<?xml version="1.0" encoding="UTF-8"?>
<compound>
  <id type="integer">4765</id>
  <title>T3D4710</title>
  <common-name>Prednisone</common-name>
  <description>Prednisone is only found in individuals that have used or taken this drug. It is a synthetic anti-inflammatory glucocorticoid derived from cortisone. It is biologically inert and converted to prednisolone in the liver. Prednisone is a glucocorticoid receptor 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.</description>
  <cas>53-03-2</cas>
  <pubchem-id>5865</pubchem-id>
  <chemical-formula>C21H26O5</chemical-formula>
  <weight nil="true"/>
  <appearance>White powder.</appearance>
  <melting-point>233 - 235°C</melting-point>
  <boiling-point nil="true"/>
  <density nil="true"/>
  <solubility>1.11e-01 g/L</solubility>
  <specific-gravity nil="true"/>
  <flash-point nil="true"/>
  <vapour-pressure nil="true"/>
  <route-of-exposure>Readily absorbed from the gastrointestinal tract. Rayos, the delayed-release formulation, has a 4-hour release time. To compare, the delayed-release formulation has a Tmax of 6.0 - 6.5 hours in healthy male subjects, whereas the immediate-release formulation has a Tmax of 2.0 hours. The rate of absorption, Cmax, and exposure is comparable between formulations. </route-of-exposure>
  <target nil="true"/>
  <mechanism-of-toxicity>Prednisone is a glucocorticoid receptor 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. Prednisone can stimulate secretion of various components of gastric juice. Suppression of the production of corticotropin may lead to suppression of endogenous corticosteroids. Prednisone has slight mineralocorticoid activity, whereby entry of sodium into cells and loss of intracellular potassium is stimulated. This is particularly evident in the kidney, where rapid ion exchange leads to sodium retention and hypertension.</mechanism-of-toxicity>
  <metabolism>Prednisone is completely converted to the active metabolite prednisolone by 11‘_-hydroxysteroid dehydrogenases. It is then further metabolized mainly in the liver. The exposure of prednisolone is 4-6 fold higher than that of prednisone.Route of Elimination: Excreted in the urine as sulfate and glucuronide conjugates. Half Life: Half life of both the immediate- and delayed- release formulation is 2 to 3 hours. </metabolism>
  <toxicity nil="true"/>
  <lethaldose nil="true"/>
  <carcinogenicity>Prednisone is not classifiable as to its carcinogenicity to humans (Group 3). Prednisone is part of MOPP, a combination chemotherapy regimen that is carcinogenic to humans (Group 1). (L135)</carcinogenicity>
  <use-source>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.</use-source>
  <min-risk-level nil="true"/>
  <health-effects nil="true"/>
  <symptoms nil="true"/>
  <treatment nil="true"/>
  <created-at type="dateTime">2014-09-11T02:05:57Z</created-at>
  <updated-at type="dateTime">2026-05-14T16:44:43Z</updated-at>
  <interacting-proteins nil="true"/>
  <wikipedia>http://en.wikipedia.org/wiki/Prednisone</wikipedia>
  <uniprot-id nil="true"/>
  <kegg-compound-id>C07370</kegg-compound-id>
  <omim-id nil="true"/>
  <chebi-id>8382</chebi-id>
  <biocyc-id nil="true"/>
  <ctd-id nil="true"/>
  <stitch-id nil="true"/>
  <drugbank-id>DB00635</drugbank-id>
  <pdb-id nil="true"/>
  <actor-id nil="true"/>
  <organism nil="true"/>
  <export type="boolean">true</export>
  <metabolizing-proteins nil="true"/>
  <transporting-proteins nil="true"/>
  <moldb-smiles>[H][C@@]12CC[C@](O)(C(=O)CO)[C@@]1(C)CC(=O)[C@@]1([H])[C@@]2([H])CCC2=CC(=O)C=C[C@]12C</moldb-smiles>
  <moldb-formula>C21H26O5</moldb-formula>
  <moldb-inchi>InChI=1S/C21H26O5/c1-19-7-5-13(23)9-12(19)3-4-14-15-6-8-21(26,17(25)11-22)20(15,2)10-16(24)18(14)19/h5,7,9,14-15,18,22,26H,3-4,6,8,10-11H2,1-2H3/t14-,15-,18+,19-,20-,21-/m0/s1</moldb-inchi>
  <moldb-inchikey>XOFYZVNMUHMLCC-ZPOLXVRWSA-N</moldb-inchikey>
  <moldb-average-mass type="decimal">358.4281</moldb-average-mass>
  <moldb-mono-mass type="decimal">358.178023942</moldb-mono-mass>
  <origin>Exogenous</origin>
  <state>Solid</state>
  <logp>1.46</logp>
  <hmdb-id>HMDB14773</hmdb-id>
  <chembl-id>CHEMBL635</chembl-id>
  <chemspider-id>5656</chemspider-id>
  <structure-image-file-name nil="true"/>
  <structure-image-content-type nil="true"/>
  <structure-image-file-size type="integer" nil="true"/>
  <structure-image-updated-at type="dateTime" nil="true"/>
  <biodb-id nil="true"/>
  <synthesis-reference>&lt;p&gt;Jean Buendia, Michel Vivat, &amp;#8220;Process for the production of prednisone 17.21-diacylates.&amp;#8221; U.S. Patent US4601854, issued May, 1982.&lt;/p&gt;</synthesis-reference>
  <structure-image-caption nil="true"/>
  <chemdb-id>CHEM003668</chemdb-id>
  <dsstox-id>DTXSID4021185</dsstox-id>
  <toxcast-id nil="true"/>
  <stoff-ident-origin nil="true"/>
  <stoff-ident-id nil="true"/>
  <susdat-id>NS00007844</susdat-id>
  <iupac>(1R,3aS,3bS,9aR,9bS,11aS)-1-hydroxy-1-(2-hydroxyacetyl)-9a,11a-dimethyl-1H,2H,3H,3aH,3bH,4H,5H,7H,9aH,9bH,10H,11H,11aH-cyclopenta[a]phenanthrene-7,10-dione</iupac>
  <moldb-polar-surface-area>91.66999999999999</moldb-polar-surface-area>
  <moldb-refractivity>97.56809999999999</moldb-refractivity>
  <moldb-polarizability>38.16717892160918</moldb-polarizability>
  <moldb-rotatable-bond-count>2</moldb-rotatable-bond-count>
  <moldb-acceptor-count>5</moldb-acceptor-count>
  <moldb-donor-count>2</moldb-donor-count>
  <moldb-pka-strongest-acidic>12.57619881791117</moldb-pka-strongest-acidic>
  <moldb-pka-strongest-basic>-3.32998911888836</moldb-pka-strongest-basic>
  <moldb-physiological-charge>0</moldb-physiological-charge>
  <moldb-number-of-rings>4</moldb-number-of-rings>
  <moldb-alogps-logp>2.07</moldb-alogps-logp>
  <moldb-alogps-logs>-3.51</moldb-alogps-logs>
  <moldb-alogps-solubility>1.11e-01 g/l</moldb-alogps-solubility>
</compound>
