MF63, a lead compound from a series of phenanthrene imidazole inhibitors made by Merck Frost, Quebec, Canada, with antipyretic and analgesic properties, is a candidate anti-inflammatory drug. MF63 is a selective inhibitor of mPGES-1 with high degree of selectivity over mPGES-2, PGI2, PGD2, and thromboxane (TX) synthases, Cox-1, Cox-2, 5-lipoxygenase, and various prostanoid and leukotriene receptors. It is a potent inhibitor of human (IC50 of 1.3 nM) and guinea pig (IC50 of 0.9 nM) mPGES-1, but displays little activity toward the rat or mouse enzyme. In a knock-in (KI) mouse, expressing human mPGES-1 and in guinea pig the compound selectively suppressed the synthesis of PGE(2), but not other prostaglandins inhibitable by nonsteroidal anti-inflammatory drugs (NSAIDs), yet retained NSAID-like efficacy at inhibiting lipopolysaccharide-induced pyresis, hyperalgesia, and iodoacetate-induced osteoarthritic pain. MF63 demonstrated effective relief of both pyresis and inflammatory pain in mice or nonhuman primates’ preclinical models of inflammation. In the guinea pig, MF63 strongly inhibited LPS-induced pyresis and hyperalgesia and relieved chronic osteoarthritic pain at 30–100 mg/kg. MF63 did not cause NSAID-like gastrointestinal toxic effects, such as mucosal erosions or leakage in mice.

Thiadiazole-pyridazine derivative MF-438 has been identified as a potent stearoyl-CoA desaturase 1 (SCD1) inhibitor. Recently it has been shown that the upregulation of lung-cancer stem cell (CSC) markers can be reverted with a combination of MF-438 and cisplatin. The combination of MF-438 and cisplatin strongly synergizes the inhibition of 3D spheroid formation and induces CSC apoptosis.

5,6-Dihydro-6-methyl-4h-thieno(2,3-b)thiopyran-4-ol 7,7-dioxide, (4S,6S)- is an intermediate for the synthesis of topically-active carbonic anhydrase inhibitor MK-0507.

L-760735 is a non-peptide substance P receptor (Neurokinin 1 (NK1) receptor) antagonist. It exerts anxiolytic, antidepressant and antinociceptive actions in animals. Merck was developing an L- 760735 as a potential antidepressant.

L-365,260 is an antagonist of gastrin and brain CCK-B receptor. In vivo, oral administration of L-365,260 antagonized gastrin-stimulated acid secretion. L-365,260 is used as a tool compound to investigate gastrin and brain CCK-B and their role in psysiology and disease. In a double-blind placebo-controlled study L-365,260 did not augment the analgesic effect of morphine in subjects with chronic neuropathic pain. Preclinical studies demonstrated modes activity of L-365,260 in models of anxiety and ulcers.

Rofecoxib is a nonsteroidal anti-inflammatory drug which selectively inhibits COX-2 and subsequent prostaglandin synthesis. The drug was developed by Merk and approved by FDA in 1999 for relief of signs and symptoms of arthritis, acute pain in adults, and painful menstrual cycles under the name Vioxx. Later on Merck voluntarily withdrawn Vioxx from the market due to safety concerns (high risk of heart attack and stroke).

Indinavir is an antiretroviral drug for the treatment of HIV infection. Indinavir is a protease inhibitor with activity against Human Immunodeficiency Virus Type 1 (HIV-1). Protease inhibitors block the part of HIV called protease. HIV-1 protease is an enzyme required for the proteolytic cleavage of the viral polyprotein precursors into the individual functional proteins found in infectious HIV-1. Indinavir binds to the protease active site and inhibits the activity of the enzyme. This inhibition prevents cleavage of the viral polyproteins resulting in the formation of immature non-infectious viral particles. Protease inhibitors are almost always used in combination with at least two other anti-HIV drugs.

Aniledrine is a narcotic pain reliver. The drug was prescribed as an analgesic in anaesthesia (Leritine brand name), however, it is no longer available on the market. Although the exact mechanism is not fully understood, aniledrine appears to elicit its action by binding to endorphine receptors in CNS.

Methbarbital is a barbiturate anticonvulsant, discovered by Merck in 1905. It was introduced to market for treatment of epolepsy by Abbott in 1952, and discontinued in 1990.

Vinyl ether (divinyl ether) is a clear colorless liquid with a characteristic odor. Less dense than water. Vapors heavier than air. Toxic by inhalation. Leake and Chen in 1930 demonstrated that vinyl ether possessed anaesthetic properties, and in 1931 a purer and more stable product was prepared in the research laboratories of Merck and Co. by Ruigh and Major and was used as ananaesthetic on dogs by Knoefel, Guedel, and Leake. These investigators found that dogs were more easily anaesthetized by vinyl ether than by chloroform. They also found that the period of recovery was rapid and free from vomiting; moreover, they did not notice any significant pathological effect on the various organs.The first experiments on human beings were conducted in 1933 by Gelfan and Bell. The first extensive account of vinyl ether anaesthesia in man was published in 1934, when Goldschmidt et al. reported having used it in operations in 461 mixed cases. In all these cases vinyl ether appeared to have no undesirable effect on respiration, the circulation, the liver, or the kidneys. Vinyl ether was widely used in Europe and North America for at least 30 years, until it was replaced by halothane. Vinyl ether was marketed under the name of Vinethine in the United States, Vinesthine in the United Kingdom, and Vinydan in continental Europe. Vinyl ether outlasted many of the inhalation agents introduced in recent years, and served a very useful purpose until safer, non-flammable agents, became available in the mid1960s.