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Systematic (IUPAC) name
Clinical data
  • AU: A
  • US: C (Risk not ruled out)
Legal status
Legal status
Pharmacokinetic data
Biological half-life 2-3 hours
Excretion Prednisolone is excreted via urine
CAS Number 50-24-8
ATC code A07EA01 (WHO) C05AA04, D07AA03, D07XA02, H02AB06, R01AD02, S01BA04, S01CB02, S02BA03, S03BA02
PubChem CID 5755
DrugBank APRD00197
ChemSpider 5552
Synonyms 11,17-dihydroxy-17- (2-hydroxyacetyl)- 10,13-dimethyl-6,7,8,9,10,11,12,13,14,15,16,17- dodecahydrocyclopenta [a]phenanthren-3-one
Chemical data
Formula C21H28O5
Molar mass 360.444 g/mol[[Script error: No such module "String".]]
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Prednisolone is the active metabolite of prednisone.[1]


Prednisolone is a corticosteroid drug with predominantly glucocorticoid and low mineralocorticoid activity, making it useful for the treatment of a wide range of inflammatory and auto-immune conditions[2] such as asthma[3], uveitis, Pyoderma Gangrenosum, rheumatoid arthritis, ulcerative colitis, temporal arteritis and Crohn's disease, Bell's palsy, multiple sclerosis[4], cluster headaches, vasculitis, acute lymphoblastic leukemia and autoimmune hepatitis[5], systemic lupus erythematosus and dermatomyositis.

It can also be used as an immunosuppressive drug for organ transplants and in cases of adrenal insufficiency (Addison's). Prednisolone acetate ophthalmic suspension is an adrenocortical steroid product, prepared as a sterile ophthalmic suspension and used to reduce swelling, redness, itching, and allergic reactions affecting the eye.

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 with inflammation.

Mechanism of Action

Prednisolone irreversibly binds with glucocorticoid receptors (GR) alpha and beta for which they have a high affinity. AlphaGR and BetaGR are found in virtually all tissues with variable numbers between 3000 - 10000 per cell depending on the tissue involved. Prednisolone can activate and influence biochemical behaviour of most cells. The steroid/receptor complexes dimerise and interact with cellular DNA in the nucleus, binding to steroid-response elements and modifying gene transcription. They both induce synthesis of some genes and therefore some proteins, and inhibit synthesis of others. [6] [7]

Metabolic action: Not all actions on genes are known. Most mediator proteins are enzymes, e.g. cAMP-dependent kinase

Anti-inflammatory and immunosuppressive actions: -Inhibition of gene transcription for COX-2, cytokines, cell adhesion molecules and inducible NO synthetase -Blockage of Vit D3-mediated induction of osteocalcin gene in osteoblasts and modification of collegenase gene transcription -Increase synthesis annexin-1, important in negative feedback on hypothalamus and anterior pituitary gland, may have anti-inflammatory action.

Regulation of gene suppression leads to systemic suppression of inflammation and immune response. this is the clinical usefulness but ultimately leads to glyconeogenesis protolysis and lypolysis. Gene transcription returns to normal after cessation but sudden stoppage can cause Addison's disease. Osteoporosis is permanent.

Adverse effects

Possible side effects include fluid retention of the face (moon face, Cushing's syndrome), acne, constipation, and mood swings.

A lengthy course of prednisolone can cause bloody or black tarry stools; filling or rounding out of the face; muscle cramps or pain; muscle weakness; nausea; pain in back, hips, ribs, arms, shoulders, or legs; reddish-purple stretch marks on arms, face, legs, trunk or groin; thin and shiny skin; unusual bruising; urinating at night; rapid weight gain; and wounds that will not heal.

Swelling of the pancreas has also been reported.

Prednisolone can cause increased blood sugar levels for diabetics.

Other effects include decreased or blurred vision, increased eye pressure, increased thirst, confusion, rare cases of dementia in otherwise healthy elderly patients and nervousness.

It also is reported to cause insomnia when taken.

Banned status in athletics

As a glucocorticosteroid, prednisolone is banned under WADA anti-doping rules.[8]


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es:Prednisolona fr:Prednisolone ko:프레드니솔론 it:Prednisolone hu:Prednizolon nl:Prednisolon ja:プレドニゾロン pl:Prednizolon pt:Prednisolona ro:Prednisolon ru:Преднизолон sv:Prednisolon

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  2. Czock D, Keller F, Rasche FM, Häussler U. Pharmacokinetics and pharmacodynamics of systemically administered glucocorticoids. Clin Pharmacokinet. 2005;44(1):61-98. Review. PMID 15634032
  3. Fiel SB, Vincken W. Systemic corticosteroid therapy for acute asthma exacerbations. J Asthma. 2006 Jun-Jul;43(5):321-31. Review. PMID 16801135
  4. Thrower BW. Relapse management in multiple sclerosis. Neurologist. 2009 Jan;15(1):1-5. Review. PMID 19131851
  5. Lambrou GI, Vlahopoulos S, Papathanasiou C, Papanikolaou M, Karpusas M, Zoumakis E, Tzortzatou-Stathopoulou F. Prednisolone exerts late mitogenic and biphasic effects on resistant acute lymphoblastic leukemia cells: Relation to early gene expression. Leuk Res. 2009 May 16. [Epub ahead of print] PMID 19450877
  6. Prednisolone. Australian Medicines Handbook 2010. Adelaide: Australian Medicines handbook Pty Ltd.; 2010. 497, 598.,
  7. Rang HP, Dale MM, Ritter JM, Moore PK. The pituitary and the adrenal Cortex. Hunter l, editor. Pharmacology. 5th ed. London: Churchill Livingstone; 2003. 413, 415.
  8. "The 2008 Prohibited List".