Prednisone delayed-release tablets are indicated in the treatment of the following diseases or conditions: 1.1 Allergic Conditions Control of severe or incapacitating allergic conditions intractable to adequate trials of conventional treatment in adults and pediatric populations with: Atopic dermatitis Drug hypersensitivity reactions Seasonal or perennial allergic rhinitis Serum sickness 1.2 Dermatologic Diseases ...
Dosage of prednisone delayed-release tablets should be individualized according to the severity of the disease and the response of the patient. For pediatric patients, the recommended dosage should be governed by the same considerations rather than strict adherence to the ratio indicated by age or body weight. The maximal activity of the adrenal cortex is between 2 am and 8 am and is minimal between 4 pm and midni...
Prednisone delayed-release tablets (1 mg prednisone) are white to off-white colored, round, unscored, delayed release tablet, debossed with "1" on one side and plain on other side, mottled appearance, free from physical defects. NDC Number Size 74157-010-30 Bottle of 30 tablets Prednisone delayed-release tablets (2 mg prednisone) are light peach to peach colored, round, unscored, delayed release tablet, debossed w...
www.fda.gov/medwatchPrednisone delayed-release tablets are indicated in the treatment of the following diseases or conditions:
1.1 Allergic Conditions
Control of severe or incapacitating allergic conditions intractable to adequate trials of conventional treatment in adults and pediatric populations with:
1.2 Dermatologic Diseases
1.3 Endocrine Conditions
1.4 Gastrointestinal Diseases
During acute episodes in:
1.5 Hematologic Diseases
1.6 Neoplastic Conditions
For the treatment of:
1.7 Nervous System Conditions
1.8 Ophthalmic Conditions
1.9 Conditions Related to Organ Transplantation
1.10 Pulmonary Diseases
1.11 Renal Conditions
1.12 Rheumatologic Conditions
As adjunctive therapy for short-term administration (to tide the patient over an acute episode or exacerbation) in:
During an exacerbation or as maintenance therapy in selected cases of:
1.13 Specific Infectious Diseases
Dosage of prednisone delayed-release tablets should be individualized according to the severity of the disease and the response of the patient. For pediatric patients, the recommended dosage should be governed by the same considerations rather than strict adherence to the ratio indicated by age or body weight.
The maximal activity of the adrenal cortex is between 2 am and 8 am and is minimal between 4 pm and midnight. Exogenous corticosteroids suppress adrenocorticoid activity the least when given at the time of maximal activity. Prednisone delayed-release tablet is a delayed-release formulation of prednisone which releases the active substance beginning approximately 4 hours after intake [ see Clinical Pharmacology (12.3) ]. The timing of prednisone delayed-release tablets administration should take into account the delayed-release pharmacokinetics and the disease or condition being treated.
The initial dosage of prednisone delayed-release tablets may vary from 5 to 60 mg per day depending on the specific disease entity being treated. Patients currently on immediate release prednisone, prednisolone, or methylprednisolone should be switched to prednisone delayed-release tablets at an equivalent dose based on relative potency (2.4).
In situations of less severity, lower doses will generally suffice while in selected patients higher initial doses may be required. The initial dosage should be maintained or adjusted until a satisfactory response is noted. If after a reasonable period there is a lack of satisfactory clinical response, prednisone delayed-release tablets should be discontinued and the patient transferred to other appropriate therapy. It should be emphasized that dosage requirements are variable and must be individualized on the basis of the disease under treatment and the response of the patient.
After a favorable response is noted, the proper maintenance dosage should be determined by decreasing the initial drug dosage in small decrements at appropriate time intervals until the lowest dosage which will maintain an adequate clinical response is reached. It should be kept in mind that constant monitoring is needed in regard to drug dosage. Included in the situations which may make dosage adjustments necessary are changes in clinical status secondary to remissions or exacerbations in the disease process, the patient's individual drug responsiveness, and the effect of patient exposure to stressful situations not directly related to the disease entity under treatment. In this latter situation it may be necessary to increase the dosage of prednisone delayed-release tablets for a period of time consistent with the patient's condition. If a period of spontaneous remission occurs in a chronic condition, treatment should be discontinued. If after long-term therapy the drug is to be stopped, it is recommended that it be withdrawn gradually rather than abruptly.
Blood pressure, body weight, routine laboratory studies (including 2-hour postprandial blood glucose and serum potassium), and chest X-ray should be obtained at regular intervals during prolonged therapy with prednisone delayed-release tablets. Upper GI X-rays are desirable in patients with known or suspected peptic ulcer disease.
Prednisone delayed-release tablets are for oral administration.
Prednisone delayed-release tablets should be taken daily with food. [see Clinical Pharmacology (12.3)]
Prednisone delayed-release tablets should not be broken, divided, or chewed because the delayed release of prednisone is dependent on an intact coating [see Description (11)].
For the purpose of comparison, one 5 mg prednisone delayed-release tablet is the equivalent milligram dosage of the following various corticosteroids:
| Betamethasone, 0.75 mg | Paramethasone, 2 mg |
| Cortisone, 25 mg | Prednisolone, 5 mg |
| Dexamethasone, 0.75 mg | Prednisone, 5 mg |
| Hydrocortisone, 20 mg | Triamcinolone, 4 mg |
| Methylprednisolone, 4 mg |
These dose relationships apply only to oral or intravenous administration of these compounds. When these substances or their derivatives are injected intramuscularly or into joint spaces, their relative properties may be greatly altered.
