Tropicamide (Mydriacyl) is an anticholinergic used as a mydriatic.Tropicamide belongs to the group of medicines called anti-muscarinics. Tropicamide blocks the receptors in the muscles of the eye (muscarinic receptors). These receptors are involved controlling the pupil size and the shape of the lens. By blocking these receptors, tropicamide produces dilatation of the pupil (mydriasis) and prevents the eye from accommodating for near vision (cycloplegia). Tropicamide is given as eye drops to dilate the pupil and relax the lens so that eye examinations can be carried out thoroughly.

Cyclopentolate (cyclopentolate hydrochloride) is a parasympatholytic anticholinergic used solely to obtain mydriasis or cycloplegia. This anticholinergic preparation blocks the responses of the sphincter muscle of the iris and the accommodative muscle of the ciliary body to cholinergic stimulation, producing pupillary dilation (mydriasis) and paralysis of accommodation (cycloplegia). It acts rapidly, but has a shorter duration than atropine. Maximal cycloplegia occurs within 25 to 75 minutes after instillation. Complete recovery of accommodation usually takes 6 to 24 hours. Complete recovery from mydriasis in some individuals may require several days. Heavily pigmented irides may require more doses than lightly pigmented irides.

Hydrocortisone is the main glucocorticoid secreted by the adrenal cortex. Its synthetic counterpart is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Topical hydrocortisone is used for its anti-inflammatory or immunosuppressive properties to treat inflammation due to corticosteroid-responsive dermatoses. Hydrocortisone binds to the cytosolic glucocorticoid receptor. After binding the receptor the newly formed receptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes preventing the phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products in inflammation Prostaglandins and Leukotrienes are inhibited by the action of Glucocorticoids. Glucocorticoids also stimulate the lipocortin-1 escaping to the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines etc.) from neutrophils, macrophages and mastocytes. Additionally the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding. For the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. Also used to treat endocrine (hormonal) disorders (adrenal insufficiency, Addisons disease). Hydrocortisone is also used to treat many immune and allergic disorders, such as arthritis, lupus, severe psoriasis, severe asthma, ulcerative colitis, and Crohn's disease.

Atropine inhibits the muscarinic actions of acetylcholine on structures innervated by postganglionic cholinergic nerves, and on smooth muscles which respond to endogenous acetylcholine but are not so innervated. As with other antimuscarinic agents, the major action of atropine is a competitive or surmountable antagonism which can be overcome by increasing the concentration of acetylcholine at receptor sites of the effector organ (e.g., by using anticholinesterase agents which inhibit the enzymatic destruction of acetylcholine). The receptors antagonized by atropine are the peripheral structures that are stimulated or inhibited by muscarine (i.e., exocrine glands and smooth and cardiac muscle). Responses to postganglionic cholinergic nerve stimulation also may be inhibited by atropine but this occurs less readily than with responses to injected (exogenous) choline esters. Atropine is relatively selective for muscarinic receptors. Its potency at nicotinic receptors is much lower, and actions at non-muscarinic receptors are generally undetectable clinically. Atropine does not distinguish among the M1, M2, and M3 subgroups of muscarinic receptors.

The alkaloid L-(-)-scopolamine [L-(-)-hyoscine], a belladonna alkaloid, competitively inhibits muscarinic receptors for acetylcholine and acts as a nonselective muscarinic antagonist, producing both peripheral antimuscarinic properties and central sedative, antiemetic, and amnestic effects. Scopolamine acts: i) as a competitive inhibitor at postganglionic muscarinic receptor sites of the parasympathetic nervous system, and ii) on smooth muscles that respond to acetylcholine but lack cholinergic innervation. It has been suggested that scopolamine acts in the central nervous system (CNS) by blocking cholinergic transmission from the vestibular nuclei to higher centers in the CNS and from the reticular formation to the vomiting center. Scopolamine can inhibit the secretion of saliva and sweat, decrease gastrointestinal secretions and motility, cause drowsiness, dilate the pupils, increase heart rate, and depress motor function. Scopolamine is used for premedication in anesthesia and for the prevention of nausea and vomiting (post operative and associated with motion sickness).

