Aceclidine is a parasympathomimetic agent used in the treatment of open-angle glaucoma as topical eye drop solution. It is as a muscarinic acetylcholine receptor agonist with weak anticholinesterase activity. Acting directly on the motor end-plate (cholinergic nerve endings) it decreases intraocular pressure and mediates the contraction of iris muscle. Aceclidine increased outflow facility in human eyes in vitro by a direct stimulation of the outflow tissues in the absence of an intact ciliary muscle. This effect was biphasic, occurring at concentrations of 10 uM and lower with no effect at higher concentrations. Passed numerous clinical trials in Russia, France, Italy and other countries and was widely used in Europe but never been in clinical use in USA.

Raclopride is a salicylamide neuroleptic, that acts as a selective antagonist of D2 dopamine receptors both in vitro and in vivo. Tritium-labelled raclopride has properties that demonstrate its usefulness as a radioligand for the labelling of dopamine-D2 receptors : 3H-Raclopride has a high affinity for the rat and human dopamine-D2 receptors, the non-specific binding of 3H-raclopride is very low, not exceeding 5% of the total binding and the distribution of the 3H-raclopride binding sites in the brain closely correlates with the dopaminergic innervation. The binding of 3H-raclopride is blocked by dopamine-D2 agonists and antagonists, while the D1 agonist SKF 38393 and the Dl antagonist SCH 23390 have much less potency. The interaction of dopamine with 3H-raclopride binding results in a shallow competition curve, which suggests that 3H-raclopride, similar to other dopamine-D2 radioligands, labels both high and low agonist affinity states of the dopamine-D2 receptor. The in vivo receptor binding studies performed with 3H-raclopride also demonstrate its favorable properties as a dopamine-D2 receptor marker in vivo In contrast to some other compounds used as radioligands, raclopride enters the brain readily and binds with a low component of non-specific binding in all dopamine-rich brain areas. A saturation curve may be achieved in vivo binding studies since injections of increasing concentrations of 3H-raclopride appears to be saturated at concentrations above 25 mkCi (corresponding to approximately 5 nmol/kg). Raclopride antagonizes apomorphine-induced hyperactivity in the rat at low doses (ED50 = 130 nM/kg i.p.) but induces catalepsy only at much higher doses (ED50 = 27 mkM/kg i.p.). Radiolabelled raclopride has been used as a ligand for in vitro and in vivo autoradiography in rat and primate brains. Raclopride C 11 is used with positron emission tomography (PET) as a clinical research tool to determine dopamine type 2 (D 2) receptor density in the human brain under normal and pathological conditions. For example, raclopride C 11 used in PET studies has served to confirm the age-related decrease in striatal dopamine D2 receptor density, which may be associated with a decline in the motor as well as cognitive functions. In patients with Alzheimer's disease, raclopride C 11 may be used to examine neuroreceptor distribution and quantities, which may help in the analysis of degenerative alterations of neuron populations and neuroreceptor systems in patients with this disease. In Huntington's disease, in which degeneration of neostriatal interneurons occurs (postsynaptic to the dopaminergic input), specific binding of raclopride C 11 to D 2 receptors may serve as one of the parameters in predicting performance in cognitive tasks.

Tilorone (trade names Amixin, Lavomax and others) is the first recognized synthetic, small molecular weight compound that is an orally active interferon inducer. Tilorone induces the formation of interferons (alpha, beta, gamma) by intestinal epithelial cells, hepatocytes, T-lymphocytes, and granulocytes. After ingestion, the maximum production of interferon is determined in the sequence of the intestine - liver - blood after 4-24 hours. Activates the stem cells of the bone marrow, stimulates humoral immunity, increases the production of IgM, IgA, IgG, affects the antibody formation, reduces the degree of immunosuppression, restores the ratio of T-helperers / T-suppressors. The mechanism of antiviral action is associated with the inhibition of translation of virus-specific proteins in infected cells, thereby suppressing the replication of the virus. Effective against influenza viruses and viruses that cause ARVI, hepato- and herpesviruses, incl. CMV and others. The mechanism of antiviral action is associated with the inhibition of translation of virus-specific proteins in infected cells, thereby suppressing the replication of the virus.

Aceclidine is a parasympathomimetic agent used in the treatment of open-angle glaucoma as topical eye drop solution. It is as a muscarinic acetylcholine receptor agonist with weak anticholinesterase activity. Acting directly on the motor end-plate (cholinergic nerve endings) it decreases intraocular pressure and mediates the contraction of iris muscle. Aceclidine increased outflow facility in human eyes in vitro by a direct stimulation of the outflow tissues in the absence of an intact ciliary muscle. This effect was biphasic, occurring at concentrations of 10 uM and lower with no effect at higher concentrations. Passed numerous clinical trials in Russia, France, Italy and other countries and was widely used in Europe but never been in clinical use in USA.

Melperone is an antipsychotic drug which is used in Europe for the treatment of sleep disorders, agitation and confusion states. The exact mechanism of melperone action is unknown.