Delayed-release Tablets
Prednisone delayed-release tablets are contraindicated in patients who have known hypersensitivity to prednisone or to any of the excipients. Rare instances of anaphylaxis have occurred in patients receiving corticosteroid therapy [ see Adverse Reactions (6) ].
Hypothalamic-pituitary-adrenal (HPA) axis suppression, Cushing's syndrome, and hyperglycemia. Monitor patients for these conditions with chronic use.
Corticosteroids can produce reversible hypothalamic-pituitary adrenal (HPA) axis suppression with the potential for corticosteroid insufficiency after withdrawal of treatment. Drug-induced secondary adrenocortical insufficiency may be minimized by gradual reduction of dosage. This type of relative insufficiency may persist for months after discontinuation of therapy; therefore, in any situation of stress occurring during that period, hormone therapy should be reinstituted. If the patient is receiving corticosteroids already, dosage may have to be increased.
Since mineralocorticoid secretion may be impaired, salt and/or a mineralocorticoid should be administered concurrently. Mineralocorticoid supplementation is of particular importance in infancy.
Metabolic clearance of corticosteroids is decreased in hypothyroid patients and increased in hyperthyroid patients. Changes in thyroid status of the patient may necessitate adjustment in dosage.
Corticosteroids, including prednisone delayed-release tablets, suppress the immune system and increase the risk of infection with any pathogen, including viral, bacterial, fungal, protozoan, or helminthic pathogens. Corticosteroids can:
Corticosteroid-associated infections can be mild but can be severe and at times fatal. The rate of infectious complications increases with increasing corticosteroid dosages.
Monitor for the development of infection and consider prednisone delayed-release tablets withdrawal or dosage reduction as needed.
Tuberculosis
If prednisone delayed-release tablets are used to treat a condition in patients with latent tuberculosis or tuberculin reactivity, reactivation of tuberculosis may occur. Closely monitor such patients for reactivation. During prolonged prednisone delayed-release tablets therapy, patients with latent tuberculosis or tuberculin reactivity should receive chemoprophylaxis.
Varicella Zoster and Measles Viral Infections
Varicella and measles can have a serious or even fatal course in non-immune patients taking corticosteroids, including prednisone delayed-release tablets. In corticosteroid-treated patients who have not had these diseases or are non-immune, particular care should be taken to avoid exposure to varicella and measles:
Hepatitis B Virus Reactivation
Hepatitis B virus reactivation can occur in patients who are hepatitis B carriers treated with immunosuppressive dosages of corticosteroids, including prednisone delayed-release tablets. Reactivation can also occur infrequently in corticosteroid-treated patients who appear to have resolved hepatitis B infection.
Screen patients for hepatitis B infection before initiating immunosuppressive (e.g., prolonged) treatment with prednisone delayed-release tablets. For patients who show evidence of hepatitis B infection, recommend consultation with physicians with expertise in managing hepatitis B regarding monitoring and consideration for hepatitis B antiviral therapy.
Fungal Infections
Corticosteroids, including prednisone delayed-release tablets, may exacerbate systemic fungal infections; therefore, avoid prednisone delayed-release tablets use in the presence of such infections unless prednisone delayed-release tablets are needed to control drug reactions. For patients on chronic prednisone delayed-release tablets therapy who develop systemic fungal infections, prednisone delayed-release tablets withdrawal or dosage reduction is recommended.
Amebiasis
Corticosteroids, including prednisone delayed-release tablets, may activate latent amebiasis. Therefore, it is recommended that latent amebiasis or active amebiasis be ruled out before initiating prednisone delayed-release tablets in patients who have spent time in the tropics or patients with unexplained diarrhea.
Strongyloides Infestation
Corticosteroids, including prednisone delayed-release tablets, should be used with great care in patients with known or suspected Strongyloides (threadworm) infestation. In such patients, corticosteroid-induced immunosuppression may lead to Strongyloides hyperinfection and dissemination with widespread larval migration, often accompanied by severe enterocolitis and potentially fatal gram-negative septicemia.
Cerebral Malaria
Avoid corticosteroids, including prednisone delayed-release tablets, in patients with cerebral malaria.
Corticosteroids can cause elevation of blood pressure, salt, and water retention, and increased excretion of potassium and calcium. These effects are less likely to occur with the synthetic derivatives except when used in large doses. Dietary salt restriction and potassium supplementation may be necessary. These agents should be used with caution in patients with congestive heart failure, hypertension, or renal insufficiency.
Literature reports suggest an apparent association between use of corticosteroids and left ventricular free wall rupture after a recent myocardial infarction; therefore, therapy with corticosteroids should be used with great caution in these patients.
There is an increased risk of gastrointestinal perforation in patients with certain GI disorders. Signs of GI perforation, such as peritoneal irritation may be masked in patients receiving corticosteroids.
Corticosteroids should be used with caution if there is a probability of impending perforation, abscess, or other pyogenic infections; diverticulitis; fresh intestinal anastomoses; and active or latent peptic ulcer.
Corticosteroids use may be associated with central nervous system effects ranging from euphoria, insomnia, mood swings, personality changes, and severe depression, to frank psychotic manifestations. Also, existing emotional instability or psychotic tendencies may be aggravated by corticosteroids.
