Ripazepam (CI 683 or pyrazapon) is a pyrazolodiazepine that has anxiolytic effects. It is related to certain benzodiazepines such as zolazepam. In animal studies, it showed anxiolytic effects without sedative or depressant effects. In rats, it did not elicit a tumorigenic potential. Although ripazepam was found significantly superior to placebo and was well tolerated in neurotic patients, it has never been marketed for clinical use.

Metalol is an antagonist at beta-adrenergic receptors.

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

Oxisuran was developed by Parke-Davis as an antineoplastic agent. It was shown that this drug was a differential inhibitor of cell-mediated hypersensitivity. Experiments on rodents with experimental autoimmune encephalomyelitis have revealed that oxisuran was pharmacologically effective. However, information about the further development of the compound is not available.

Picropodophyllin (also known as picropodophyllotoxin (PPP)), an orally active insulin-like growth factor 1 receptor (IGF1R) inhibitor that exhibits no activity at the insulin receptor, FGFR, PDGFR or EGFR. Picropodophyllin possesses antineoplastic activity. PPP is currently tested as an orally administrated single agent treatment in an open-label combined Phase I/II clinical study in advanced cancer patients with solid tumors which progress in spite of several lines of treatment. In addition, it effectively inhibits rhambodmyosarcomas tumor proliferation and metastasis in vitro and in an animal model.

Porfiromycin is an N-methyl derivative of the antineoplastic antibiotic mitomycin-C initially isolated from Streptomyces ardus. Upon administration, the drug undergoes chemical or enzymatic reduction, followed by spontaneous loss of the tertiary methoxy (hydroxyl) group and formation of an aromatic indole system. Thus activated, porfiromycin generates oxygen radicals and alkylates DNA, producing interstrand cross-links and single-strand breaks at guanosine residues. Porfiromycin was tested in phase III for head and neck carcinoma, however, its development was terminated.

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.