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HCID 5865Erstellt: 26. Oktober 2026

Prednison

PREDNISON · MOPP · Deltasone · Prednisone-d4 · Prednisone Micronised · Pregna-1,4-diene-3,11,20-trione, 17,21-dihydroxy- · Cortan · Orasone

https://huagongshe.com/de/chemical/5865

Molekülstruktur von Prednison

Identifikatoren & physikalische Daten

CAS No.53-03-2
SummenformelC21H26O5
Durchschnittliche Molmasse358,4 g/mol
Monoisotopische Masse358,17802393 g/mol
SMILESC[C@]12C=CC(=O)C=C1CC[C@@H]1[C@@H]2C(=O)C[C@@]2(C)[C@H]1CC[C@]2(O)C(=O)CO
InChIKeyXOFYZVNMUHMLCC-ZPOLXVRWSA-N
PubChem CID5865
ChEMBLCHEMBL635
ChEBICHEBI:8382
EC No.200-160-3
DTXSIDDTXSID4021185
Lokaler NamePrednison

Chemische & physikalische Eigenschaften

XLogP1,5
Polarare Oberfläche (TPSA)91,7
H-Brücken-Donoren2
H-Brücken-Akzeptoren5
Frei drehbare Bindungen2
Schwere Atome26
Formalladung0
Komplexität764
pHPrednisone-syrup has a pH of 3-4.5 and contains 2-5% alcohol. Prednisone oral solution has a pH of 2.6-3.6 and contains 4-6% alcohol, and the oral concentrate solution has a pH of 3-4 and contains about 30% alcohol.
LogP (Verteilungskoeffizient)1.46log Kow = 1.460.6
GeruchOdorless
GeschmackPersistent bitter after-taste
Color/FormCrystalsWhite to practically white, crystalline powder
LöslichkeitVery slightly soluble (NTP, 1992)Very slightly solubleVery slightly soluble in water1 g soluble in 150 mL alcohol, in 200 mL chloroformslightly soluble in methanol1.11e-01 g/LPractically insoluble in water, slightly soluble in ethanol (96 per cent) and in methylene chloride. It shows polymorphism (5.9).115mg/L(25 ºC)
DecompositionHazardous decomposition products formed under fire conditions - Carbon oxides.When heated to decomposition it emits acrid smoke and irritating fumes.
Schmelzpunkt451 to 455 °F (DEC) (NTP, 1992)230234 °C (decomposes)233 - 235 °C236-238 °C(lit.)
Optical RotationSpecific optical rotation: +172 deg at 25 °C/D (dioxane)max absorption (methanol): 238 nm (e = 15,500)
Physical DescriptionPrednisone is an odorless white crystalline powder. (NTP, 1992)Solid
Stability/Shelf LifeStable under recommended storage conditions.
Collision Cross Section253.9 Ų [M-H]- [CCS Type: DTBuffer gas: N2Ionization: ESI-Dataset: TOXCASTSource Identifier: DTXSID4021185]184.1 Ų [M+H]+ [CCS Type: DTIonization: APCI+192.2 Ų [M+Na]+ [CCS Type: DTIonization: ESI+181.8 Ų [M+H]+ [CCS Type: TWMethod: calibrated with polyalanine and drug standards]174.8 Ų [M+H-H2O]+ [CCS Type: TW180.52 Ų [M+H]+ [CCS Type: TW180.1 Ų [M+H]+ [CCS Type: TW]
Siedepunkt410.86°C (rough estimate)
Dichte1.1121 (rough estimate)
Brechungsindex170 ° (C=0.5, Dioxane)
Flammpunkt>200℃
Lagerbedingungen2-8°C
pKa (Säurekonstante)12.36±0.60(Predicted)
AggregatzustandSolid
FarbeWhite to Off-White
Merck7722
BRN2065301
Henry-Konstante3.5×104 mol/(m3Pa) at 25℃, HSDB (2015)
BCS Class1
StabilitätStable. Incompatible with strong oxidizing agents.
Hauptanwendungenclinical testing
InChIKeyXOFYZVNMUHMLCC-ZPOLXVRWSA-N
SMILESO[C@]1([C@@]2([C@H]([C@H]3[C@@H]([C@@]4(C(=CC(=O)C=C4)CC3)C)C(=O)C2)CC1)C)C(=O)CO
CAS Datenbank53-03-2(CAS DataBase Reference)
NIST chemische InformationenPrednisone(53-03-2)
EPA chemische InformationenPrednisone (53-03-2)