Corticosteroids decrease bone formation and increase bone resorption both through their effect on calcium regulation (i.e., decreasing absorption and increasing excretion) and inhibition of osteoblast function. This, together with a decrease in the protein matrix of the bone secondary to an increase in protein catabolism, and reduced sex hormone production, may lead to inhibition of bone growth in children and adolescents and the development of osteoporosis at any age. Special consideration should be given to patients at increased risk of osteoporosis (i.e., postmenopausal women) before initiating corticosteroid therapy and bone density should be monitored in patients on long term corticosteroid therapy.
Prolonged use of corticosteroids may produce posterior subcapsular cataracts, glaucoma with possible damage to the optic nerves, and may enhance the establishment of secondary ocular infections due to fungi or viruses.
The use of oral corticosteroids is not recommended in the treatment of optic neuritis and may lead to an increase in the risk of new episodes.
Intraocular pressure may become elevated in some individuals. If corticosteroid therapy is continued for more than 6 weeks, intraocular pressure should be monitored.
Corticosteroids should be used cautiously in patients with ocular herpes simplex because of possible corneal perforation. Corticosteroids should not be used in active ocular herpes simplex.
Administration of live or live, attenuated vaccines is contraindicated in patients receiving immunosuppressive doses of corticosteroids. Killed or inactivated vaccines may be administered; however, the response to such vaccines cannot be predicted. Immunization procedures may be undertaken in patients who are receiving corticosteroids as replacement therapy, e.g., for Addison's disease.
While on corticosteroid therapy, patients should not be vaccinated against smallpox. Other immunization procedures should not be undertaken in patients who are on corticosteroids, especially on high dose, because of possible hazards of neurological complications and a lack of antibody response.
Long-term use of corticosteroids can have negative effects on growth and development in children.
Growth and development of pediatric patients on prolonged corticosteroid therapy should be carefully monitored.
Prednisone can cause fetal harm when administered to a pregnant woman. Human studies suggest a small but inconsistent increased risk of orofacial clefts with use of corticosteroids during the first trimester of pregnancy. Published animal studies show prednisolone to be teratogenic in rats, rabbits, hamsters, and mice with increased incidence of cleft palate in offspring. Intrauterine growth restriction and decreased birth weight have also been reported with corticosteroid use during pregnancy, however, the underlying maternal condition may also contribute to these risks. If this drug is used during pregnancy, or if the patient becomes pregnant while using this drug, advise the patient about the potential harm to the fetus [see Use in Specific Populations (8.1)].
Although controlled clinical trials have shown corticosteroids to be effective in speeding the resolution of acute exacerbations of multiple sclerosis, they do not show that they affect the ultimate outcome or natural history of the disease. The studies do show that relatively high doses of corticosteroids are necessary to demonstrate a significant effect.
An acute myopathy has been observed with the use of high doses of corticosteroids, most often occurring in patients with disorders of neuromuscular transmission (e.g., myasthenia gravis), or in patients receiving concomitant therapy with neuromuscular blocking drugs (e.g., pancuronium). This acute myopathy is generalized, may involve ocular and respiratory muscles, and may result in quadriparesis. Elevation of creatine kinase may occur. Clinical improvement or recovery after stopping corticosteroids may require weeks to years.
Kaposi's sarcoma has been reported to occur in patients receiving corticosteroid therapy, most often for chronic conditions. Discontinuation of corticosteroids may result in clinical improvement of Kaposi’s sarcoma.
Common adverse reactions for corticosteroids include fluid retention, alteration in glucose tolerance, elevation in blood pressure, behavioral and mood changes, increased appetite and weight gain.
Allergic Reactions:Anaphylaxis, angioedema
Cardiovascular:Bradycardia, cardiac arrest, cardiac arrhythmias, cardiac enlargement, circulatory collapse, congestive heart failure, fat embolism, hypertension, hypertrophic cardiomyopathy in premature infants, myocardial rupture following recent myocardial infarction, pulmonary edema, syncope, tachycardia, thromboembolism, thrombophlebitis, vasculitis
Dermatologic:Acne, allergic dermatitis, cutaneous and subcutaneous atrophy, dry scalp, edema, facial erythema, hyper or hypopigmentation, impaired wound healing, increased sweating, petechiae and ecchymoses, rash, sterile abscess, striae, suppressed reactions to skin tests, thin fragile skin, thinning scalp hair, urticaria
Endocrine:Abnormal fat deposits, decreased carbohydrate tolerance, development of Cushingoid state, hirsutism, manifestations of latent diabetes mellitus and increased requirements for insulin or oral hypoglycemic agents in diabetics, menstrual irregularities, moon facies, secondary adrenocortical and pituitary unresponsiveness (particularly in times of stress, as in trauma, surgery or illness), suppression of growth in children
Fluid and Electrolyte Disturbances:Fluid retention, potassium loss, hypertension, hypokalemic alkalosis, sodium retention
Gastrointestinal:Abdominal distention, elevation in serum liver enzymes levels (usually reversible upon discontinuation), hepatomegaly, hiccups, malaise, nausea, pancreatitis, peptic ulcer with possible perforation and hemorrhage, ulcerative esophagitis
General:Increased appetite and weight gain
Metabolic:Negative nitrogen balance due to protein catabolism
Musculoskeletal:Osteonecrosis of femoral and humeral heads, charcot-like arthropathy, loss of muscle mass, muscle weakness, osteoporosis, pathologic fracture of long bones, steroid myopathy, tendon rupture, vertebral compression fractures
Neurological:Arachnoiditis, convulsions, depression, emotional instability, euphoria, headache, increased intracranial pressure with papilledema (pseudo-tumor cerebri) usually following discontinuation of treatment, insomnia, meningitis, mood swings, neuritis, neuropathy, paraparesis/paraplegia, paresthesia, personality changes, sensory disturbances, vertigo
Ophthalmic:Exophthalmos, glaucoma, increased intraocular pressure, posterior subcapsular cataracts, and central serous chorioretinopathy
Reproductive:Alteration in motility and number of spermatozoa
Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in practice.
