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Active ingredient: Prednisone - Brands, Medical Use, Clinical Data

Brands, Medical Use, Clinical Data

Drug Category

  • Antineoplastic Agents
  • Glucocorticoids
  • Anti-inflammatory Agents
  • Adrenergic Agents

Dosage Forms

  • Tablets
  • Ointments
  • Cream
  • Oral Solution

Brands / Synonyms

Adasone; Ancortone; Apo-prednisone; Betapar; Bicortone; Cartancyl; Colisone; Cortan; Cortancyl; Cortidelt; Cotone; Dacorten; Dacortin; Decortancyl; Decortin; Decortisyl; Dehydrocortisone; Dekortin; Delcortin; Dellacort; Dellacort A; Delta Cortelan; Delta E; Delta E.; Delta-Cortelan; Delta-Cortisone; Delta-cortone; Delta-Dome; Delta-E; Deltacortene; Deltacortisone; Deltacortone; Deltasone; Deltison; Deltisona; Deltisone; Deltra; Di-Adreson; Diadreson; Econosone; Encorton; Encortone; Enkorton; Fernisone; Fiasone; Hostacortin; In-Sone; Incocortyl; Juvason; Liquid Pred; Lisacort; Me-Korti; Metacortandracin; Meticorten; Nisona; Nizon; Novoprednisone; Nurison; Orasone; Origen Prednisone; Panafcort; Panasol; Paracort; Parmenison; Pehacort; PRD; Precort; Predeltin; Prednicen-M; Prednicorm; Prednicort; Prednicot; Prednidib; Prednilonga; Prednison; Prednisona [Inn-Spanish]; Prednisone; Prednisone Intensol; Prednisone [Ban:Inn]; Prednisonum [Inn-Latin]; Prednitone; Prednizon; Prednovister; Presone; Pronison; Rectodelt; Reserpine; Reserpine Base; Reserpine Puriss; Retrocortine; Servisone; Sk-Prednisone; Sone; Sterapred; Supercortil; Ultracorten; Ultracortene; Winpred; Wojtab; Zenadrid


Systemic use: for the treatment of drug-induced allergic reactions, perennial or seasonal allergic rhinitis, serum sickness, giant cell arteritis acute rheumatic or nonrheumatic carditis, systemic dermatomyositis, systemic lupus erythematosus, atopic dermatitis, contact dermatitis, exfoliative dermatitis, bullous dermatitis herpetiformis, severe seborrheic dermatitis, severe (Stevens-Johnson syndrome) erythema multiforme, mycosis fungoides, pemphigus, severe psoriasis, acute adrenocortical insufficiency, Addison's disease, secondary adrenocortical insufficiency, congenital adrenal hyperplasia, hypercalcemia associated with neoplasms, nonsuppurative thyroiditis, ulceratice colitis, Crohn's disease, acquired hemolytic anemia, congenital hypoplastic anemia, erythroblastopenia, adult secondary thrombocytopenia, adult idiopathic thrombocytopenia purpura, acute or subacute bursitis, epicondylitis, acute nonspecific tenosynovitis, acute or chronic lymphocytic leukemia, Hodgkin's or non-Hodgkin's lynphomas, Waldenstrom's macroglobulinemia, primary brain tumors (adjunct), nephrotic syndrome, tuberculous meningitis, multiple sclerosis, myasthenia gravis. cerebral edema, chorioretinitis, diffuse posterior choroiditis, aleergic conjunctivitis, Herpes zoster ophthalmicus, anterior segment inflammation, iridocyclitis, iritis, keratitis, optoc neuritis, sympathetic ophthalmia, corneal marginal allergic ulcers, symptomatic sarcoidosis, Loeffler's syndrome not manageable by other means, berylliosis, fulminating or disseminated pulmonary tuberculosis when used concurrently with appropriate antituberculous chemotherapy and aspiration pneumonitis.


Prednisone, the most commonly-prescribed corticosteroid, is used to treat allograft rejection, asthma, systemic lupus erythematosus, and many other inflammatory states. Prednisone has very little mineralocorticoid activity.

Mechanism of Action

Prednisone is a glucocorticoid agonist. It is first metabolized in the liver to its active form, prednisolone. Prednisolone crosses cell membranes and binds with high affinity to specific cytoplasmic receptors. The result includes inhibition of leukocyte infiltration at the site of inflammation, interference in the function of mediators of inflammatory response, suppression of humoral immune responses, and reduction in edema or scar tissue. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.


Readily absorbed from the gastrointestinal tract.


LD50=mg/kg (orally in rat)

Biotrnasformation / Drug Metabolism



Systemic fungal infections and known hypersensitivity to components.

Drug Interactions

The pharmacokinetic interactions listed below are potentially clinically important. Drugs that induce hepatic enzymes such as phenobarbital, phenytoin and rifampin may increase the clearance of corticosteroids and may require increases in corticosteroid dose to achieve the desired response. Drugs such as troleandomycin and ketoconazole may inhibit the metabolism of corticosteroids and thus decrease their clearance. Therefore, the dose of corticosteroid should be titrated to avoid steroid toxicity. Corticosteroids may increase the clearance of chronic high dose aspirin. This could lead to decreased salicylate serum levels or increase the risk of salicylate toxicity when corticosteroid is withdrawn. Aspirin should be used cautiously in conjunction with corticosteroids in patients suffering from hypoprothrombinemia. The effect of corticosteroids on oral anticoagulants is variable. There are reports of enhanced as well as diminished effects of anticoagulants when given concurrently with corticosteroids. Therefore, coagulation indices should be monitored to maintain the desired anticoagulant effect.

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