Sicherheit & Vorschriften

GHS-EinstufungDangerH360 (33.7%): May damage fertility or the unborn child [Danger Reproductive toxicity]H361 (65.1%): Suspected of damaging fertility or the unborn child [Warning Reproductive toxicity]H372 (32%): Causes damage to organs through prolonged or repeated exposure [Danger Specific target organ toxicity, repeated exposure]H373 (20.1%): May causes damage to organs through prolonged or repeated exposure [Warning Specific target organ toxicity, repeated exposure]P203, P260, P264, P270, P280, P318, P319, P405, and P501 (click each P-code to see the statement)Aggregated GHS information provided per 169 reports by companies from 21 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. For more detailed information, please visit ECHA C&L website.
Regulatorische InformationenPrednisone: Does not have an individual approval but may be used under an appropriate group standard
Weitere SicherheitsinformationenIMAP assessments - Pregna-1,4-diene-3,11,20-trione, 17,21-dihydroxy-: Environment tier I assessmentIMAP assessments - Pregna-1,4-diene-3,11,20-trione, 17,21-dihydroxy-: Human health tier I assessment
GesundheitsgefahrenSYMPTOMS: Implicated in aplastic anemia.ACUTE/CHRONIC HAZARDS: Toxic. (NTP, 1992)
FDA-AnforderungenThe Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including prednisone, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act.The Generic Animal Drug and Patent Restoration act requires that each sponsor of an approved animal drug must submit to the FDA certain information regarding patents held for the animal drug or its method of use. The Act requires that this information, as well as a list of all animal drug products approved for safety and effectiveness, be made available to the public. Prednisone is included on this list.Implantation or injectable dosage form new animal drugs. Sterile prednisone suspension. ... Indications for use: It is used /in horses, dogs and cats/ for conditions requiring an anti-inflammatory agent. ... Do not use in horses intended for human consumption. Federal law restricts this drug to use by or on the order of a licensed veterinarian.
Reaktive GruppeAlcohols and PolyolsKetonesHydrocarbons, Aliphatic Unsaturated
Special ReportsWeisburger EKBioassay Program for Carcinogenic Hazards of Cancer Chemotherapeutic AgentsCancer 40: 1935-49 (1977). Route: intraperitoneal injectionSpecies: rats and mice.
Air and Water ReactionsVery slightly water soluble (NTP, 1992).
Hazard Classes and CategoriesRepr. 1B (33.7%)Repr. 2 (65.1%)STOT RE 1 (32%)STOT RE 2 (20.1%)
Hazardous Reactivities and IncompatibilitiesIncompatible materials: Strong oxidizing agents
BrandbekämpfungTo extinguish a fire involving this chemical you may use a dry chemical, carbon dioxide, foam or halon extinguishera water spray may also be used. (NTP, 1992)
Erste HilfeEYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.SKIN: IMMEDIATELY flood affected skin with water while removing and isolating all contaminated clothing. Gently wash all affected skin areas thoroughly with soap and water. If symptoms such as redness or irritation develop, IMMEDIATELY call a physician and be prepared to transport the victim to a hospital for treatment.INHALATION: IMMEDIATELY leave the contaminated areatake deep breaths of fresh air. If symptoms (such as wheezing, coughing, shortness of breath, or burning in the mouth, throat, or chest) develop, call a physician and be prepared to transport the victim to a hospital. Provide proper respiratory protection to rescuers entering an unknown atmosphere. Whenever possible, Self-Contained Breathing Apparatus (SCBA) should be usedif not available, use a level of protection greater than or equal to that advised under Protective Clothing.INGESTION: DO NOT INDUCE VOMITING. If the victim is conscious and not convulsing, give 1 or 2 glasses of water to dilute the chemical and IMMEDIATELY call a hospital or poison control center. Be prepared to transport the victim to a hospital if advised by a physician. If the victim is convulsing or unconscious, do not give anything by mouth, ensure that the victim's airway is open and lay the victim on his/her side with the head lower than the body. DO NOT INDUCE VOMITING. IMMEDIATELY transport the victim to a hospital. (NTP, 1992)
BrandbekämpfungsverfahrenSuitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary.
LagerbedingungenKeep container tightly closed in a dry and well-ventilated place.Prednisone tablets should be stored in well closed containers at a temperature less than 40 °C, preferably between 15-30 °C. Prednisone syrup should be stored in tight containers. Prednisone oral solution and oral concentrate solution should be stored in tight containers at 15-30 °C.
ReinigungsverfahrenACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Methods and materials for containment and cleaning up: Pick up and arrange disposal without creating dust. Sweep up and shovel. Keep in suitable, closed containers for disposal.