The safety of prednisone delayed-release tablets was evaluated in 375 rheumatoid arthritis patients in two controlled trials. Patients treated with prednisone delayed-release tablets ranged in age from 20 to 80 years (median age 56 years), with 85% female, 99% Caucasian, 1% African-American, and < 1% Asian.
Patients received prednisone delayed-release tablets 3 mg to 10 mg once daily at 10 pm; the majority (84%) received ≤ 5 mg. The clinical trial experience did not raise new safety concerns beyond those already established for immediate-release prednisone.
Adverse reactions have been identified during post approval use of prednisone delayed-release tablets. Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure. The postmarketing experience has not raised new safety concerns beyond those already established for immediate-release prednisone.
7.1 Aminoglutethimide
Aminoglutethimide may lead to loss of corticosteroid-induced adrenal suppression.
7.2 Amphotericin B Injection
There have been cases reported in which concomitant use of Amphotericin B and hydrocortisone was followed by cardiac enlargement and congestive heart failure [see Drug Interactions (7.14)] .
7.3 Anticholinesterase Agents
Concomitant use of anticholinesterase agents 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.
7.4 Anticoagulant Agents
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.
7.5 Antidiabetic Agents
Because corticosteroids may increase blood glucose concentrations, dosage adjustments of antidiabetic agents may be required.
7.6 Antitubercular Drugs
Serum concentrations of isoniazid may be decreased.
7.7 CYP 3A4 Inducers (e.g., Barbiturates, Phenytoin, Carbamazepine, and Rifampin)
Drugs such as barbiturates, phenytoin, ephedrine, and rifampin, which induce hepatic microsomal drug metabolizing enzyme activity may enhance the metabolism of corticosteroids and require that the dosage of the corticosteroid be increased.
7.8 CYP 3A4 Inhibitors (e.g., Ketoconazole, Macrolide Antibiotics)
Ketoconazole has been reported to decrease the metabolism of certain corticosteroids by up to 60% leading to increased risk of corticosteroid side effects.
7.9 Cholestyramine
Cholestyramine may increase the clearance of corticosteroids.
7.10 Cyclosporine
Increased activity of both cyclosporine and corticosteroids may occur when the two are used concurrently. Convulsions have been reported with this concurrent use.
7.11 Digitalis
Patients on digitalis glycosides may be at increased risk of arrhythmias due to hypokalemia.
7.12 Estrogens, Including Oral Contraceptives
Estrogens may decrease the hepatic metabolism of certain corticosteroids, thereby increasing their effect.
7.13 Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) Including Aspirin and Salicylates
Concomitant use of aspirin or other nonsteroidal anti-inflammatory drugs and corticosteroids increases the risk of gastrointestinal side effects. Aspirin should be used cautiously in conjunction with corticosteroids in hypoprothrombinemia. The clearance of salicylates may be increased with concurrent use of corticosteroids; this could lead to decreased salicylate serum levels or increase the risk of salicylate toxicity when corticosteroid is withdrawn.
7.14 Potassium-Depleting Agents (e.g., Diuretics, Amphotericin B)
When corticosteroids are administered concomitantly with potassium-depleting agents, patients should be observed closely for development of hypokalemia.
7.15 Skin Tests
Corticosteroids may suppress reactions to skin tests.
7.16 Toxoids and Live or Attenuated Vaccines
Patients on corticosteroid therapy may exhibit a diminished response to toxoids and live or inactivated vaccines due to inhibition of antibody response. Corticosteroids may also potentiate the replication of some organisms contained in live attenuated vaccines. Routine administration of vaccines or toxoids should be deferred until corticosteroid therapy is discontinued if possible [ see Warnings and Precautions (5.8) ].
Risk Summary
Based on findings from human and animal studies, corticosteroids, including prednisone delayed-release tablets, can cause fetal harm when administered to a pregnant woman (see Data) [see Warnings and Precautions (5.10)]. Published epidemiological studies suggest a small but inconsistent increased risk of orofacial clefts with use of corticosteroids during the first trimester. Intrauterine growth restriction and decreased birth weight have also been reported with maternal use of corticosteroids during pregnancy; however, the underlying maternal condition may also contribute to these risks (see Clinical Considerations). Published animal studies show prednisolone to be teratogenic in rats, rabbits, hamsters, and mice with increased incidence of cleft palate in offspring (see Data). Advise a pregnant woman about the potential harm to a fetus.
The estimated background risk of major birth defects and miscarriage for the indicated populations is unknown. All pregnancies have a background risk of birth defect, loss or other adverse outcomes. In the US general population, the estimated background risk of major birth defects and miscarriage in clinical recognized pregnancies is 2% to 4% and 15% to 20%, respectively.
