Pralidoxime is a cholinesterase reactivator used as the antidote to organophosphate pesticides or acetylcholinesterase inhibitors (nerve agents) in conjunction with atropine and diazepam. Organophosphates bind to the esteratic site of acetylcholinesterase, which results initially in reversible inactivation of the enzyme. Acetylcholinesterase inhibition causes acetylcholine to accumulate in synapses, producing continuous stimulation of cholinergic fibers throughout the nervous systems. If given within 24 hours after organophosphate exposure, pralidoxime reactivates the acetylcholinesterase by cleaving the phosphate-ester bond formed between the organophosphate and acetylcholinesterase. Pralidoxime is indicated as an adjunct in the treatment of moderate and severe poisoning caused by organophosphate pesticides that have anticholinesterase activity or by chemicals with anticholinesterase activity such as some chemicals used as nerve agents during chemical warfare. Pralidoxime is also indicated as an adjunct in the management of the overdose of cholinesterase inhibitors, such as ambenonium, neostigmine, and pyridostigmine, used in the treatment of myasthenia gravis. Pralidoxime, used in conjunction with atropine, reverses nicotinic effects, such as muscle weakness and fasciculation, respiratory depression, and central nervous system (CNS) effects, associated with toxic exposure to organophosphate anticholinesterase pesticides and chemicals and with cholinesterase inhibitor overdose. Atropine, by antagonizing the action of cholinesterase inhibitors at muscarinic receptor sites, reverses muscarinic effects, such as tracheobronchial and salivary secretion, bronchoconstriction, bradycardia, and, to a moderate extent, CNS effects.

Niacin (also known as vitamin B3 and nicotinic acid) is bio converted to nicotinamide which is further converted to nicotinamide adenine dinucleotide (NAD+) and the hydride equivalent (NADH) which are coenzymes necessary for tissue metabolism, lipid metabolism, and glycogenolysis. Niacin (but not nicotinamide) in gram doses reduces LDL-C, Apo B, Lp(a), TG, and TC, and increases HDL-C. The increase in HDL-C is associated with an increase in apolipoprotein A-I (Apo A-I) and a shift in the distribution of HDL subfractions. These shifts include an increase in the HDL2:HDL3 ratio, and an elevation in lipoprotein A-I (Lp A-I, an HDL-C particle containing only Apo A-I). The mechanism by which niacin alters lipid profiles is not completely understood and may involve several actions, including partial inhibition of release of free fatty acids from adipose tissue, and increased lipoprotein lipase activity (which may increase the rate of chylomicron triglyceride removal from plasma). Niacin decreases the rate of hepatic synthesis of VLDL-C and LDL-C, and does not appear to affect fecal excretion of fats, sterols, or bile acids. As an adjunct to diet, the efficacy of niacin and lovastatin in improving lipid profiles (either individually, or in combination with each other, or niacin in combination with other statins) for the treatment of dyslipidemia has been well documented. The effect of combined therapy with niacin and lovastatin on cardiovascular morbidity and mortality has not been determined. In addition, preliminary reports suggest that niacin causes favorable LDL particle size transformations, although the clinical relevance of this effect is not yet clear. April 15, 2016: Based on several large cardiovascular outcome trials including AIM-HIGH, ACCORD, and HPS2-THRIVE, the FDA decided that "scientific evidence no longer supports the conclusion that a drug-induced reduction in triglyceride levels and/or increase in HDL-cholesterol levels in statin-treated patients results in a reduction in the risk of cardiovascular events" Consistent with this conclusion, the FDA has determined that the benefits of niacin ER tablets for coadministration with statins no longer outweigh the risks, and the approval for this indication should be withdrawn.

Methyl salicylate (or methyl 2-hydroxybenzoate), also known as wintergreen oil, is a natural product and is present in white wine, tea, porcini mushroom Boletus edulis, Bourbon vanilla, clary sage, red sage and fruits including cherry, apple, raspberry, papaya and plum. Methyl salicylate is topically used in combination with methanol and under brand name SALONPAS to temporarily relieves mild to moderate aches and pains of muscles and joints associated with: strains, sprains, simple backache, arthritis, bruises. The precise mechanism of action of methyl salicylate is not known, but there is suggested, that it cause dilation of the capillaries thereby increasing blood flow to the area.

Sulverapride is a methylsulfamoylbenzamide derivative patented by Societe d'Etudes Scientifiques et Industrielles de l'Ile-de-France for the treatment of lower urinary tract disorders

MK-0767 is a potent hypoglycaemic insulin sensitizer being evaluated by Kyorin with potential as an antidiabetic agent. MK-0767 acts as a dual agonist of the peroxisome proliferator-activated receptors alpha and gamma, induced high-affinity interactions of PPARα and PPARγ with the transcriptional coactivator CBP in vitro. In ob/ob mice, MK-0767 normalized hyperglycemia and hyperinsulinemia with equal or greater potency and efficacy than pioglitazone. Treatment of hamsters with MK-0767 produced substantial reductions in blood cholesterol and triglycerides. In dogs, MK-0767 reduced serum cholesterol levels with a potency more than 10-fold greater than simvastatin. The efficacies of MK-0767 and simvastatin were additive when given together.

Trigonelline is a pyridine derivative known to contribute indirectly to the formation of desirable flavor products, including furans, pyrazine, alkyl-pyridines, and pyrroles, during coffee roasting. The amount of trigonelline in arabica is higher than that in robusta green coffee beans, and thus it can be used as a marker compound to distinguish the coffee bean species. During the roasting process of coffee beans, trigonelline changes into N-methylpyridinium and nicotinic acid as its major products, which makes it a useful index of the degree of roasting. The importance of trigonelline in coffee is connected to nutritional aspects. It has been revealed in recent studies that the administration of trigonelline allows diabetic rats to avoid diabetes-related organ damage and live longer, which can make it a potentially strong candidate for industrial application as a pharmacological agent for the treatment of hyperglycemia, hyperlipidemia, and liver/kidney dysfunctions. In addition, the urinary concentrations of trigonelline and its thermal product N-methylpyridinium of coffee drinkers are higher than those of noncoffee drinkers, which indicates that trigonelline and N-methylpyridinium may have potential as dietary biomarkers that could be used as analytical probes to control compliance in human intervention studies on coffee. Trigonelline has been isolated from many plants: fenugreek seeds (Trigonella foenum-graecum, hence the name), garden peas, hemp seed, oats, potatoes, Stachys species, dahlia, Strophanthus species, and Dichapetalum cymosum. In a randomized cross-over trial, the critical effect of Trigonelline on glucose tolerance has been studied during a 2-hour oral glucose tolerance test (OGTT) in 15 overweight men. Results showed that glucose and insulin concentrations significantly reduced 15minutes after Trigonelline consumption compared with placebo.