Freisetung ohne BrandSMALL SPILLS AND LEAKAGE: Should a spill occur while you are handling this chemical, you should dampen the solid spill material with alcohol, then transfer the dampened material to a suitable container. Use absorbent paper dampened with alcohol to pick up any remaining material. Seal the absorbent paper, and any of your clothes, which may be contaminated, in a vapor-tight plastic bag for eventual disposal. Solvent wash all contaminated surfaces with alcohol followed by washing with a strong soap and water solution. Do not reenter the contaminate area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.STORAGE PRECAUTIONS: You should keep this material in a tightly-closed container under an inert atmosphere, and store it in a freezer. (NTP, 1992)
EntsorgungsverfahrenSRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubberContaminated packaging: Dispose of as unused product.
Preventive MeasuresACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains.Precautions for safe handling: Avoid contact with skin and eyes. Avoid formation of dust and aerosols. Provide appropriate exhaust ventilation at places where dust is formed. Normal measures for preventive fire protection.Appropriate engineering controls: Handle in accordance with good industrial hygiene and safety practice. Wash hands before breaks and at the end of workday.Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants. Ensure that the local ventilation moves the contaminant away from the worker.
Personal Protective Equipment (PPE)RECOMMENDED RESPIRATOR: Where the neat test chemical is weighed and diluted, wear a NIOSH-approved half face respirator equipped with an organic vapor/acid gas cartridge (specific for organic vapors, HCl, acid gas and SO2) with a dust/mist filter.RECOMMENDED GLOVE MATERIALS: Permeation data indicate that neoprene gloves may provide protection to contact with this compound. Neoprene over latex gloves is recommended. However, if this chemical makes direct contact with your gloves, or if a tear, puncture or hole develops, remove them at once. (NTP, 1992)Eye/face protection: Safety glasses with side-shields conforming to EN166. Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU).Skin protection: Handle with gloves.Body Protection: Impervious clothing. The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace.Respiratory protection: Where risk assessment shows air-purifying respirators are appropriate use a full-face particle respirator type N100 (US) or type P3 (EN 143) respirator cartridges as a backup to engineering controls. If the respirator is the sole means of protection, use a full-face supplied air respirator. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU).
WechselwirkungenConcomitant use of anticholinesterase agents (e.g., neostigmine, pyridostigmine) and corticosteroids may produce severe weakness in patients with myasthenia gravis. If possible, anticholinesterase agents should be withdrawn at least 24 hours before initiating corticosteroid therapy. If concomitant therapy must occur, it should take place under close supervision and the need for respiratory support should be anticipated. /Corticosteroids/Co-administration of corticosteroids and warfarin usually results in inhibition of response to warfarin, although there have been some conflicting reports. Therefore, coagulation indices should be monitored frequently to maintain the desired anticoagulant effect. /Corticosteroids/Because corticosteroids may increase blood glucose concentrations, dosage adjustments of antidiabetic agents may be required. /Corticosteroids/Cholestyramine may increase the clearance of corticosteroids. /Corticosteroids/For more Interactions (Complete) data for PREDNISONE (25 total), please visit the HSDB record page.
UmweltverhaltenTERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 110(SRC), determined from a structure estimation method(2), indicates that prednisone is expected to have high mobility in soil(SRC). Volatilization of prednisone from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 2.8X10-10 atm-cu m/mole(SRC), using a fragment constant estimation method(3). Prednisone is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 3.8X10-13 mm Hg at 25 °C(SRC), determined from a fragment constant method(2). Biodegradation data in soil were not available(SRC, 2016).AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 110(SRC), determined from a structure estimation method(2), indicates that prednisone is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 2.8X10-10 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of 4(SRC), from its log Kow of 1.46(6) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Biodegradation data in water were not available(SRC, 2016).ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), prednisone, which has an estimated vapor pressure of 3.8X10-13 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase prednisone may be removed from the air by wet and dry deposition(SRC). Prednisone contains chromophores that absorb at wavelengths >290 nm(3) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).