Clinical Considerations
Fetal/Neonatal Adverse Reactions
Infants born to pregnant women who have received corticosteroids should be carefully monitored for signs and symptoms of hypoadrenalism [see Warnings and Precautions (5.1)]
Data
Human Data
Published epidemiological studies on the association between prednisolone and fetal outcomes have reported inconsistent findings and have important methodological limitations. Multiple cohort and case-controlled studies in humans suggest that maternal corticosteroid use during the first trimester increases the incidence of cleft lip with or without cleft palate from about 1/1000 infants to 3-5/1000 infants; however, a risk for orofacial clefts has not been observed in all studies. Methodological limitations of these studies include non-randomized design, retrospective data collection, and the inability to control for confounders such as underlying maternal disease and use of concomitant medications.
Two prospective case control studies showed decreased birth weight in infants exposed to maternal corticosteroids in utero. In humans, the risk of decreased birth weight appears to be dose related and may be minimized by administering lower corticosteroid doses. It is likely that underlying maternal conditions contribute to intrauterine growth restriction and decreased birth weight, but it is unclear to what extent these maternal conditions contribute to the increased risk of orofacial clefts.
Animal Data
Prednisolone, the active metabolite of prednisone, administered during the period of organogenesis, has been shown to be teratogenic in rats, rabbits, hamsters, and mice with increased incidence of cleft palate in offspring. In teratogenicity studies, cleft palate along with elevation of fetal lethality (or increase in resorptions) and reductions in fetal body weight were seen in rats at maternal doses of 30 mg/kg (equivalent to 290 mg in a 60 kg individual based on mg/m 2body surface comparison) and higher. Cleft palate was observed in mice at a maternal dose of 20 mg/kg (equivalent to 100 mg in a 60 kg individual based on mg/m 2comparison). Additionally, constriction of the ductus arteriosus has been observed in fetuses of pregnant rats exposed to prednisolone. Prednisone delayed-release tablets was not formally evaluated in animal reproduction studies.
Risk Summary
Prednisolone has been found to be present in human milk following administration to lactating women. Published reports suggest infant daily doses are estimated to be less than 1% of the maternal daily dose. No adverse effects in the breastfed infant have been reported following maternal exposure of prednisolone during breastfeeding. There are no available data on the effects of prednisolone on milk production. High doses of corticosteroids administered to lactating women for long periods could potentially produce problems in the breastfed infant including growth and development and interfere with endogenous corticosteroid production (see Clinical Considerations) [see Use in Specific Populations (8.4)]. The developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for prednisone delayed-release tablets and any potential adverse effects on the breastfed child from prednisone delayed-release tablets or from the mother's underlying condition.
Clinical Considerations
In order to minimize exposure, the lowest dose should be prescribed to lactating women to achieve the desired clinical effect.
Data
Human Data
Reports suggest that prednisolone concentrations in human milk are 5% to 25% of maternal serum levels, and that total infant daily doses are small, about 0.14% of the maternal daily dose.
The efficacy and safety of prednisone in the pediatric population are based on the well-established course of effect of corticosteroids which is similar in pediatric and adult populations. Published studies provide evidence of efficacy and safety in pediatric patients for the treatment of nephrotic syndrome (> 2 years of age), and aggressive lymphomas and leukemias (> 1 month of age). However, some of these conclusions and other indications for pediatric use of corticosteroid, e.g., severe asthma and wheezing, are based on adequate and well-controlled trials conducted in adults, on the premises that the course of the diseases and their pathophysiology are considered to be substantially similar in both populations. The adverse effects of prednisone in pediatric patients are similar to those in adults [ see Adverse Reactions (6) ]. Like adults, pediatric patients should be carefully observed with frequent measurements of blood pressure, weight, height, intraocular pressure, and clinical evaluation for the presence of infection, psychosocial disturbances, thromboembolism, peptic ulcers, cataracts, and osteoporosis.
Children who are treated with corticosteroids by any route, including systemically administered corticosteroids, may experience a decrease in their growth velocity. This negative impact of corticosteroids on growth has been observed at low systemic doses and in the absence of laboratory evidence of HPA axis suppression (i.e., cosyntropin stimulation and basal cortisol levels). Growth velocity may therefore be a more sensitive indicator of systemic corticosteroid exposure in children than some commonly used tests of HPA axis function. The linear growth of children treated with corticosteroids by any route should be monitored, and the potential growth effects of prolonged treatment should be weighed against clinical benefits obtained and the availability of other treatment alternatives. In order to minimize the potential growth effects of corticosteroids, children should be titrated to the lowest effective dose [ see Warnings and Precautions (5.9) ].
No overall differences in safety or effectiveness were observed between elderly subjects and younger subjects, and other reported clinical experience with prednisone has not identified differences in responses between the elderly and younger patients. However, the incidence of corticosteroid-induced side effects may be increased in geriatric patients and are dose-related. Osteoporosis is the most frequently encountered complication, which occurs at a higher incidence rate in corticosteroid-treated geriatric patients as compared to younger populations and in age-matched controls. Losses of bone mineral density appear to be greatest early on in the course of treatment and may recover over time after steroid withdrawal or use of lower doses (i.e., ≤ 5 mg/day). Prednisone doses of 7.5 mg/day or higher have been associated with an increased relative risk of both vertebral and nonvertebral fractures, even in the presence of higher bone density compared to patients with involution osteoporosis. Routine screening of geriatric patients, including regular assessments of bone mineral density and institution of fracture prevention strategies, along with regular review of prednisone indication should be undertaken to minimize complications and keep the prednisolone dose at the lowest acceptable level. Co-administration of certain bisphosphonates have been shown to retard the rate of bone loss in corticosteroid-treated males and postmenopausal females, and these agents are recommended in the prevention and treatment of corticosteroid-induced osteoporosis [ see Warnings and Precautions (5.6) ].
