Dicyclomine is an anticholinergic tertiary amine used frequently by oral and parenteral route as an effective anti-spasmodic agent. Dicyclomine hydrochloride salt is approved under brand name bentyl for the treatment of functional bowel/irritable bowel syndrome. In addition is known, that dicyclomine is also used in morning and motion sickness, dysmenorrheal, intestinal hypermotility. It was shown, that Dicyclomine is a selective M1 and M3 muscarinic receptors antagonist, but os shown pharmacological activity via the M1 receptor.

Acetaminophen, also known as paracetamol, is commonly used for its analgesic and antipyretic effects. Its therapeutic effects are similar to salicylates, but it lacks anti-inflammatory, antiplatelet, and gastric ulcerative effects. Acetaminophen (USAN) or Paracetamol (INN) is a widely used analgesic and antipyretic drug that is used for the relief of fever, headaches, and other minor aches and pains. It is a major ingredient in numerous cold and flu medications and many prescription analgesics. It is extremely safe in standard doses, but because of its wide availability, deliberate or accidental overdoses are not uncommon. Acetaminophen, unlike other common analgesics such as aspirin and ibuprofen, has no anti-inflammatory properties or effects on platelet function, and it is not a member of the class of drugs known as non-steroidal anti-inflammatory drugs or NSAIDs. At therapeutic doses, acetaminophen does not irritate the lining of the stomach nor affect blood coagulation, kidney function, or the fetal ductus arteriosus (as NSAIDs can). Acetaminophen is thought to act primarily in the CNS, increasing the pain threshold by inhibiting both isoforms of cyclooxygenase, COX-1, COX-2, and COX-3 enzymes involved in prostaglandin (PG) synthesis. Unlike NSAIDs, acetaminophen does not inhibit cyclooxygenase in peripheral tissues and, thus, has no peripheral anti-inflammatory affects. Acetaminophen indirectly blocks COX, and that this blockade is ineffective in the presence of peroxides. This might explain why acetaminophen is effective in the central nervous system and in endothelial cells but not in platelets and immune cells, which have high levels of peroxides. Studies also report data suggesting that acetaminophen selectively blocks a variant of the COX enzyme that is different from the known variants COX-1 and COX-2. This enzyme is now referred to as COX-3. Its exact mechanism of action is still poorly understood, but future research may provide further insight into how it works. The antipyretic properties of acetaminophen are likely due to direct effects on the heat-regulating centers of the hypothalamus resulting in peripheral vasodilation, sweating and hence heat dissipation.

Dicyclomine is an anticholinergic tertiary amine used frequently by oral and parenteral route as an effective anti-spasmodic agent. Dicyclomine hydrochloride salt is approved under brand name bentyl for the treatment of functional bowel/irritable bowel syndrome. In addition is known, that dicyclomine is also used in morning and motion sickness, dysmenorrheal, intestinal hypermotility. It was shown, that Dicyclomine is a selective M1 and M3 muscarinic receptors antagonist, but os shown pharmacological activity via the M1 receptor.

