Beclometasone dipropionate or beclomethasone dipropionate is sold under the brand name Qvar among others. Beclomethasone dipropionate is a corticosteroid demonstrating potent anti-inflammatory activity. The precise mechanism of corticosteroid action on asthma is not known. Corticosteroids have been shown to have multiple anti-inflammatory effects, inhibiting both inflammatory cells (e.g., mast cells, eosinophils, basophils, lymphocytes, macrophages, and neutrophils) and release of inflammatory mediators (e.g., histamine, eicosanoids, leukotrienes, and cytokines). These anti-inflammatory actions of corticosteroids may contribute to their efficacy in asthma. Beclomethasone dipropionate is a prodrug that is rapidly activated by hydrolysis to the active monoester, 17 monopropionate (17-BMP). Beclomethasone 17 monopropionate has been shown in vitro to exhibit a binding affinity for the human glucocorticoid receptor, which is approximately 13 times that of dexamethasone, 6 times that of triamcinolone acetonide, 1.5 times that of budesonide and 25 times that of beclomethasone dipropionate. The clinical significance of these findings is unknown. Studies in patients with asthma have shown a favorable ratio between topical anti-inflammatory activity and systemic corticosteroid effects with recommended doses of QVAR. Beclometasone dipropionate was first patented in 1962 and used medically in 1972. Common side effects with the inhaled form include respiratory infections, headaches, and throat inflammation. Serious side effects include an increased risk of infection, cataracts, Cushing’s syndrome, and severe allergic reactions. Long term use of the pill form may cause adrenal insufficiency. The pills may also cause mood or personality changes. The inhaled form is generally regarded as safe in pregnancy. Beclometasone is mainly a glucocorticoid.

Medrysone is a synthetic glucocorticoid used to to treat inflammatory eye diseases such as allergic conjunctivitis, vernal conjunctivitis, and episcleritis.

Trimeprazine (also known as Alimemazine), a phenothiazine used as antipsychotic drug. This drug is used in Russia under brand name TERALIGEN and has anti-histamine, sedative, and anti-emetic (anti-nausea) effects. Teraligen is used to treat neurosis, depression and anxiety of different origins. It prevents and relieves allergic conditions, which cause pruritus and urticaria by blocking histamine produced by the body during an allergic reaction. Trimeprazine competes with free histamine for binding at HA-receptor sites. This antagonizes the effects of histamine on HA-receptors, leading to a reduction of the negative symptoms brought on by histamine HA-receptor binding. Trimeprazine is not approved for use in humans in the United States. Nevertheless, combination of alimemazine and prednisolone (commonly sold under the brand name Temaril-P) is licensed as an antipruritic and antitussive in dogs.

Triamcinolone is a long-acting synthetic corticosteroid primarily used for their anti-inflammatory effects in disorders of many organ systems. Triamcinolone diacetate injectable suspension is indicated for intramuscular use as follows: Allergic States Control of severe or incapacitating allergic conditions intractable to adequate trials of conventional treatment in asthma, atopic dermatitis, contact dermatitis, drug hypersensitivity reactions, perennial or seasonal allergic rhinitis, serum sickness, transfusion reactions. Bullous dermatitis herpetiformis, exfoliative erythroderma, mycosis fungoides, pemphigus, severe erythema multiform (Stevens-Johnson syndrome). Endocrine Disorders Primary or secondary adrenocortical insufficiency, congenital adrenal hyperplasia, hypercalcemia associated with cancer, nonsuppurative thyroiditis. To tide the patient over a critical period of the disease in regional enteritis and ulcerative colitis. Hematologic Disorders Acquired (autoimmune) hemolytic anemia, Diamond-Blackfan anemia, pure red cell aplasia, selected cases of secondary thrombocytopenia. Trichinosis with neurologic or myocardial involvement, tuberculous meningitis with subarachnoid block or impending block when used with appropriate ant tuberculous chemotherapy. For palliative management of leukemia’s and lymphomas. Nervous System Acute exacerbations of multiple sclerosis; cerebral edema associated with primary or metastatic brain tumor, or craniotomy. Sympathetic ophthalmia, uveitis and ocular inflammatory conditions unresponsive to topical corticosteroids. To induce diuresis or remission of proteinuria in idiopathic nephrotic syndrome or that due to lupus erythematosus. Berylliosis, fulminating or disseminated pulmonary tuberculosis when used concurrently with appropriate ant tuberculous chemotherapy, idiopathic eosinophilic pneumonias, symptomatic sarcoidosis. As adjunctive therapy for short-term administration in acute gouty arthritis; acute rheumatic carditis. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins that, through inhibition of arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Firstly, however, these glucocorticoids bind to the glucocorticoid receptors, which translocate into the nucleus, bind DNA (GRE), and change genetic expression both positively and negatively. 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.