It has been reported that equivalent weight-based doses yield higher total and unbound prednisolone plasma concentrations and reduced renal and non-renal clearance in elderly patients compared to younger populations. Dose selection for an elderly patient should be cautious, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy.
This drug is known to be substantially excreted by the kidney, and the risk of toxic reactions to this drug may be greater in patients with impaired renal function. Because elderly patients are more likely to have decreased renal function, care should be taken in dose selection, and it may be useful to monitor renal function.
The effects of accidental ingestion of large quantities of prednisone over a very short period of time have not been reported, but prolonged use of the drug can produce mental symptoms, moon face, abnormal fat deposits, fluid retention, excessive appetite, weight gain, hypertrichosis, acne, striae, ecchymosis, increased sweating, pigmentation, dry scaly skin, thinning scalp hair, increased blood pressure, tachycardia, thrombophlebitis, decreased resistance to infection, negative nitrogen balance with delayed bone and wound healing, headache, weakness, menstrual disorders, accentuated menopausal symptoms, neuropathy, fractures, osteoporosis, peptic ulcer, decreased glucose tolerance, hypokalemia, and adrenal insufficiency. Hepatomegaly and abdominal distention have been observed in children.
Treatment of acute overdosage is by immediate gastric lavage or emesis followed by supportive and symptomatic therapy. For chronic overdosage in the face of severe disease requiring continuous steroid therapy the dosage of prednisone may be reduced only temporarily, or alternate day treatment may be introduced.
The active ingredient in prednisone delayed-release tablet is prednisone (a corticosteroid). Corticosteroids are adrenocortical steroids, both naturally occurring and synthetic. The molecular formula for prednisone is C 21H 26O 5. The chemical name for prednisone is 17,21-dihydroxypregna-1,4-diene-3,11,20-trione, and the structural formula is:
Prednisone, USP is a white to practically white crystalline powder and has a molecular weight of 358.44 g/mol. Prednisone, USP is practically insoluble in water, slightly soluble in ethanol (96 per cent) and in methylene chloride.
Prednisone delayed-release tablet is a delayed-release prednisone tablet. It consists of a prednisone-containing core tablet in an inactive shell, which delays the onset of in vitro drug dissolution by approximately 4 hours. Each tablet contains 1 mg, or 2 mg of prednisone, USP with the following inactive ingredients: dibasic calcium phosphate dihydrate, colloidal silicon dioxide, croscarmellose sodium, glycerol dibehenate, lactose monohydrate, magnesium stearate, povidone, yellow ferric oxide and red ferric oxide.
Each prednisone delayed-release tablet contains 30 mg of phosphorous.
Each prednisone delayed-release tablet contains less than 5 mg of sodium.
Naturally occurring corticosteroids (hydrocortisone and cortisone), which also have salt-retaining properties, are used as replacement therapy in adrenocortical deficiency states. Their synthetic analogs, such as prednisone, are primarily used for their potent anti-inflammatory effects in disorders of many organ systems.
Corticosteroids, such as prednisone, cause profound and varied metabolic effects. In addition, they modify the body's immune responses to diverse stimuli.
Prednisone is a synthetic adrenocortical steroid drug with predominantly corticosteroid properties. Some of these properties reproduce the physiological actions of endogenous glucocorticosteroids, but others do not necessarily reflect any of the adrenal hormones' normal functions; they are seen only after administration of large therapeutic doses of the drug. The pharmacological effects of prednisone which are due to its corticosteroid properties include: promotion of gluconeogenesis; increased deposition of glycogen in the liver; inhibition of the utilization of glucose; anti-insulin activity; increased catabolism of protein; increased lipolysis; stimulation of fat synthesis and storage; increased glomerular filtration rate and resulting increase in urinary excretion of urate (creatinine excretion remains unchanged); and increased calcium excretion.
Depressed production of eosinophils and lymphocytes occurs, but erythropoiesis and production of polymorphonuclear leukocytes are stimulated. Inflammatory processes (edema, fibrin deposition, capillary dilatation, migration of leukocytes and phagocytosis) and the later stages of wound healing (capillary proliferation, deposition of collagen, cicatrization) are inhibited.
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.
The pharmacokinetic profile of prednisone delayed-release tablets has an approximately 4-hour lag time from that of immediate-release prednisone formulations. While the pharmacokinetic profile of prednisone delayed-release tablets when given with food differs in terms of lag time from IR prednisone, its absorption, distribution, and elimination processes are comparable.
Absorption
Prednisone is released from prednisone delayed-release tablets when taken with food approximately 4 hours after oral ingestion. This causes a delay in the time until peak plasma concentrations (T max) are achieved. Median T maxof prednisone delayed-release tablets in 27 healthy male subjects was 6.0 - 6.5 hours compared to 2.0 hours for an immediate-release (IR) formulation. Subsequently, prednisone was absorbed at the same rate as the IR formulation. Peak plasma concentrations (C max) and exposure, as indicated by AUC 0-lastand AUC 0-∞, were comparable for both prednisone IR and prednisone delayed-release tablets administered 2.5 hours after a light meal or with normal meal (Figure 1).