Pizotifen (INN) or pizotyline (USAN), trade name Sandomigran, is a benzocycloheptene-based drug used as a medicine, primarily as a preventative to reduce the frequency of recurrent migraine headaches. Pizotifen is a serotonin antagonist acting mainly at the 5-HT2A and 5HT2C receptors. It also has some activity as an antihistamine as well as some anticholinergic activity. The main medical use for pizotifen is for the prevention of vascular headache including migraine and cluster headache. Pizotifen is one of a range of medications used for this purpose, other options include propranolol, topiramate, valproic acid and amitriptyline. While pizotifen is reasonably effective, its use is limited by side effects, principally drowsiness and weight gain, and it is usually not the first choice medicine for preventing migraines, instead being used as an alternative when other drugs have failed to be effective. It is not effective in relieving migraine attacks once in progress. Pizotifen has also been reported as highly effective in a severe case of erythromelalgia, a rare neurovascular disease that is sometimes refractory to the other drugs named above. Side effects include sedation, dry mouth, drowsiness, increased appetite and weight gain. Occasionally it may cause nausea, headaches, or dizziness. In rare cases, anxiety, aggression and depression may also occur. Pizotifen is well absorbed from the gastro-intestinal tract, peak plasma concentrations occurring approximately 5 hours after oral administration. The absorption of pizotifen is fast (absorption half life 0.5 to 0.8 hours) and nearly complete (80%). Over 90% is bound to plasma proteins. Pizotifen undergoes extensive metabolism. Over half of a dose is excreted in the urine, chiefly as metabolites; a significant proportion is excreted in the faeces. The primary metabolite of pizotifen (N-glucuronide conjugate) has a long elimination half-life of about 23 hours.

Hymecromone (4-methylumbelliferone) is already approved drug in Europe and Asia where it is used to treat biliary spasm. It is used as choleretic and antispasmodic drugs and as a standard for the fluorometric determination of enzyme activity. The concomitant administration of Hymecromone with products, containing metoclopramide, leads to mutual decrease of their action. Due to a danger of diarrhea with subsequent hypokalemia, Hymecromone should be applied with caution to patients on cardiac glycosides therapy (in these cases the sensitivity to them is increased). Hymecromone can be administered simultaneously with otherspasmolytics and analgesics. Very rare allergic reactions, itching, erythema, rashes; diarrhea which normally disappears by reduction of dose or discontinuance of therapy.

Temocapril is a prodrug-type angiotensin-I converting enzyme (ACE) inhibitor not approved for use in the United States but is approved in Japan and South Korea. Temocapril can also be used in hemodialysis patients without risk of serious accumulation.

Dexamethasone is an anti-inflammatory agent that is FDA approved for the treatment of many conditions, including rheumatic problems, a number of skin diseases, severe allergies, asthma, chronic obstructive lung disease, croup, brain swelling and others. Dexamethasone is a glucocorticoid agonist. Unbound dexamethasone crosses cell membranes and binds with high affinity to specific cytoplasmic glucocorticoid receptors. Adverse reactions are: Glaucoma with optic nerve damage, visual acuity and field defects; cataract formation; secondary ocular infection following suppression of host response; and perforation of the globe may occur; muscle weakness; osteoporosis and others. Aminoglutethimide may diminish adrenal suppression by corticosteroids. Macrolide antibiotics have been reported to cause a significant decrease in corticosteroid clearance.

Glucose is a sugar with the molecular formula C6H12O6. The D-isomer (D-glucose), also known as dextrose, occurs widely in nature, but the L-isomer (L-glucose) does not. Glucose is made during photosynthesis from water and carbon dioxide, using energy from sunlight. The reverse of the photosynthesis reaction, which releases this energy, is a very important source of power for cellular respiration. Glucose is stored as a polymer, in plants as starch and in animals as glycogen, for times when the organism will need it. Glucose circulates in the blood of animals as blood sugar. Glucose can be obtained by hydrolysis of carbohydrates such as milk, cane sugar, maltose, cellulose, glycogen etc. It is however, manufactured by hydrolysis of cornstarch by steaming and diluting acid. Glucose is the human body's key source of energy, through aerobic respiration, providing about 3.75 kilocalories (16 kilojoules) of food energy per gram. Breakdown of carbohydrates (e.g. starch) yields mono- and disaccharides, most of which is glucose. Use of glucose as an energy source in cells is by either aerobic respiration, anaerobic respiration, or fermentation. All of these processes follow from an earlier metabolic pathway known as glycolysis. The insulin reaction, and other mechanisms, regulate the concentration of glucose in the blood. Glucose supplies almost all the energy for the brain, so its availability influences psychological processes. When glucose is low, psychological processes requiring mental effort (e.g., self-control, effortful decision-making) are impaired. Ingested glucose is absorbed directly into the blood from the intestine and results in a rapid increase in the blood glucose level. Glucose is used to manage hypoglycemia and for intravenous feeding. Nausea may occur after ingesting glucose, but this also may be an effect of the hypoglycemia which is present just prior to ingestion. Other adverse effects include increased blood glucose, injection site leakage of fluid (extravasation), injection site inflammation, and bleeding in the brain.