Vetrabutine is a spasmolytic agent. As a musculotropic spasmolytic agent vatrabutine was reported to act directly on the smooth muscle fibers and to have no neurotropic activity. In pigs, its activity was specific to the uterine body and cervical musculature where it acted on the myometrial cells, sealing off the membrane against the passage of potassium ions, thereby increasing membrane potential and lowering tonus. Vetrabutine was of moderate acute oral toxicity. Vetributine hydrochloride has been used in human medicine as a spasmolytic agent in obstetrics.

Adrenochrome monoaminoguanidine (S-Adchnon) is a hemostatic capillary-stabilizing agent demonstrating pharmacological effects against radiation injury by reducing side effects of radiation therapy on hematopoietic organ. Synthesized by a dehydrating reaction of adrenochrome and aminoguanidine it has superior properties than adrenochrome, an oxidation product of adrenalin remarkable for its efficiency as a haemostatic agent at very small doses and for its more rapid and equally intense action than that of adrenalin. Adrenochrome does not alter the cardiac rhythm and does not cause any hypertension or internal haemorrhages and would be suitable for therapeutic applications, however, its instability, in aqueous or alcoholic solution, makes its use substantially impossible. S-Adchnon was devised, approved by the Japanese Ministry of Health, Labor and Welfare in 1962 and used widely in Japan. Adrenochrome monoaminoguanidine has negligible toxicity, stable and could be made into salts for aqueous dosage, especially for injection. Adrenochrome monoaminoguanidine methanesulfonate (AMM) enhances the recovery from radiation-induced leukopenia in rabbits and in humans, and inhibits the increases in chromosome aberrations in peripheral lymphocytes of patients with cervical carcinoma under radiotherapy. It has been shown that the radiation-induced initial decrease in number of peripheral blood leukocytes (PBL) is not affected by AMM, but recovery from the decrease is enhanced, shortening the period of leukopenia. This suggests that AMM may not exert its effects by protecting PBL directly but by protecting stem and/or progenitor cells in hematogenesis which proliferate and differentiate to PBL after irradiation. In in vitro colony formation method AMM demonstrated a protective effect on the survival of GM-CFC, a hematopoietic progenitor cells. Differential action on cancer and normal tissue by AMM and cytochrome C combined with radiotherapy was demonstrated. AMM in combination with cytochrome C augumented natural killer (NK) cells activity in KSN nude mice, protected potent NK cells in patients with lung cancer against radiotherapy and sensitized the human lung cancer xenografts to radiotherapy. Thus, AMM and cytochrome C may have the potential as a differential modulator of radiosensitivity of normal tissues and of tumors.

Roxindole (EMD-49,980) is a dopaminergic and serotonergic drug which was originally developed for the treatment of schizophrenia. Roxindole has also been investigated as a therapy for the major depressive disorder, Parkinson's disease, and prolactinoma. Roxindole is dopamine autoreceptor-selective agonistic drug with high affinity to D2-like receptors and with much lower affinities to D1-like, % and ol2, muscarinic and 5HT 2 receptors. Additionally, Roxindole exerts 5HT uptake inhibition and 5HT1A agonistic effects. The bioavailability of Roxindole has been estimated at 5% due to a high first-pass metabolization. On the other hand, in 14C distribution studies, Roxindole has crossed the blood-brain barrier readily and the brain concentrations at all intervals have been much higher than corresponding plasma levels. In clinical trials, Roxindole ‘s antipsychotic efficacy was only modest but it was unexpectedly found to produce potent and rapid antidepressant and anxiolytic effects. However, the clinical development of Roxindole was discontinued.

Picloxydine is a heterocyclic biguanide with antibacterial and antiplaque activity. 0.4% Picloxydine produces a highly significant drop in the number of aerobic organisms. 0.4% Picloxydine is far more effective than 0.2% Picloxydine or chlorhexidine in reducing the total viable count of oral aerobic and anaerobic organisms. It is used to treat superficial eye infections. Picloxydine is also used in eye drops in the topical therapy of trachoma. This drug can cause side effects - local intolerance reactions (temporary irritation, allergic reactions).

THALLOUS OXIDE (Thallium (1) Oxide) has been used in the manufacturing of glass of a high coefficient of refraction for optical purposes (thallium flint glass) and for artificial gems. Thallium oxide is black in color and is the inorganic compound of Thallium and Oxygen. THALLOUS OXIDE compounds are typically insoluble in aqueous solutions (water) and extremely stable making them useful in ceramic structures as simple as producing clay bowls to advanced electronics (e.g. tablets) and in light weight structural components in aerospace and electrochemical applications such as fuel cells. THALLOUS OXIDE is toxic by ingestion. It has previously been used as rat poison and ant killer, but its use is prohibited since 1972.

Hexobendine (Ustimon or ST7090) is a vasodilator. It inhibits uptake of adenosine and cAMP. Hexobendine was investigated in clinical trials for the treatment of cerebrovascular and coronary artery diseases.

Tiemonium (often used in a form of iodide or methylsulphate salt) is a muscarinic acetylcholine receptor antagonist, which is available in Asia (mainly Bangladesh) for the alleviation of muscle spasms of the intestine, biliary system, uterus and urinary bladder in gastrointestinal, biliary, urinary and gynecological diseases.

Viquidil is an isomer of quinidine and papaverine derivative. Viquidil is used for treatment of disturbances of cerebral blood flow and metabolism. Viquidil, however, appeared to be approximately twice as potent as papaverine in inhibition of thrombus formation in the microvasculature and was apparently without toxic side-effects.

Nizofenone (Ekonal, Midafenone) is a neuroprotective drug which protects neurons from death following cerebral anoxia (interruption of oxygen supply to the brain). It might thus be useful in the treatment of acute neurological conditions such as stroke. Nizofenone ameliorates various pathophysiologic events during ischemia, such as ATP depletion, lactate accumulation, glutamate release, free fatty acid liberation, edema, and neuronal degeneration; in particular, ischemia-induced excessive glutamate release has been completely blocked by this drug. This drug has also radical-scavenging action, comparable to vitamin E, and inhibits oxygen radical-induced lipid peroxidation. The potent cerebroprotective effect of nizofenone has been demonstrated in various experimental models of cerebral hypoxia, ischemia (focal and global), ischemia-reperfusion, and infarction. The clinical efficacy of nizofenone has been proved by pioneering double-blind studies in acute subarachnoid hemorrhage patients. Nizofenone is clinically used for preventing the delayed ischemic neurologic deficits due to late vasospasm following subarachnoid hemorrhage.

Aescin, the major active principle from Aesculus hippocastanum (Hippocastanaceae) the horse chestnut tree, has shown satisfactory evidence for a clinically significant activity in chronic venous insufficiency (CVI), haemorrhoids and post-operative oedema. In one controlled trial aescin was shown to be as effective as compression therapy as an alternative to medical treatment for CVI. The therapeutic benefit is well supported by a number of experimental investigations in different animal models, indicative of clearcut anti-oedematous, anti-inflammatory and venotonic properties, mainly related to the molecular mechanism of the agent, allowing improved entry of ions into channels, thus raising venous tension in both in vitro and in vivo conditions. Other mechanisms, i.e. release of PGF2 from veins, antagonism to 5-HT and histamine, reduced catabolism of tissue mucopolysaccharides, further underline the wide ranging mechanisms of the therapeutic activity of aescin. Aescin exists in two forms, α and β. β-aescin (b-escin) appears to be the active component of the mixture and is the molecular form present in major available pharmaceutical products. Beta-aescin has cytotoxic activity toward human colon adenocarcinoma cell lines.