Miconazole is a synthetic imidazole derivative, a topical antifungal agent for use in the local treatment of vaginal, and skin and nail infections due to yeasts and dermatophytes. It is particularly active against Candida spp., Trichophyton spp., Epidermophyton spp., Microsporum spp. and Pityrosporon orbiculare (Malassezia furfur), but also possesses some activity against Gram-positive bacteria. It binds to the heme moiety of the fungal cytochrome P-450 dependent enzyme lanosterol 14-alpha-demethlyase. Inhibits 14-alpha-demethlyase, blocks formation of ergosterol and leads to the buildup of toxic methylated 14-a-sterols. Miconazole also affects the synthesis of triglycerides and fatty acids and inhibits oxidative and peroxidative enzymes, increasing the amount of active oxygen species within the cell.

Tetracaine (INN, also known as amethocaine; trade name Pontocaine. Ametop and Dicaine) is a potent local anesthetic of the ester group. It is mainly used topically in ophthalmology and as an antipruritic, and it has been used in spinal anesthesia. Tetracaine blocks sodium ion channels required for the initiation and conduction of neuronal impulses thereby affecting local anesthesia. In biomedical research, tetracaine is used to alter the function of calcium release channels (ryanodine receptors) that control the release of calcium from intracellular stores. Tetracaine is an allosteric blocker of channel function. At low concentrations, tetracaine causes an initial inhibition of spontaneous calcium release events, while at high concentrations, tetracaine blocks release completely.

Butyric acid (butanoic acid) belongs to a group of short-chain fatty acids and is thought to play several beneficial roles in the gastrointestinal tract. The butyric anion is easily absorbed by enteric cells and used as a main source of energy. Moreover, butyric acid is an important regulator of colonocyte proliferation and apoptosis, gastrointestinal tract motility and bacterial microflora composition in addition to its involvement in many other processes including immunoregulation and anti-inflammatory activity. Butyric acid shows a protective effect in inflammatory response secondary to inflammatory bowel diseases. A beneficial effect of butyric acid as one constituent of a multifaceted mechanism modulating gastrointestinal function has also been stressed in patients with the stoma and coexisting constipation. Butyric acid supplementation combined with the use of probiotics should be adopted as one of the basic therapeutic strategies in this patient group, preceding treatment with laxatives. Sodium butyrate in the form of enemas (combined in a mixture with A-300 silicon dioxide) may be a successful method of therapeutic management in patients with radiation proctitis. Sodium butyrate may also prevent diarrhea through an increased passive absorption of water in the colon and its effects on the gut microflora.

Resocortol butyrate is a corticosteroid which has a high intrinsic glucocorticoid activity. Its mineralocorticoid and progestational activity is very low. Resocortol butyrate has local and systemic glucocorticoid effects. The expression of these effects depends on the mode of application and the dosage applied. After topical application on the skin, a local anti-inflammatory effect is seen, which is accompanied by a moderate and reversible adrenal suppression at higher doses. After oral administration in dogs few systemic effects were observed. Resocortol butyrate was marketed under the brand name Pruban as the topical cream for the treatment of acute localised moist dermatitis in dogs. It was discontinued.

Amphomycin is a natural antibacterial lipopeptide initially reported by researchers at Bristol-Myers in 1953 from Streptomyces canus. Lipopeptides are cyclic depsipeptides with a peptidyl side chain capped with a saturated alkyl tail. They preferentially target Gram-positive bacteria and may be useful against drug resistant strains. Amphomycin is closely related to a number of "lost" antibiotics, such as aspartocin, crystallomycin, glumamycin, friulimicin, laspartocin, tsushimycin and zaomycin. Interest in amphomycin was re-awakened with the discovery of friulimicin activity against antibiotic resistant strains. Whole cell analysis by solid-state NMR indicates that in vivo mode of action for amphomycin is complex. While the downstream effect of purine biosynthesis inhibition by amphomycin is unknown, presumably it would directly alter the overall metabolism of bacteria.