Unerwünschte WirkungenAdverse effects are common in patients receiving glucocorticoids in high doses or over a long period. Regimens involving prednisone administration of ≥40 mg daily are considered "high-dose." The primary adverse effects associated with prednisone therapy include hyperglycemia, insomnia, increased appetite, hypertension, osteoporosis, edema, adrenal suppression, cataracts, delayed wound healing, skin fragility, weight gain, increased risk of infections, and fractures. Potential cardiovascular and metabolic effects include hypertension, hyperglycemia, and dyslipidemia.Other adverse reactions include adrenal insufficiency, particularly for patients with sepsis or undergoing stressful proceduresthis is typically diagnosable when the patient is hypotensive and not responsive to fluids, vasopressors, or cardiogenic medications. Once adrenal insufficiency is suspected, treatment should be initiated immediately with a dose of 100 mg of hydrocortisone every 8 hours. Osteonecrosis of the femoral head has also been reported.Drug-Drug Interactions* Amphotericin B: Prednisone combined with amphotericin B or other potassium-lowering drugs may cause hypokalemia. Therefore, clinicians are advised to monitor electrolyte levels in patients receiving these medications.* Macrolides: Some macrolide antibiotics (eg, clarithromycin) may slow the breakdown of prednisone, leading to increased steroid levels.* Warfarin: When warfarin is taken with prednisone, the former's anticoagulant effects can become inconsistent. Frequent INR checks are recommended.* Isoniazid: Isoniazid levels may drop when given with prednisone, which might lower its effectiveness.* Bupropion: Combining prednisone with bupropion may increase seizure risk. If used together, doses should start low and increase slowly.* Cholestyramine: Cholestyramine may reduce how long prednisone stays active by increasing its elimination rate.* Cyclosporine: When prednisone and cyclosporine are used together, the risk of immunosuppression increases.* Digoxin: Individuals receiving digoxin could be more prone to abnormal heart rhythms if potassium levels fall due to steroid therapy.* Estrogens: Estrogens can slow prednisone metabolism, leading to prolonged steroid action.* Fluoroquinolones: Tendon injuries, including ruptures, have been reported in patients receiving fluoroquinolones like ciprofloxacin together with prednisone, especially in older adults.* CYP3A4 inducers/inhibitors: Drugs that increase CYP3A4 enzyme activity (eg, phenytoin or rifampin) can make prednisone less effective. On the flip side, CYP3A4 inhibitors (like ketoconazole) may increase steroid levels and the risk of adverse effects.* Ketoconazole: Ketoconazole may also hinder natural steroid production, which can lead to problems if prednisone is stopped too quickly.* NSAIDs: Taking NSAIDs (eg, aspirin) with prednisone increases the risk of stomach ulcers or bleeding.
ExpositionspfadeReadily 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.
Milk ConcentrationsIt passes into breast milk in small amounts. /Adrenocorticosteroids/ /from table II/
ToxizitätsübersichtIDENTIFICATION AND USE: Prednisone is white crystalline powder with a persistent bitter after-taste. It is glucocorticoid, anti-inflammatory agent and antineoplastic agent. HUMAN EXPOSURE AND TOXICITY: Prednisone causes profound and varied metabolic effects when used at therapeutic doses, given on a continuous basis. When given in large doses it can induce cardiac complications. In addition, it modifies the body's immune response to diverse stimuliamong the changes that occur are lymphopenia, monocytopenia and suppression of delayed hypersensitivity skin tests. Fluid and electrolyte disturbances may occur, including sodium and fluid retention, which may lead to congestive heart failure and hypertension. With large doses, potassium loss, hypokalemic alkalosis, and increased calcium excretion may occur. Glucocorticoids may cause fetal damage when administered to pregnant women. One retrospective study of 260 women who received pharmacologic dosages of glucocorticoids during pregnancy revealed 2 instances of cleft palate, 8 stillbirths, 1 spontaneous abortion, and 15 premature births. Another study reported 2 cases of cleft palate in 86 births. No chromosomal damage was detected in peripheral lymphocytes of patients treated with 3 mg/kg bw per day prednisone alone for 28 days and then with 0.5-1 mg/kg bw per day for 18-120 months. ANIMAL STUDIES: Carcinogenicity studies have been conducted in rats and mice. Of treated males, 7/20 developed tumors, among which were 3 pituitary tumors and 1 tumor of the breast16/18 female rats developed tumors, 8 of the breast, 5 of the pituitary, 2 of the adrenal and 1 of the liver. The