2-methyl-4,6-dinitrophenol (4,6-Dinitro-ortho-cresol, DNOC) is a yellow crystalline solid. DNOC is used agriculturally as a larvicide, ovicide and insecticide (against locusts and other insects) as well as a potato haulm desiccant. It is also used as a polymerization inhibitor and as an intermediate in the chemical industry. For agricultural uses, DNOC is mainly formulated as emulsifiable concentrate, either aqueous or oily. 4,6-Dinitro-o-cresol is an uncoupler of the mitochondrial respiratory system. It causes an increase in basal metabolic rate with raised temperature and weight loss in man and animals. After metabolic activation, 4,6-dinitro-o-cresol has mutagenic potential in vitro. In vivo, evidence of clastogenic effects was obtained with a herbicide containing 4,6-dinitro-o-cresol but not with the pure substance. A long-term study with rats yielded no evidence of carcinogenic effects. During the 1930s, DNOC, along with dinitrophenol, was used therapeutically as a weight-loss agent after animal experiments had demonstrated that dinitrophenols increased the basal metabolic rate (BMR). The earliest mention of the use of these compounds for weight loss is a publication by Cutting and Tainter (1933) in which the authors reported clinical studies of dinitrophenol for this purpose. Dodds and Robertson (1933) reported that the related compound, DNOC, exhibited a greater effect on metabolism than dinitrophenol, leading to the marketing of DNOC for weight loss. Following the publication of these reports, dinitrophenol, and to a lesser extent, DNOC, began selling in drug stores and was prescribed by physicians for weight loss. DNOC acts mainly as an inhibitor of oxidative phosphorylation at the mitochondrial level, inducing a significant increase in basal metabolism and hyperthermy. The oxidation of carbohydrate forms the main source of energy of the body and the energy is “stored” in the form of compounds containing phosphate (high energy phosphate bonds of adenosine triphosphate or ATP). This compound is then a source of energy to the body. DNOC inhibits the formation of ATP. In the presence of DNOC the oxidative process continues and is even increased, but the energy cannot be converted to a useable form and it is therefore dissipated as heat. In muscle ATP cannot be re-synthesized and is progressively broken down to adenylic acid. The shortage of ATP may lead to muscular paralysis which for critical organs, such as heart and respiratory muscles, includes a blocking of their vital functions and in the case of death by DNOC poisoning, to early rigor mortis.