducing side effects of radiation therapy on hematopoietic organ. Synthesized by a dehydrating reaction of adrenochrome and aminoguanidine it has superior properties than adrenochrome, an oxidation product of adrenalin remarkable for its efficiency as a haemostatic agent at very small doses and for its more rapid and equally intense action than that of adrenalin. Adrenochrome does not alter the cardiac rhythm and does not cause any hypertension or internal haemorrhages and would be suitable for therapeutic applications, however, its instability, in aqueous or alcoholic solution, makes its use substantially impossible. S-Adchnon was devised, approved by the Japanese Ministry of Health, Labor and Welfare in 1962 and used widely in Japan. Adrenochrome monoaminoguanidine has negligible toxicity, stable and could be made into salts for aqueous dosage, especially for injection. Adrenochrome monoaminoguanidine methanesulfonate (AMM) enhances the recovery from radiation-induced leukopenia in rabbits and in humans, and inhibits the increases in chromosome aberrations in peripheral lymphocytes of patients with cervical carcinoma under radiotherapy. It has been shown that the radiation-induced initial decrease in number of peripheral blood leukocytes (PBL) is not affected by AMM, but recovery from the decrease is enhanced, shortening the period of leukopenia. This suggests that AMM may not exert its effects by protecting PBL directly but by protecting stem and/or progenitor cells in hematogenesis which proliferate and differentiate to PBL after irradiation. In in vitro colony formation method AMM demonstrated a protective effect on the survival of GM-CFC, a hematopoietic progenitor cells. Differential action on cancer and normal tissue by AMM and cytochrome C combined with radiotherapy was demonstrated. AMM in combination with cytochrome C augumented natural killer (NK) cells activity in KSN nude mice, protected potent NK cells in patients with lung cancer against radiotherapy and sensitized the human lung cancer xenografts to radiotherapy. Thus, AMM and cytochrome C may have the potential as a differential modulator of radiosensitivity of normal tissues and of tumors.

Exatecan (DX-8951f), a new hexacyclic camptothecin analogue, is a second-generation topoisomerase inhibitor that prevents rapidly dividing cells from replicating by interrupting DNA transcription, ultimately leading to cell death. Preclinical studies showed exatecan to have broad-spectrum antitumor efficacy. Exatecan is in phase III clinical trials for the treatment of pancreas cancer. However, there is no recent report of this research. The compound was co-developed by Daiichi Pharmaceutical (now Daiichi Sankyo) and Yakult Honsha.

Nemonoxacin is a non-fluorinated quinolone antibiotic in clinical development in an oral and intravenous formulation. It exhibits potent antibacterial activities against Gram-positive, Gram-negative, and atypical pathogens, especially methicillin-resistant Staphylococcus aureus. The molecule inhibits bacterial DNA synthesis by forming a ternary complex with a DNA molecule and gyrase and topoisomerase IV enzymes, thus blocking bacterial DNA supercoiling. Nemonoxacin is developed by TaiGen Biotechnology Company and has reached worldwide approval in 2014 and is marketed under the name Taigexyn®.

Eperisone is an antispasmodic drug approved in Japan for the treatment of of diseases characterized by muscle stiffness and pain. It is believed that eperisone exerts its effect through inhibition of sodium channels. The drug is still being marketed in Asia under the name Myonal (Square Pharmaceuticals).

Fluocortolone is a topical corticosteroid (class of steroid hormones formed in the adrenal gland). Is primary indicated in condition like, Ana fissure, Dermatosis haemorrhoids, proctitis. The signs and symptoms that are produced after the acute overdosage include convulsions, respiratory arrest, allergic skin reactions. Glucocorticoids, such as fluocortolone, act through nuclear hormone receptors Schaaf and Cidlowski (2002). The two members of this family are glucocorticoid receptor (GR) type I and GR type I I. Activation of these sites alters gene expression of endogenous agents that influence immune and inflammatory responses.

Ximelagatran (Exanta or Exarta, H 376/95) is an anticoagulant that has been investigated extensively as a replacement for warfarin that would overcome the problematic dietary, drug interaction, and monitoring issues associated with warfarin therapy. In 2006, its manufacturer AstraZeneca announced that it would withdraw pending applications for marketing approval after reports of hepatotoxicity (liver damage) during trials, and discontinue its distribution in countries where the drug had been approved (Germany, Portugal, Sweden, Finland, Norway, Iceland, Austria, Denmark, France, Switzerland, Argentina and Brazil). Ximelagatran is a prodrug that is rapidly converted after oral administration to the active compound melagatran. Melagatran is able to inhibit thrombin activity directly and quickly. The melagatran molecule binds to the arginine side pocket of thrombin, inactivating the thrombin. Following oral administration of ximelagatran, oral bioavailability (measured as melagatran) is 18% to 25%. Peak melagatran levels after a ximelagatran dose of 48 mg twice daily are achieved within approximately 2 hours. Ximelagatran is rapidly and extensively converted to melagatran in the liver and other tissues. This conversion is achieved by ester hydrolysis and reduction via two intermediate metabolites, hydroxymelagatran, and ethylmelagatran. The predominant compound in plasma is the active drug, melagatran. The elimination half-life of melagatran after an oral dose of ximelagatran is 2.5 to 4.3 hours.

Cicletanine is a diuretic, developed by Ipsen for the treatment of hypertension. The drug was marketed in France by Recordati under the name Tenstaten. The mechanism(s) by which cicletanine exerts its biological effects has not been definitely established. The salidiuretic activity appears to be the result of an action of the sulfoconjugated metabolite of cicletanine, which inhibits the apical Na+-dependent Cl-/HCO3- anion exchanger in the distal convoluted tubule. The mechanism of the vasodilating effect of cicletanine may include stimulation of vascular prostaglandin synthesis, inhibition of the low Km cyclic GMP phosphodiesterases, and blockade of Ca2+ channels either directly or indirectly. The drug has also been shown to interact with other proteins, including alpha-adrenergic, vascular histamine, and muscarinic receptors.