overall tumor incidence in females was 1.5-2-fold higher than that in controls. However in mice, the tumor incidence in treated males was 4/19 (21%), with 2 lymphosarcomas and 2 lung tumors, and that in treated females was 8/27 (30%), with 4 lung tumors, 2 lymphosarcomas and 2 uterine tumors. These incidences were not significantly greater than thoseSigns and Symptoms of OverdoseLike any anti-inflammatory agent, steroid toxicity is treated similarly to any non-steroidal anti-inflammatory drug overdose or toxicity. Although the frequency of life-threatening complications from steroids and NSAID overdose is low, the overdose response ranges from no symptoms to death despite intensive-care treatment. Most symptoms are due to the excessive pharmacological action of steroids and NSAIDs and include abdominal pain, nausea, vomiting, drowsiness, dizziness, headache, ear ringing, and nystagmus. A significant dose-response relationship occurs with the long-term use of systemic corticosteroids and the development of systemic corticosteroid-related complications for patients with severe asthma, resulting in an increased burden and costs on the healthcare system.Management of OverdoseAssessment of all organ systems can help identify problems. If necessary, hypertension and salt retention should be treated with salt restriction and diuretics. Gastrointestinal perforation requires surgical intervention. Antibiotics and antifungals should be prescribed for infections. An iatrogenic crushing syndrome caused by a supplement containing dexamethasone has been reported. Gradual tapering of corticosteroids is advisable to prevent adrenal insufficiency. Potent proton pump inhibitors should be prescribed for gastroprotection. Hypokalemia can be treated by replacement. Steroid-induced psychosis can be managed with antipsychotics. Hyperglycemia should be treated with insulin in critically ill patients. After stabilization, patients should be prescribed vitamin D and calcium. Mitotane and ketoconazole decrease cortisol production and should be used only under the supervision of an endocrinologist.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.
Ökotoxizitätsauszüge/AQUATIC SPECIES/ Solar simulator irradiation of an aqueous suspension of prednisone, a widely prescribed drug, produces seven photochemical derivatives. The compounds have been identified on the basis of their physical features. All the chemicals have been tested to evaluate their toxic effects on freshwater organisms from different trophic levels. The rotifer Brachionus calyciflorus and two crustaceans, the cladoceran Daphnia magna and the anostracan Thamnocephalus platyurus, were used to perform acute toxicity tests. Chronic toxicity tests have been performed on the alga Pseudokirchneriella subcapitata (formerly known as Selenastrum capricornutum) and the crustacean Ceriodaphnia dubia. The results showed low acute and chronic toxicity of prednisone. Some of the photoproducts had high toxic effects on C. dubia.
Ongoing Test StatusEPA has released the Interactive Chemical Safety for Sustainability (iCSS) Dashboard. The iCSS Dashboard provides an interactive tool to explore rapid, automated (or in vitro high-throughput) chemical screening data generated by the Toxicity Forecaster (ToxCast) project and the federal Toxicity Testing in the 21st century (Tox21) collaboration. /The title compound was tested by ToxCast and/or Tox21 assays/[USEPAICSS Dashboard ApplicationAvailable from, as of October 28, 2016: http://actor.epa.gov/dashboard/]The following link will take the user to the National Toxicology Program (NTP) Test Agent Search Results page, which tabulates all of the "Short-Term Toxicity Studies," "Long-Term Carcinogenicity Studies," and "Genetic Toxicology Studies" performed with this chemical. Clicking on the "Testing Status" link will take the user to the status (i.e., in review, in progress, in preparation, on test, completed, etc.) and results of all the studies that the NTP has done on this chemical.[Available from: http://ntp.niehs.nih.gov/testing/status/agents/ts-10936-e.html]
Effluent ConcentrationsPrednisone concentration in sewage influent samples in the Ebre, Ter and Llobregat Rivers, Tarragona area, Spain ranged from 21-285 ng/L(1). Prednisone was detected in 23 of 37 water samples collected from the River Wenyu and tributaries, Beijing China between Aug 9-12, 2006 at concentrations ranging from not detected to 0.25 ng/L. No farms or livestock areas were located within the sampling area(2).
Soil Adsorption/MobilityUsing a structure estimation method based on molecular connectivity indices(1), the Koc of prednisone can be estimated to be 110(SRC). According to a classification scheme(2), this estimated Koc value suggests that prednisone is expected to have high mobility in soil
