METHYLPARABEN SUBEROHYDROXAMIC ACID PHENYL ESTER (more known as Remetinostat), a histone deacetylase (HDAC) inhibitor, was developed for the treatment of cutaneous T cell lymphoma (CTCL). This drug is participating in phase II clinical trial to evaluate the efficacy, safety, and tolerability to skin lesions in patients with early-stage cutaneous T-cell lymphoma. In May 2019 was announced the positive results from phase II trial of remetinostat in basal cell carcinoma (BCC) patients. Initial results suggest that remetinostat gel offers a potentially effective and well-tolerated, non-surgical intervention for the treatment of localized BCCs. The unique design of remetinostat enables topical application, making it active only in the skin. As soon as it reaches the blood stream, it is degraded, avoiding the side effects associated with other HDAC inhibitors. Besides, remetinostat was studied as the treatment of plaque psoriasis; however, this study was discontinued.

Menitrazepam is a cyclohexene-substituted benzodiazepine. It is a muscle relaxant.

Mefeclorazine is a non-steroidal anti-inflammatory drug. It inhibits prostaglandin synthesis.

Dexamisole is the dextro-isomer of tetramisole, a broad spectrum anthelmintic. Dexamisole significantly improves mood and psychotonicity. In adrenergically innervated blood vessels dexamisole inhibits neuronal uptake of norepinephrine more than levamisole. Dexamisole antagonized the reserpine-induced hypothermia but was ineffective in the apomorphine-induced hypothermia in mice. It reduced ptosis produced by reserpine in mice but this effect was very weak. The effect of dexamisole on the amphetamine-induced hyperactivity depended upon the animal species. Dexamisole reduced the duration of immobility in the despair test in rats. It did not modify the 5-HTP-induced head twitch reaction in mice but produced stimulation of the hind limb flexor reflex in spinal rats. The latter effect was blocked by phenoxybenzamine but not by cyproheptadine and metergoline. Dexamisole also exerted a sedative and hypothermic effect. The above findings indicate that the pharmacological profile of dexamisole resembles in some respects that of tricyclic antidepressants; they also point out that this drug has a central noradrenergic activity.

Axomadol is a centrally active analgesic agent with opioid agonistic properties and with inhibitory effects on the reuptake of the monoamines noradrenaline and, to serotonin [5‐hydroxytrypyamine (5‐HT)]. The drug participated in phase II clinical trials in the treatment of patients with moderate to severe chronic low back pain. As a result, the axomadol didn’t meet predetermined study endpoint, and studies were discontinued.

Alletorphine (R & S 218-M) is a potent analgesic said to have a reduced respiratory depressant action. It was isolated by Bentley and Hardy (1967) while they were examining a series of derivatives of tetrahydrothebaine of which the potent analgesic etorphine (propylorvinolhydrochloride: M99 Reckitt) is a member. R&S 218-M bears the same relationship to etorphine as does nalorphine to morphine. It has been the subject of experiments in animals and human volunteers.

Sulmepride (also known as TER 1546) is a sulfamoylbenzamide derivative patented by Heumann, Ludwig, und Co. G.m.b.H. as neuroleptic. Sulmepride acts as a specific antagonist of dopamine D-2 receptors.

Traboxopine (EGYT-2509) revealed specific dopamine-antagonistic activity with potentially minimal undesirable side effects. EGYT-2509 behaved as a dopamine receptor antagonist in all functional in vitro biochemical-pharmacological tests (striatal adenylate cyclase, striatal dopamine release, prolactin release from pituitary). The drug exhibited a marked preference for adenylate cyclase-coupled (D1) dopamine receptors, followed by the 3H-spiperone displacing potency at striatal receptors. Traboxopine exerts pharmacological and biochemical effects that seem to be partially similar to those of traditional neuroleptics, except for some undesirable side effects (e.g. cataleptogenic, influencing prolactin level). Traboxopine proved to be diversely influential on the dopaminergic components of the integration of sympathetic output and somato-autonomic reflexes. The apomorphine-induced stereotypy was potentiated by lower, and antagonized by higher doses of EGYT-2509. The in vitro potency of EGYT-2509 to block dopamine-mediated inhibition of prolactin release was weaker by three orders of magnitude than that of haloperidol.