Cortisone is a hormone that is FDA approved for the treatment of primary and secondary adrenocortical deficiency, rheumatic disorders, psoriasis, exfoliative dermatitis, bronchial asthma, allergic conjunctivitis, hemolytic anemia, enteritis, tuberculosis, trichnosis. Cortisone acetate 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. Common adverse reactions include convulsions, increased intracranial pressure with papilledema, vertigo, headache, psychic disturbances, hirsuitism, glaucoma, exophthalmos. Aminoglutethimide may lead to a loss of corticosteroid-induced adrenal suppression. Co-administration of corticosteroids and warfarin usually results in inhibition of response to warfarin, although there have been some conflicting reports. Cortisone is a natural steroid hormone. Its sulfate analog has been detected in in umbilical vein blood fetus plasma between 19 and 32 weeks of gestation with a significant increase at 29-30 weeks and in amniotic fluid. Base on the experiments with rats it was suggested that cortisone sulfate in mammals could be hydrolyzed enzymatically liberating sulfate ions from cortisone. Cortisone sulfate has been proposed for use as one of the glycosaminoglycan compound materials in a cartilage prosthesis and biological nasal bridge implant manufacture as well as auxiliary agent in powder aerosol composition for use in baby powder, dry shampoo, water-eczema remedy and antiperspirant.

Loteprednol (as the ester loteprednol etabonate) is a corticosteroid used to treat inflammations of the eye. It is marketed by Bausch and Lomb as Lotemax. It is a topical corticoid anti-inflammatory. It is used in ophthalmic solution for the treatment of steroid responsive inflammatory conditions of the eye such as allergic conjunctivitis, uveitis, acne rosacea, superficial punctate keratitis, herpes zoster keratitis, iritis, cyclitis, and selected infective conjunctivitis’s. Lotemax is less effective than prednisolone acetate 1% in two 28-day controlled clinical studies in acute anterior uveitis, where 72% of patients treated with Lotemax experienced resolution of anterior chamber cells, compared to 87% of patients treated with prednisolone acetate 1%. Lotemax is also indicated for the treatment of post-operative inflammation following ocular surgery. Corticosteroids inhibit the inflammatory response to a variety of inciting agents and probably delay or slow healing. They inhibit the edema, fibrin deposition, capillary dilation, leukocyte migration, capillary proliferation, fibroblast proliferation, deposition of collagen, and scar formation associated with inflammation. There is no generally accepted explanation for the mechanism of action of ocular corticosteroids. However, corticosteroids are thought to act by the induction of phospholipase A2 inhibitory proteins, collectively called lipocortins. It is postulated that these proteins control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of their common precursor arachidonic acid. Arachidonic acid is released from membrane phospholipids by phospholipase A2. Corticosteroids are capable of producing a rise in intraocular pressure (IOP). Loteprednol etabonate is structurally similar to other corticosteroids. However, the number 20 position ketone group is absent. It is highly lipid soluble, which enhances its penetration into cells. Loteprednol etabonate is synthesized through structural modifications of prednisolone-related compounds so that it will undergo a predictable transformation to an inactive metabolite. Based upon in vivo and in vitro preclinical metabolism studies, loteprednol etabonate undergoes extensive metabolism to inactive carboxylic acid metabolites. Lotemax possesses some adverse reactions associated with ophthalmic steroids include elevated intraocular pressure, which may be associated with optic nerve damage, visual acuity and field defects, posterior subcapsular cataract formation, secondary ocular infection from pathogens including herpes simplex, and perforation of the globe where there is thinning of the cornea or sclera.