Human Toxicity Excerpts/SIGNS AND SYMPTOMS/ Prednisone causes profound and varied metabolic effects when used at therapeutic doses, given on a continuous basis. When given in large doses it can induce cardiac complications. In addition, it modifies the body's immune response to diverse stimuliamong the changes that occur are lymphopenia, monocytopenia and suppression of delayed hypersensitivity skin tests. Fluid and electrolyte disturbances may occur, including sodium and fluid retention, which may lead to congestive heart failure and hypertension. With large doses, potassium loss, hypokalemic alkalosis, and increased calcium excretion may occur./SIGNS AND SYMPTOMS/ Moderate- to high-dose glucocorticoid therapy is associated with loss of bone and an increased risk of fracture. There also is evidence that long-term, low-dose (e.g., mean of 5.6 mg of prednisone daily) glucocorticoid therapy is associated with a risk of bone loss. Thus, while the American College of Rheumatology (ACR) previously considered patients who received at least 7.5 mg of prednisone (or its equivalent) daily for 6 months or longer to be at risk for glucocorticoid-induced osteoporosis, they currently consider patients receiving or planning to receive at least 5 mg of prednisone daily for 3 months or longer to be at risk for such bone loss. Skeletal wasting is most rapid during the initial 6 months of therapy, and trabecular bone is affected to a greater degree than is cortical bone. The adverse skeletal effects of glucocorticoids appear to be both dose and duration dependent, with prednisone dosages of at least 7.5 mg daily for 6 months or longer often resulting in clinically important bone loss and increased fracture risk./SIGNS AND SYMPTOMS/ Children with acute lymphoblastic leukemia (ALL) receive as part of induction therapy a 4-week course of high-dose glucocorticoid, which is either abruptly discontinued or shortly tapered. The aim of this study was to evaluate the signs and symptoms of steroid withdrawal syndrome and performance status (according to Lansky scale) during the 9-day tapering period and 1 week after withdrawal of the steroid in 63 children randomly allocated to receive prednisone or dexamethasone as part of induction treatment according the AIEOP ALL 2000 protocol. Twenty of 28 (75%) patients on dexamethasone versus 18 of 35 (51.4%) on prednisone (P < 0.05) developed at least one steroid withdrawal symptom during the study period. Three or more symptoms were observed in 39.3% (11/28) of the dexamethasone group and 8.6% (3/35) of the prednisone group (P < 0.05). Dexamethasone patients developed clinical signs earlier (within 3 days from the steroid tapering) than symptomatic prednisone patients. In the prednisone group, the symptoms were less severe and the performance status was higher (P < 0.05). .../SIGNS AND SYMPTOMS/ Glucocorticoids, especially in large doses, increase susceptibility to and mask symptoms of infection. Infections with any pathogen, including viral, bacterial, fungal, protozoan, or helminthic infections in any organ system, may be associated with glucocorticoids alone or in combination with other immunosuppressive agents. These infections may be mild, but they can be severe or fatal, and localized infections may disseminate. Patients who become immunosuppressed while receiving glucocorticoids have increased susceptibility to infections compared with healthy individuals. Some infections such as varicella (chickenpox) and measles can have a more serious or even fatal outcome in such patients, particularly in children. /Corticosteroids/For more Human Toxicity Excerpts (Complete) data for PREDNISONE (21 total), please visit the HSDB record page.
Artificial Pollution SourcesPrednisone's production and use as a glucocorticoid, veterinary adrenocortical steroid, veterinary glucocorticoid, and veterinary anti-inflammatory(1) may result in its release to the environment through various waste streams(SRC).
Wassergefährdungsklasse (WGK)WGK 2
TSCA-Inventar-StatusTSCA listed
GefahrensymboleXn
Sicherheitshinweise (S)36/37/39-45-26-16
Lagerklasse3 - Flammable liquids
Gefahrstoffdaten53-03-2(Hazardous Substances Data)
GefahrenklasseAcute Tox. 4 DermalAcute Tox. 4 InhalationAcute Tox. 4 OralEye Irrit. 2Flam. Liq. 2

Anwendungen & Verwendung

History

The first isolation and structure identifications of prednisone and prednisolone were done in 1950 by Arthur Nobile. 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. They discovered that cortisone could be microbiologically oxidized to prednisone by the bacterium Corynebacterium simplex. Prednisone was introduced in 1955 by Schering, under the brand name Meticorten.Prednisone was patented in 1954 and approved for medical use in the United States in 1955. In 2023, it was the 38th most commonly prescribed medication in the United States, with more than 15 million prescriptions.

Verwenden

Prednisone is used for the same indications as cortisone for inflammatory processes, allergies, and adrenal gland insufficiency; however, it is somewhat more active than cortisone and has less of an effect on mineral volume.