Ethynerone (MK 665) is an oral contraceptive steroid. In preclinical studies, it induced mammary tumors.

Ciprocinonide (RS-2386) is a synthetic glucocorticoid corticosteroid. It was developed in the 1980s for a topical administration as a component of the Triple Corticoid Integrated System.

Procinonide is a derivative of fluocinolone acetonide that has been applied topically with fluocinonide and ciprocinonide in the management of various skin disorders.

KETAZOCINE, a benzomorphan derivative, is a kappa opioid receptor agonist. It is used in opioid receptor research.

Disobutamide suppresses ventricular arrhythmias in several in vivo animal models. In particular, disobutamide suppressed ventricular arrhythmias in ouabain-toxic dogs and in dogs in which myocardial infarction. Clear cytoplasmic vacuolation associated with disobutamide is an example of a remarkable morphologic change not associated with apparent overt toxicity based on various functional tests. Clinically in the dog if vacuolation was associated with cell injury, one might expect a chronic debilitating condition as seen in the case of many spontaneous genetic storage diseases. Chronic heart failure or a gastrointestinal motility disorder might occur as a result of the changes in the musculature of coronary arteries or gastrointestinal wall, respectively. Disobutamide, because of its apparent low toxicity, can be recommended as useful for investigations aimed at determining the borderline between physiologic limits and toxicity of intracellular drug storage and for advancing knowledge of mechanisms involved in xenobiotics entry and storage in cells. Disobutamide was withdrawn from clinical testing when clear cytoplasmic vacuoles were found in the rat and dog during toxicity studies. Disobutamide induced vacuoles in all cell types except rat leukaemia. The drug induced cell death and reduction in confluency or cell count in cultures of all cell types except rat carcinoma and rabbit aorta muscle.

Chloralose (alpha-Chloralose, 1,2-O-(2,2,2-Trichloroethylidene)-α-D-glucofuranose) is an avicide, and a rodenticide commonly used for the control of mice and birds. Since its initial description in 1893, alpha-chloralose has undergone extensive pharmacologic evaluation. It has been characterized as a compound possessing potent CNS activity and has been evaluated in humans and animal models for its therapeutic properties. Though the toxicity of the compound prohibits its use as a human therapeutic agent, it has been employed widely as an animal anesthetic in the laboratory setting. α-Chloralose is widely used as an anesthetic in studies of the cerebrovasculature because of its presumed minimal depression of autonomic function. α-Chloralose acts as the positive allosteric modulator of GABA-A receptor and increases the affinity for GABA 5-fold and produced a small increase in the efficacy of GABA. Studies of α-Chloralose interactions with other allosteric modulators determined that α-Chloralose binds to a site on the GABAA receptor complex distinct from the benzodiazepine, neurosteroid and barbiturate sites.

SR 202 is an antagonist of peroxisome proliferator-activated receptor γ (PPARγ) transcriptional activity induced by troglitazone but not of basal PPARγ activity. It is selective for PPARγ, not affecting basal or agonist-induced transcriptional activity of PPARα, PPARβ, or the farnesoid X receptor (FXR). It inhibits PPARγ-dependent differentiation of preadipocyte 3T3-L1 cells in a dose-dependent manner. SR 202 (400 mg/kg) decreases the amount of weight gained and white adipose tissue mass accumulated by mice fed a standard or high-fat diet for ten weeks and is associated with lower PPARγ mRNA levels. It protects against high-fat diet-induced insulin resistance in wild-type mice and improves insulin sensitivity in ob/ob mice.

Halofenate (MK-185) was invented as a hypolipidemic and hypouricemic agent. It was shown that halofenate lower serum triglycerides and uric acid in patients with a variety of hyperlipidemias. Treatment of dyslipidemic type 2 diabetic patients also showed triglyceride lowering and, surprisingly, significant reductions in plasma glucose and insulin. Halofenate is a selective PPAR-γ modulator (SPPARγM). SPPARγMs are believed to bind in distinct manners to the ligand-binding pocket of PPAR-γ, leading to altered receptor conformational stability and resulting in distinct patterns of gene expression. Thus, was suggested that halofenate hold promising therapeutic potential in the treatment of type 2 diabetes, without the side effects. However, information about the current use of this compound is not available.