Benzoclidine (Oxylidin) exerts tranquilizing and hypotensive actions. It reduces the excitability of the central nervous system, enhances the effect of hypnotic drugs, analgesics and local anesthetics, has a moderate antihypertensive effect, reduces the excitability of the vasomotor centers, has anti-arrhythmic activity. Benzoclidine is marke indicated for the treatment of anxiety and depression of various origins (particularly mild expressed and associated with cerebrovascular insufficiency), neurosis, personality disorder, cyclothymia, hypertension with cerebral disorders, sinus tachycardia, paroxysmal tachycardia.

Meprylcaine (also known as Epirocaine and Oracaine) is a local anesthetic with stimulant properties that is structurally related to dimethocaine. Meprylcaine has a relatively potent inhibitory action on the monoamine transporter and inhibits the reuptake of dopamine, norepinephrine and serotonin. Oracaine is commonly used as the hydrochloride salt and is compatible with the known vasoconstrictors. It has a slightly more rapid onset than procaine with a slight increase in potency. The earliest symptoms of a toxic overdose are stimulation to the central nervous system, thus following the same symptoms as procaine. Not more than 400 mg. (20 ml. of a 2 per cent solution) should be used at any one time for the ambulatory patient. Oracaine, like metycaine, may be used for patients sensitive to the para-aminobenzoic acid derivatives. Oracaine hydrochloride is used at present mainly by the dental profession and in dermatologic surgery.

Benfluorex under trade name Mediator was launched in 1976 for controlling blood sugar levels in people with type 2 diabetes. In 2009 this drug together with others medicines containing it was withdrawn because of the risk of heart valve disease. The mechanisms by which benfluorex reduces hepatic gluconeogenesis are markedly different from those of metformin, the main antidiabetic compound used in the world. It was suggested that inhibition of gluconeogenesis by benfluorex was, at least in part, due to a decrease in mitochondrial β-oxidation. First, benfluorex decreased acetyl-CoA concentration, which in turn would reduce pyruvate carboxylase activity and release its inhibitory effect on pyruvate dehydrogenase. Second, benfluorex decreased both the ATP-to-ADP and the NAD+-to-NADH ratios, leading to a reduced gluconeogenic flux at the level of 3-phosphoglycerate kinase and GAPDH. Changes in cellular redox state represent probably the main mechanism by which benfluorex reduces glucose production in hepatocytes.