Fluticasone is a medium-potency synthetic trifluorinated corticosteroid which is used in some countries to manage nasal symptoms of allergic and non-allergic rhinitis. Fluticasone binds and activates glucocorticoid receptor, resulting in the activation of lipocortin. Lipocortin, in turn, inhibits cytosolic phospholipase A2, which triggers a cascade of reactions involved in the synthesis of inflammatory mediators, such as prostaglandins and leukotrienes. Both the furoate and propanoate esters, fluticasone furoate and fluticasone propionate, are much more commonly used as topical anti-inflammatories and inhaled corticosteroids.

Neomycin is an aminoglycoside antibiotic found in many topical medications such as creams, ointments, and eye drops. In vitro tests have demonstrated that neomycin is bactericidal and acts by inhibiting the synthesis of protein in susceptible bacterial cells. It is effective primarily against gram-negative bacilli but does have some activity against gram-positive organisms. Neomycin is active in vitro against Escherichia coli and the Klebsiella-Entero. Topical uses include treatment for superficial eye infections caused by susceptible bacteria (used in combination with other anti-infective), treatment of otitis externa caused by susceptible bacteria, treatment or prevention of bacterial infections in skin lesions, and use as a continuous short-term irrigant or rinse to prevent bacteriuria and gram negative rod bacteremia in bacteriuria patients with indwelling catheters. May be used orally to treat hepatic encephalopathy, as a perioperative prophylactic agent, and as an adjunct to fluid and electrolyte replacement in the treatment of diarrhea caused to enter pathogenic E. coli (EPEC). Neomycin sulfate has been shown to be effective adjunctive therapy in hepatic coma by reduction of the ammonia forming bacteria in the intestinal tract. The subsequent reduction in blood ammonia has resulted in neurologic improvement. To reduce the development of drug-resistant bacteria and maintain the effectiveness of Neomycin Sulfate Oral Solution and other antibacterial drugs, susceptible bacteria should use Neomycin Sulfate Oral Solution only to treat or prevent infections that are proven or strongly suspected to be caused. When culture and susceptibility information are available, they should be considered in selecting or modifying antibacterial therapy. In the absence of such data, local epidemiology and susceptibility patterns may contribute to the empiric selection of therapy. Neomycin binds to four nucleotides of 16S rRNA and a single amino acid of protein S12. This interferes with decoding site near nucleotide 1400 in 16S rRNA of 30S subunit. This region interacts with the wobble base in the anticodon of tRNA. This leads to interference with the initiation complex, misreading of mRNA so incorrect amino acids are inserted into the polypeptide leading to nonfunctional or toxic peptides and the breakup of polysomes into nonfunctional monosomes

Deflazacort is a glucocorticoid developed for the treatment of different inflammatory and immune conditions. The drug is rapidly metabolized to an active metabolite, 21-hydroxy-deflazaxort that may cross the blood brain barrier. Deflazacort acts by suppressing inflammatory response.

Flunisolide is a synthetic corticosteroid. It is administered either as an oral metered-dose inhaler for the treatment of asthma or as a nasal spray for treating allergic rhinitis. Corticosteroids are naturally occurring hormones that prevent or suppress inflammation and immune responses. When given as an intranasal spray, flunisolide reduces watery nasal discharge (rhinorrhea), nasal congestion, postnasal drip, sneezing, and itching oat the back of the throat that are common allergic symptoms. Flunisolide is a glucocorticoid receptor agonist. The antiinflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. 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. Flunisolide binds to plasma transcortin, and it becomes active when it is not bound to transcortin. It is used for the maintenance treatment of asthma as a prophylactic therapy. Flunisolide is marketed as AeroBid, Nasalide, Nasarel.