Figure 1. Mean Plasma Levels of Prednisone After a Single Dose of 5 mg Prednisone Administered as a 5 mg Prednisone Delayed-Release Tablet or a 5 mg Immediate-Release (IR) Tablet
A: 5 mg IR tablet under fasting conditions, administered at 2 am, B: 5 mg prednisone delayed-release tablets, administered 2.5 hours after a light evening meal, and C: 5 mg prednisone delayed-release tablets administered immediately after dinner
In a study with 24 healthy subjects, oral absorption of prednisone from prednisone delayed-release tablets was significantly affected by the intake of food. Under standard fasting conditions, both the maximum plasma concentration (C max) and the bioavailability of prednisone delayed-release tablets were significantly lower than under fed conditions, shortly after intake of a high fat meal.
Prednisone delayed-release tablets at dose levels of 1 mg, 2 mg, and 5 mg showed dose-proportionality in terms of peak and systemic exposure (C max, AUC 0-∞, and AUC 0-last) for the parent drug prednisone as well as for the active metabolite prednisolone.
Metabolism
Prednisone is completely converted to the active metabolite prednisolone, which is further metabolized mainly in the liver and excreted in the urine as sulfate and glucuronide conjugates. The exposure of prednisolone is 4-6 fold higher than that of prednisone.
Excretion
The terminal half-life of both prednisone and prednisolone from the administration of prednisone delayed-release tablets was 2-3 hours, which is comparable to that from the IR formulation.
Special Populations
The effects of gender, age, renal impairment, and hepatic impairment on the pharmacokinetics of prednisone or prednisolone after administration of prednisone delayed-release tablets have not been evaluated.
Prednisone was not formally evaluated in carcinogenicity studies. Review of the published literature identified carcinogenicity studies of prednisolone, the active metabolite of prednisone, at doses which were less than the typical clinical doses. In a 2-year study, male Sprague-Dawley rats administered prednisolone in drinking water at a dose of 368 mcg/kg/day (equivalent to 3.5 mg/day in a 60-kg individual based on a mg/m 2body surface area comparison) developed increased incidences of hepatic adenomas. Lower doses were not studied, and therefore, a no effect level could not be identified. In an 18-month study, intermittent oral gavage administration of prednisolone did not induce tumors in female Sprague-Dawley rats when given 1, 2, 4.5, or 9 times per month at 3 mg/kg prednisone (equivalent to 29 mg in a 60-kg individual based on a mg/m 2body surface area comparison).
Prednisone was not formally evaluated for genotoxicity. However, in published studies prednisolone was not mutagenic with or without metabolic activation in the Ames bacterial reverse mutation assay using Salmonella typhimuriumand Escherichia coli, or in a mammalian cell gene mutation assay using mouse lymphoma L5178Y cells, according to current evaluation standards. In a published chromosomal aberration study in Chinese Hamster Lung (CHL) cells, a slight increase was seen in the incidence of structural chromosomal aberrations with metabolic activation at the highest concentration tested, however, the effect appears to be equivocal. Prednisolone was not genotoxic in an in vivomicronucleus assay in the mouse, though the study design did not meet current criteria.
Prednisone was not formally evaluated in fertility studies. Corticosteroids have been shown to impair fertility in male rats. Menstrual irregularities have been described with clinical use [ see Adverse Reactions (6) ].
The efficacy of prednisone delayed-release tablets in the treatment of rheumatoid arthritis was assessed in one multicenter, double-blind, placebo-controlled, randomized, 12-week trial in patients ≥18 years with active rheumatoid arthritis diagnosed according to American College of Rheumatology (ACR) criteria. Patients were enrolled who were not currently treated with corticosteroids but had received non-biologic DMARD therapy for at least 6 months before receipt of study medication, and had an incomplete response to DMARD therapy alone. Patients were randomized in a 2:1 ratio to treatment with prednisone delayed-release tablets 5 mg (n=231) or placebo (n=119) administered at 10 pm. A total of 350 patients were enrolled and ranged in age from 27 to 80 years (median age 57 years) with 84% females. Race was distributed as follows: 98% Caucasian, 1% African-American, and <1% Asian.
The percentage of patients with improvement in rheumatoid arthritis at 12 weeks using ACR response criteria (ACR20) was assessed as the primary endpoint, and ACR20, ACR50 and ACR70 responses for patients treated with prednisone delayed-release tablets 5 mg versus placebo are shown in Table 1. The relative efficacy of prednisone delayed-release tablets compared to immediate-release prednisone has not been established.
| ACR Response at 12 Weeks | Prednisone delayed-release tablets 5 mg | Placebo | Prednisone delayed-release tablets 5 mg –
Placebo (95% CI) |
|---|---|---|---|
| N = 231 | N = 119 | ||
| All missing values were imputed as non-responders. | |||
| ACR20 | 47% | 29% | 17%
(7.2, 27.6) |
| ACR50 | 22% | 10% | 12%
(4.4, 19.6) |
| ACR70 | 7% | 3% | 4%
(0.1, 8.7) |
The results of the components of the ACR response criteria are shown in Table 2.
