(R)-Sulindac is the (R)-enantiomer of nonsteroidal anti-inflammatory drug (NSAID) Sulindac, that is marketed in the U.S. by Merck as Clinoril. Sulindac is a prodrug, derived from sulfinylindene, that is converted in vivo to an active sulfide compound by liver methionine sulfoxide reductases (Msr). The (Msr) family of enzymes includes two major classes, MsrA and MsrB, that specifically reduce the S- and R-epimers of Sulindac. Reduction of (R)-Sulindac to Sulindac Sulfide catalyzed by methionine sulfoxide reductase (Msr)-B. The oxidation of both epimers to sulindac sulfone is catalyzed primarily by the microsomal cytochrome P450 (P450) system. (S)-Sulindac increases the activity of the P450 system better than (R)-sulindac, but both epimers increase primarily the enzymes that oxidize (R)-sulindac. Both epimers can protect normal lung cells against oxidative damage and enhance the killing of lung cancer cells exposed to oxidative stress.

Azumolene is a direct-acting, skeletal muscle relaxant with structural similarities to dantrolene. It is a muscle relaxant that inhibits the release of calcium from skeletal muscle sarcoplasmic reticulum. Azumolene inhibits a component of store-operated calcium entry (SOCE) coupled to activation of type 1 ryanodine receptor (RyR1) by caffeine and ryanodine, whereas the SOCE component induced by thapsigargin is not affected. Azumolene distinguishes between two mechanisms of cellular signaling to SOCE in skeletal muscle, one that is coupled to and one independent from RyR1. Azumolene is equipotent to dantrolene sodium in blocking pharmacologic-induced muscle contractures and that azumolene is efficacious for treatment/prevention of malignant hyperthermia.

Pyritinol is a semi natural analogue of water soluble vitamin B6. Pyritinol was synthetized way back in 1961 by Merck Laboratories. After years of research, it entered the market in the 1970s, where it was used for clinical applications – including treating stroke patients and those with Alzheimer’s. Since the 1990s, it has been sold as a nootropic dietary supplement in the United States and many other parts of the world. Pyritinol, unlike many other nootropics, has been approved for use as a medical treatment in countries around the world. Doctors in many European countries use Pyritinol to treat patients with chronic degenerative brain disorders – like dementia. Countries where Pyritinol is an approved treatment include Austria, Germany, France, Greece, Italy, and Portugal. France has approved the use of Pyritinol – but only as a treatment for rheumatoid arthritis. Pyritinol is not currently licensed for use in the United Kingdom, but in most other countries, it’s available online or through drug stores as an over the counter substance. Pyritinol is marketed under the brand names Encephabol, Encefabol and Cerbon 6. One of the known mechanisms of action of Pyritinol involves increasing choline uptake into your neurons and thereby increasing acetylcholine levels. Pyritinol is also a great effective precursor to dopamine, which is one of the neurotransmitter mood-boosters in the brain. Pyritinol has better conversion into the neurochemical. This drug increases dopamine, which can keep the brain from anxiety because a lower dopamine level is connected to mood disorders and depression.

Fenoctimine is a nonanticholinergic inhibitor of gastric acid secretion in dogs and rats. Fenoctimine was more potent than cimetidine in the reduction of basal acid secretion in the gastric fistula rat and inhibited the production of gastric acid stimulated by histamine, gastrin tetrapeptide or bethanechol in the chronic gastric fistula dog. This compound is not an H2-antagonist but does inhibit the H+/K+-ATPase of hog gastric mucosa. The in vitro metabolism of fenoctimine by rat liver homogenates resulted in the oxidation of the aliphatic chain at the seven carbon, initially to an alcohol and then to a ketone. The unexpectedly weak effect of fenoctimine as a gastric antisecretory agent in humans, as well as anticholinergic effects, may be due to its extensive metabolism, which is different from that seen in dog and rat. The development of fenoctimine has been discontinued for unspecified reason.

Incadronate (Disodium Cycloheptylaminomethylene diphosphate) is used to treat malignancy-associated hypercalcemia (MAH) in Japan. Experiments on rodents have revealed that this drug could be an effective agent for the treatment of various arthritic conditions, including human rheumatoid arthritis. In addition was shown, that incadronate induced growth inhibition and apoptotic death of pancreatic cancer cells. Incadronate also inhibited migration presumably by preventing the activation of Rho by lysophosphatidic acid. Thus, this drug can be of value in regimens for the treatment of pancreatic cancer.

Loprazolam is a hypnotic drug which stimulates GABA-A receptors. Due to its hypnotic activity the drug is used to treat short-term sleep disordes.

Loprazolam is a hypnotic drug which stimulates GABA-A receptors. Due to its hypnotic activity the drug is used to treat short-term sleep disordes.

Obidoxime is an antidote for organophosphorous nerve agent poisoning including chlorosarin, cyclosarin (GF), R-33 (VR), R-VX, sarin (GB), tabun (GA), VX, chlorosoman, soman (GD), and organophosphorous pesticides. It acts as an acetylcholinesterase (AChE) reactivator. In combination with atropine obidoxime can be used to treat super toxic organophosphate poisoning by relieving the symptoms of skeletal neuromuscular blocking that occurs during a cholinergic crisis.

Fenoctimine is a nonanticholinergic inhibitor of gastric acid secretion in dogs and rats. Fenoctimine was more potent than cimetidine in the reduction of basal acid secretion in the gastric fistula rat and inhibited the production of gastric acid stimulated by histamine, gastrin tetrapeptide or bethanechol in the chronic gastric fistula dog. This compound is not an H2-antagonist but does inhibit the H+/K+-ATPase of hog gastric mucosa. The in vitro metabolism of fenoctimine by rat liver homogenates resulted in the oxidation of the aliphatic chain at the seven carbon, initially to an alcohol and then to a ketone. The unexpectedly weak effect of fenoctimine as a gastric antisecretory agent in humans, as well as anticholinergic effects, may be due to its extensive metabolism, which is different from that seen in dog and rat. The development of fenoctimine has been discontinued for unspecified reason.

Carumonam is a monobactam antibacterial agent. It was highly active in vitro against members of the family Enterobacteriaceae, Pseudomonas aeruginosa, and Haemophilus influenzae and weakly active against Streptococcus pneumoniae, but it was not active against Staphylococcus aureus. The excellent activity of carumonam against Gram-negative bacteria is related to its high affinity for their penicillin-binding proteins. It is indicated for the treatment of urinary tract infections, chronic respiratory infections, biliary tract infections, peritonitis, sepsis. Another factor that contributes to the excellent activity of carumonam against Gram-negative bacteria is its resistance to beta-lactamases. Adverse effects of the carumonam were limited to phlebitis at the intravenous infusion site; bloody diarrhea.