Sulfur dioxide (SO2) is a colorles, highly toxic gas with a choking or suffocating odor. It is used as a pharmaceutical aid and antioxidant. It reacts easily with other substances to form harmful compounds, such as sulfuric acid, sulfurous acid and sulfate particles. About 99% of the sulfur dioxide in air comes from human sources. The main source of sulfur dioxide in the air is industrial activity that processes materials that contain sulfur, eg the generation of electricity from coal, oil or gas that contains sulfur. Some mineral ores also contain sulfur, and sulfur dioxide is released when they are processed. In addition, industrial activities that burn fossil fuels containing sulfur can be important sources of sulfur dioxide. Sulfur dioxide affects human health when it is breathed in. It irritates the nose, throat, and airways to cause coughing, wheezing, shortness of breath, or a tight feeling around the chest. The effects of sulfur dioxide are felt very quickly and most people would feel the worst symptoms in 10 or 15 minutes after breathing it in. Sulfur dioxide is used to increase the storage life and preserve the color and flavor of fruits and vegetables and as a disinfectant in breweries, wineries and food factories. It prevents the formation of nitroamines in beer and reduces free chlorine after water treatment. It is used as a bleaching agent in the textile, paper pulp, wool and fresh produce industries and as a fumigant for grain and against lice and mites in veterinary practice. It also serves as a chemical intermediate in the manufacture of chlorine dioxide, sodium sulfate, thionyl chloride and organic sulfonates. It is used as a reducing agent of iron in mineral processing, as a cleaning agent for metallic oxides, as an oxidizing agent in lithium batteries, as an oxygen scavenger and extractive solvent in petroleum refining, in glass manufacture and as a neutralizing agent. SO2 can be generated endogenously in mammals. In contrast to the toxic effects of SO2, protective effects have also been found in mammals. Endogenous SO2 has antioxidant, anti-inflammatory, anti-hypertension, and anti-atherogenic effects and regulates vascular tone and cardiac function in mammals. SO2 may have a dual role in regulating physiological and pathophysiological effects in mammals. Studies have shown that SO2 can also regulate levels of lipid metabolism. In male Sprague–Dawley rats on a normal or a high cholesterol diet, inhalation of 5 ppm and 10 ppm SO2 gas (for 14 days) increased plasma triglyceride levels and decreased high-density lipoprotein cholesterol levels. However, in rats treated with a high cholesterol diet for 8 weeks, plasma total cholesterol increased and high-density lipoproteincholesterol decreased. After treatment with an SO2 donor the plasma levels of triglyceride and low-density lipoprotein cholesterol were markedly decreased. In addition, the SO2 donor significantly decreased atherosclerotic lesions. These data suggest that SO2 regulates lipid metabolism. The mechanism may be related to upregulation of the disturbed endogenous H2S pathway, increased plasma glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) activities, aortic tissue SOD1 and SOD2 protein expression, and decreased malondialdehyde generation. The antioxidant effect of SO2 might involve one of these mechanisms, which could directly prevent the progression of atherosclerotic lesions. Sulfur dioxide and its derivatives have significant vasodilatory effects. SO2 decreased systolic blood pressure in spontaneously hypertensive rats which may be related to its vasorelaxing effect. Compared with exogenous SO2 vasoactive effects, it was discovered that endogenous SO2 had an important vasorelaxing function which is necessary for maintaining normal blood vascular tone.

EUPROCIN, a cupreine derivative, is a local anesthetic.

Tyloxapol is a nonionic liquid polymer of the alkyl aryl polyether alcohol type that is used as a surfactant to aid liquefaction and removal of mucopurulent (containing mucus and pus) bronchopulmonary secretions. Tyloxapol is also used as a detergent, dispersing agent, encapsulating agent and a hydroxy radical scavenger. Tyloxapol has been used as a mucolytic agent for over 50 years and has proven to be well tolerated during this time. Tyloxapol influences the respiratory system by the following four different action mechanisms: secretolytic action, reduction of surface tension, dissolution of coatings and down-regulation of inflammation. Several studies have shown that small quantities of Tyloxapol applied as an aerosol liquefy sputum. The viscosity of sputum is reduced by 10% to 20% according to rotational viscosimetry measurements. Tyloxapol also penetrates the mucous wall and dissolves viscous and dried secretions, thus enabling increased ciliary activity in the respiratory tract. Although the mechanism of Tyloxapol has been well described, and there is a long-standing basis for its clinical usefulness, there are almost no randomized, double-blind, placebo-controlled trials available that demonstrate the superiority of Tyloxapol vs. saline. Side-effects in the form of hypersensitivity reactions have only occurred very rarely.

Pramoxine (also known as pramocaine or pramoxine HCI) is a topical anesthetic and antipruritic. Pramoxine is used to temporarily relieve itching and pain caused by minor skin irritation such as minor burns/cuts/scrapes, sunburn, eczema, insect bites, cold sores, or rashes from poison ivy, poison oak, or poison sumac. Some products containing pramoxine are also used to temporarily relieve the itching and discomfort from hemorrhoids and certain other problems of the genital/anal area (such as anal fissures, itching around the vagina/rectum). Pramocaine is available by itself and in combination with other medications in various topical preparations. It works by preventing ionic fluctuations needed for neuron membrane depolarization and action potential propagation. Pramoxine reversibly binds and inhibits voltage gated sodium channels on neurons decreasing sodium permeability into the cell. This stabilizes the membrane and prevents ionic fluctuations needed for depolarization stopping any action potential propagation.

Phenyltoloxamine is an ethanolamine derivative with antihistaminic property, which is used in combination with some analgesics for the temporary relief of minor aches and pains associated with headache; backache; muscular aches; temporarily reduces fever and some others disorders. Phenyltoloxamine blocks H1 histamine receptor, thereby inhibiting phospholipase A2 and production of endothelium-derived relaxing factor, nitric oxide. Subsequent lack of activation of guanylyl cyclase through nitric oxide results in decreased cyclic GMP levels, thereby inhibiting smooth muscle constriction of various tissues, decreasing capillary permeability and decreasing other histamine-activated allergic reactions.