Prednisone: Wikis


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Systematic (IUPAC) name
(8S,9S,10R,13S,14 S,17R)-

17-hydroxy-17-(2-hydroxyacetyl)-10,13-dimethyl-7,8,9,10,12,13,14,15,16,17- decahydro-3H-cyclopenta[a]phenanthrene-3,11(6H)-dione

CAS number 53-03-2
ATC code A07EA03 H02AB07
PubChem 5865
DrugBank APRD00340
ChemSpider 5656
Chemical data
Formula C 21H26O5  
Mol. mass 358.428 g/mol
SMILES eMolecules & PubChem
Pharmacokinetic data
Bioavailability 70%
Metabolism prednisolone (liver)
Half life 1 hour
Excretion Renal
Therapeutic considerations
Pregnancy cat. C
Legal status Rx Only (US)
Routes Oral, Nasal, Rectal, Injection, IV
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Prednisone is a synthetic corticosteroid drug that is particularly effective as an immunosuppressant, and affects virtually all of the immune system. It is used to treat certain inflammatory diseases and (at higher doses) cancers, but has significant adverse effects. It is usually taken orally but can be delivered by intramuscular injection or intravenous injection. It has a mainly glucocorticoid effect. Prednisone is a prodrug that is converted by the liver into prednisolone, which is the active drug and also a steroid.



Prednisone can, therefore, be used in autoimmune diseases, inflammatory diseases (such as severe asthma, severe allergies, Juvenile dermatomyositis, angioedema episodes, severe urushiol-induced contact dermatitis, systemic lupus erythematosus, ulcerative colitis, rheumatoid arthritis, Still's disease, Bell's palsy, Crohn's disease, pemphigus and sarcoidosis), uveitis, various kidney diseases including nephrotic syndrome, mononucleosis Epstein-Barr virus, and to prevent and treat rejection in organ transplantation. Prednisone has also been used in the treatment of migraine headaches and cluster headaches and for severe aphthous ulcer ("Cankersore") outbreaks. It can also be used to treat autoimmune pancreatitis.

Prednisone is used as an antitumor drug. Prednisone is very important in the treatment of acute lymphoblastic leukemia, Non-Hodgkin lymphomas, Hodgkin's lymphoma, multiple myeloma, and other tumors in combination with other anticancer drugs.

Furthermore, the pharmaceutical industry uses prednisone tablets for the calibration of dissolution testing equipment according to the United States Pharmacopeia (USP).

Intravenous application may be employed for cerebral inflammation, as in the periodic attacks caused by multiple sclerosis.

Prednisone is also used for the treatment of the Herxheimer reaction which is common during the treatment of syphilis, and to delay the onset of symptoms of Duchenne muscular dystrophy. The mechanism for the delay of symptoms is unknown.

Because it suppresses the adrenals, it is also sometimes used in the treatment of congenital adrenal hyperplasia.


The first commercially feasible synthesis of prednisone was carried out in 1955 in the laboratories of Schering Corporation, which later became Schering-Plough Corporation, by Arthur Nobile and coworkers.[1] They discovered that cortisone could be microbiologically oxidized to prednisone by the bacterium Corynebacterium simplex. The same process was used to prepare prednisolone from hydrocortisone.[2] Their discovery was protected by US Patents 2,837,464 (1958); 2,897,216 (1959); and 3,134,718 (1964).

The enhanced adrenocorticoid activity of these compounds over cortisone and hydrocortisone was demonstrated in mice.[3]

Prednisone and prednisolone were introduced by Schering in the mid-1960s under the brand names Meticorten and Meticortelone respectively.

These prescription medicines are now available from a number of manufacturers as generic drugs.


Adrenal suppression will occur if prednisone is taken for longer than 7 days. This will cause the body to lose the ability to synthesize natural corticosteroids, resulting in dependence on prednisone. For this reason, prednisone should not be abruptly stopped if taken for more than seven days, and instead, the dosage should be gradually reduced. This weaning process may be over a few days if the course of prednisone was short, but may take weeks or months if the patient had been on long-term treatment. Abrupt withdrawal may lead to an Addisonian crisis. For those on chronic therapy, alternate-day dosing may preserve adrenal function, thereby reducing side-effects.[4]

Glucocorticoids act to feedback inhibit both the hypothalamus (decreasing Corticotropin-releasing hormone [CRH]) and corticotrophs in the anterior pituitary gland (decreasing the amount of Adrenocorticotropic hormone [ACTH]). For this reason exogenous glucocorticoid analogues down-regulate the body's ability to naturally produce glucocorticoids. This mechanism leads to dependence in a short time and can be very dangerous if medications are withdrawn too quickly. The body must have time to begin synthesis of CRH and ACTH and for the adrenal glands to begin functioning normally again.


Short-term side-effects, as with all glucocorticoids, include high blood glucose levels, especially in patients who already have diabetes mellitus or are on other medications that increase blood glucose (such as tacrolimus), and mineralocorticoid effects such as fluid retention (it is worth noting, however, that the mineralocorticoid effects of prednisone are very minor; this is why it is not used in the management of adrenal insufficiency unless a more potent mineralocorticoid is administered concomitantly).

Additional short-term side-effects include insomnia, euphoria, and, rarely, mania (particularly in those suffering from Bipolar I and II).

Long-term side-effects include Cushing's syndrome, truncal weight gain, osteoporosis, glaucoma, type II diabetes mellitus, and depression upon withdrawal.


Micrograph of fatty liver, as may be seen due to long-term prednisone use. Trichrome stain.



Lodotra is the trade name of an oral formulation which releases prednisone four hours after application. It is indicated for rheumatoid arthritis with morning stiffness. Taken at 10 pm, it releases the drug at around 2 am. The plasma peak level is reached at 4 am which is considered to be the optimal time for relieving morning stiffness. The drug was approved in the European Union in January 2009.[5][6]


  1. ^ Merck Index, 14th Edition, p.1327. Published by Merck & Co. Inc.
  2. ^ A.Nobile "et al." Journal of the American Chemical Society Vol 77, p.4184 (1955).
  3. ^ H.L. Herzog et al. Science, Vol. 121, p 176 (1955).
  4. ^ "Therapeutic and Adverse Effects of Glucocorticoids". U.S. Pharmacist.  
  5. ^ Wan, Yuet (8 January 2009). "Delayed-release prednisone (Lodotra™) approved in EU for treatment of rheumatoid arthritis". Retrieved 22 November 2009.  
  6. ^ Buttgereit, F.; Doering, G.; Schaeffler, A.; Witte, S.; Sierakowski, S.; Gromnica-Ihle, E.; Jeka, S.; Krueger, K. et al. (2008). "Efficacy of modified-release versus standard prednisone to reduce duration of morning stiffness of the joints in rheumatoid arthritis (CAPRA-1): a double-blind, randomised controlled trial". The Lancet 371: 205. doi:10.1016/S0140-6736(08)60132-4.   edit

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Simple English

Prednisone is a Corticosteroid. It can be used to treat Sarcoidosis, Autoimmune disease, and a variety of other diseases.

Diseases treated by prednisone

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