Norethisterone (INN, BAN), also known as Norethindrone (USAN) (brand names Micronor, AYGESTIN, numerous others) is a synthetic progestational hormone (progestin) with actions similar to those of progesterone but functioning as a more potent inhibitor of ovulation. It has weak estrogenic and androgenic properties. The hormone has been used for the treatment of secondary amenorrhea, endometriosis, and abnormal uterine bleeding due to hormonal imbalance in the absence of organic pathology, such as submucous fibroids or uterine cancer. AYGESTIN® is not intended, recommended or approved to be used with oncomitant estrogen therapy in postmenopausal women for endometrial protection. Progestins diffuse freely into target cells and bind to the progesterone receptor. Target cells include the female reproductive tract, the mammary gland, the hypothalamus, and the pituitary. Once bound to the receptor, progestins slow the frequency of release of gonadotropin releasing hormone (GnRH) from the hypothalamus and blunt the pre-ovulatory LH surge. Allergic reaction could be: Itching or hives, swelling in your face or hands, swelling or tingling in your mouth or throat, chest tightness, trouble breathing.

Methylprednisolone is a prednisolone derivative with similar anti-inflammatory and immunosuppressive action. It is adjunctive therapy for short-term administration in rheumatoid arthritis. It is indicated in the following conditions: endocrine disorders, rheumatic disorders, collagen diseases, allergic states etc. Methylprednisolone is marketed in the USA and Canada under the brand names Medrol and Solu-Medrol. Methylprednisolone is a GR receptor agonist.

Fludrocortisone acetate (approved as Florinef) is a synthetic adrenocortical steroid possessing very potent mineralcorticoid properties and high glucocorticoid activity. Main indications are Partial replacement therapy for primary and secondary adrenocortical insufficiency in Addison's disease and for the treatment of salt losing adrenogenital syndrome.

Prednisolone hemisuccinate is a prodrug of a glucocorticoid agonist prednisolone, which is marketed under trade name Prednisolut in Germany and Austria. Prednisolone hemisuccinate is used in emergency medicine to treate shock due to allergic reaction, insect and snake bites, in neurology to treat brain edema and meningitis, in transplantation medicine to reduce risk of organ refection after kidney transplane, in pneumology to treat acute asthma attack, pulmonary edema, in severe or life-threatening situation in rheumatic diseases.

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.

Mafenide is a sulfonamide-type medication used as an antibiotic. It is indicated for use as an adjunctive topical antimicrobial agent to control bacterial infection when used under moist dressings over meshed autografts on excised burn wounds. Mafenide is not antagonized by pABA, serum, pus or tissue exudates, and there is no correlation between bacterial sensitivities to mafenide and to the sulfonamides. A single case of bone marrow depression and a single case of an acute attack of porphyria have been reported following therapy with mafenide acetate. Fatal hemolytic anemia with disseminated intravascular coagulation, presumably related to a glucose-6-phosphate dehydrogenase deficiency, has been reported following therapy with mafenide acetate. Other adverse reactions are: pain or burning sensation, rash and pruritis, erythema, skin maceration from prolonged wet dressings, facial edema, swelling, hives, blisters, eosinophilia.

Proguanil is a prophylactic antimalarial drug, which works by stopping the malaria parasite, Plasmodium falciparum and Plasmodium vivax, from reproducing once it is in the red blood cells. Proguanil in combination with atovaquone are marked under the brand name malarone, which is indicated for the treatment of acute, uncomplicated P. falciparum malaria and for the prophylaxis of Plasmodium falciparum malaria, including in areas where chloroquine resistance has been reported. Atovaquone and proguanil, interfere with 2 different pathways involved in the biosynthesis of pyrimidines required for nucleic acid replication. Atovaquone is a selective inhibitor of parasite mitochondrial electron transport. Proguanil hydrochloride primarily exerts its effect by means of the metabolite cycloguanil, a dihydrofolate reductase inhibitor. Inhibition of dihydrofolate reductase in the malaria parasite disrupts deoxythymidylate synthesis. Recently were done experiments, which confirmed the hypothesis that proguanil might act on another target than dihydrofolate reductase. In addition, was made conclusion, that effectiveness of malarone was due to the synergism between atovaquone and proguanil and may not require the presence of cycloguanil.

Dimercaprol (2, 3-dimercapto-1-propanol) or British anti-Lewisite (BAL), is a colorless or almost colorless liquid chelating agent having a disagreeable, mercaptan-like odor. Dimercaprol was developed at Oxford University during World War II as a means of treating and reversing poisoning from Lewisite, an arsenical gas used in chemical warfare (and thus initially called British anti-Lewisite [BAL]). The sulfhydryl groups of dimercaprol form complexes with certain heavy metals thus preventing or reversing the metallic binding of sulfhydryl-containing enzymes. Parenterally administered dimercaprol is used to treat arsenic, gold, copper and mercury poisoning. It is indicated in acute lead poisoning when used concomitantly with edetate clcium disodium. Dimercaprol is occasionally used in the initial treatment of severe, symptomatic Wilson disease, but generally for a short time only.

Ethinyl estradiol is a synthetic derivative of the natural estrogen estradiol. It is one of two estrogens currently used in oral contraceptive pills. The other, mestranol, is converted to ethinyl estradiol before it is biologically active. Ethinyl estradiol and norethindrone are used together as an oral contraceptive agent. Estrogens diffuse into their target cells and interact with a protein receptor. Target cells include the female reproductive tract, the mammary gland, the hypothalamus, and the pituitary. Estrogens increase the hepatic synthesis of sex hormone binding globulin (SHBG), thyroid-binding globulin (TBG), and other serum proteins and suppress follicle-stimulating hormone (FSH) from the anterior pituitary. This cascade is initiated by initially binding to the estrogen receptors. The combination of an estrogen with a progestin suppresses the hypothalamic-pituitary system, decreasing the secretion of gonadotropin-releasing hormone (GnRH). Used for treatment of moderate to severe vasomotor symptoms associated with the menopause, female hypogonadism, prostatic carcinoma-palliative therapy of advanced disease, breast cancer, as an oral contraceptive, and as emergency contraceptive.

Estradiol benzoate is the synthetic benzoate ester of estradiol, a steroid sex hormone vital to the maintenance of fertility and secondary sexual characteristics in females. As the primary, most potent estrogen hormone produced by the ovaries, estradiol binds to and activates specific nuclear receptors. This agent exhibits mild anabolic and metabolic properties, and increases blood coagulability. Although estradiol benzoate is not approved by the FDA for use in humans in the United States, it is approved for veterinary use as a subdermal implant both alone (CELERIN®) and in combination with the anabolic steroid trenbolone acetate (SYNOVEX® Plus).