MK-0941 is selective, allosteric glucokinase activator (GKA) that activates glucokinase (hexokinase subtype IV) with greater selectivity than over different hexokinase isoforms. In chronic oral toxicity studies in animals with MK-0941, cataracts were observed in rats and dogs at drug exposures of 3 and 1.5 times, respectively, the maximum predicted human exposure based on doses planned for further clinical development. No cataracts were observed in either species at drug exposures equal to the maximum predicted human exposure. In patients receiving stable-dose insulin glargine, the glucokinase activator MK-0941 led to improvements in glycemic control that were not sustained. MK-0941 was associated with an increased incidence of hypoglycemia and elevations in triglycerides and blood pressure.

Fenaftic acid is a choleretic agent.

FENFLUMIZOLE, an imidazole derivative, is a nonsteroidal, anti-inflammatory agent. It is a potent cyclooxygenase inhibitor with anti-phlogistic potency equalling that of indomethacin.

Levisoprenaline (l-isoproterenol) is beta1- and beta2-adrenoreceptor agonist. In Japan, continuous inhalation of levisoprenaline is a recommended treatment for pediatric patients with acute severe exacerbation. Compared with salbutamol, l-isoproterenol reduced modified pulmonary index score more rapidly. But in most countries do not recommend continuous inhalation of l-isoproterenol to treat pediatric patients with acute severe exacerbation of asthma due to worsening asthma control. Levisoprenaline was used to cause experimental chronic heart failure in rats.

Piconol (2-Pyridinemethanol) is a pyridylalcohol devivative with hypoglycemic activity.

FIBRACILLIN is a semisynthetic antibacterial agent.

IRINDALONE is an antihypertensive agent. It is a serotonin receptor antagonist with weak alpha 1-adrenoceptor blocking properties.

Pirinixil is an ethanolamine derivative of Wy-14,643 [4-chloro-6-(2,3-xylidino)-2-pyrimidinythio]acetic acid. It is the hypolipidemic agent of low toxicity. It has been reported to increase high density lipoprotein cholesterol levels in experimental animals. Pirinixil increased plasma cholesterol levels significantly without affecting plasma triglycerides. Pirinixil exerted a powerful antilipolytic activity against epinephrine, ACTH, nicotine and cold exposure. It is a potent inducer of liver peroxisones and of mitochondrial carmitine acetyltransferase. Pirinixil was developed treatment of hyperlipidemias and atherosclerosis. Pirinixil can increase generation of ROS, leading to DNA damage and p53 phosphorylation, which, in turn, induces the activation of Bax, release of cytochrome-c from mitochondria and activation of caspases, culminating in rat hepatoma FaO cell death.

Odiparcil is a novel, orally active beta-d-thioxyloside analog with antithrombotic activity associated with a reduced risk of adverse bleeding events. Its unique mechanism of action is postulated by means of an elevation in circulating endogenous chondroitin sulfate-related glycosaminoglycans (GAGs) levels. Odiparcil has demonstrated good tolerability, safety and efficacy in phase I and phase IIa studies, in approximately 700 healthy volunteers and 1100 patients. The drug has been investigated in several preclinical models and its potential has been proven in MPS. It may be therefore anticipated that Odiparcil could prove beneficial to MPS patients (MPS I, II and VI) as a substrate reduction therapy as a stand-alone treatment on in adjunction to current treatments. U.S. Food and Drug Administration (FDA) has granted Orphan Drug Designation to odiparcil (formerly known as IVA336) for the treatment of mucopolysaccharidosis VI (MPS VI), also known as Maroteaux-Lamy syndrome.

Indiplon is a nonbenzodiazepine, hypnotic sedative that was proposed for the treatment of insomnia. It is a high-affinity allosteric potentiator of GABAA responses that demonstrates preference for α1 subunit-containing GABAA receptors. There is minimal potential for adverse effects, residual daytime sedation, tolerance, respiratory depression. The simultaneous administration of indiplon and alcohol did not result in any significant pharmacokinetic changes. There is little risk of pharmacokinetic interaction between indiplon and any co-administered drugs. Developer (Neurocrine) decided to discontinue all clinical and marketing development of Indiplon in the United States.