| Parameter | Prednisone delayed-release tablets 5 mg + DMARD
N = 231 | Placebo + DMARD
N = 119 | ||
|---|---|---|---|---|
| Baseline | Week 12 | Baseline | Week 12 | |
| Mean (SD) is presented. Baseline values were carried forward for patients with missing data at Week 12. | ||||
| Tender joint count a | 12.6 (6.2) | 7.9 (6.8) | 12.5 (5.9) | 9.8 (6.7) |
| Swollen joint count a | 8.4 (4.4) | 4.8 (4.8) | 8.6 (4.7) | 6.1 (5.4) |
| Patient assessment of pain b | 55.3 (21.9) | 33.0 (24.5) | 50.5 (23.3) | 39.6 (24.7) |
| Patient global assessment c | 57.4 (20.1) | 36.2 (24.5) | 50.9 (20.9) | 43.0 (22.4) |
| Physician global assessment c | 55.2 (16.1) | 31.9 (19.7) | 54.1 (17.4) | 40.4 (21.8) |
| Disability index (HAQ-DI) d | 1.3 (0.6) | 1.1 (0.6) | 1.3 (0.6) | 1.2 (0.6) |
| ESR (mm/hr) | 33.0 (16.6) | 25.2 (16.8) | 32.9 (20.0) | 26.5 (19.7) |
| CRP (mg/dL) | 9.3 (13.2) | 7.5 (10.7) | 11.8 (18.0) | 9.7 (12.1) |
a 28-joint count
b Patient assessment of arthritis pain. Visual analog scale: 0 = no pain, 100 = very intensive pain
cPatient or physician global assessment of disease activity. Visual analog scale: 0 = not active at all, 100 = extremely active
dHealth Assessment Questionnaire Disability Index; 0 = best, 3 = worst, measures the patient’s ability to perform the following: dress/groom, arise, eat, walk, reach, grip, maintain hygiene, and maintain daily activity
The percentage of patients achieving ACR20 responses by visit is shown in Figure 2.
| Figure 2. ACR20 Response Over 12 Weeks |
|---|
|
a The same patients may not have responded at each time point.
The percent change from baseline in the duration of morning stiffness at 12 weeks was assessed as a prespecified secondary endpoint. Patients treated with prednisone delayed-release tablets had a median decrease in the duration of morning stiffness of 55% compared to 33% in placebo-treated patients (20% estimated median difference between treatment groups with 95% confidence interval [7, 32]). This corresponds to a median duration of morning stiffness of 46 minutes in the prednisone delayed-release tablets group and 85 minutes in the placebo group.
Prednisone delayed-release tablets (1 mg prednisone) are white to off-white colored, round, unscored, delayed release tablet, debossed with "1" on one side and plain on other side, mottled appearance, free from physical defects.
| NDC Number | Size |
| 74157-010-30 | Bottle of 30 tablets |
Prednisone delayed-release tablets (2 mg prednisone) are light peach to peach colored, round, unscored, delayed release tablet, debossed with "2" on one side and plain on other side, mottled appearance, free from physical defects.
NDC Number | Size |
| 74157-019-30 | Bottle of 30 tablet |
Store at 20°C to 25°C (68°F to 77°F); excursions permitted to 15°C to 30°C (59°F to 86°F) [See USP Controlled Room Temperature].
Protect prednisone delayed-release tablets from light and moisture.
Dispense in a tight, light-resistant container as defined in the USP using a child-resistant closure.
Patients should be informed of the following information before initiating therapy with prednisone delayed-release tablets and periodically during the course of ongoing therapy.
Manufactured For:
INA Pharmaceutics Inc
Fairmont, WV 26554
Product of Spain
Issued: 11/2025
NDC 74157-010-30
predniSONE Delayed-release Tablets
1 mg
30 Tablets
Swallow whole. Do not crush,
divide, or chew tablets.
Rx Only
NDC 74157-019-30
predniSONE Delayed-release Tablets
2 mg
30 Tablets
Swallow whole. Do not crush,
divide, or chew tablets.
Rx Only
| Class | Version | Type | Effective |
|---|---|---|---|
| PREDNISONE Pharmacologic Class Indexing | 1 | Indexing - Pharmacologic Class | 20190419 |
| Product concept | Relation | Version | Effective |
|---|---|---|---|
| 2205d503-be51-445b-bb34-c209cc557b3c | Product name | 5 | 20230105 |
| 9492a99d-61c8-491f-9086-1c6a7e98c040 | Product name | 6 | 20230105 |
| 205c2cdd-a63b-cbc9-6bcb-6be6001edf81 | Product name | 2 | 20170705 |
| Package NDC | Product | Description | Form | Quantity | Strength | SPL version |
|---|---|---|---|---|---|---|
| 74157-010-30 | Prednisone delayed release | 1 in 1 CARTON | TABLET, DELAYED RELEASE | 1 | 1 | |
| 74157-010-30 | Prednisone delayed release | 30 in 1 BOTTLE | TABLET, DELAYED RELEASE | 30 | 1 | |
| 74157-019-30 | Prednisone delayed release | 30 in 1 BOTTLE | TABLET, DELAYED RELEASE | 30 | 1 | |
| 74157-019-30 | Prednisone delayed release | 1 in 1 CARTON | TABLET, DELAYED RELEASE | 1 | 1 |
| Package NDC | Billing unit | Product NDC | DailyMed indexing SPL | SPL version | Effective |
|---|---|---|---|---|---|
| 74157-010-30 | EA - Each | 74157-010 | e2cc38ee-76e8-4ca2-8cbd-483a4258db10 | 1 | 2026-01-08 |
| 74157-019-30 | EA - Each | 74157-019 | 4ea9eaa9-54c8-48e2-b8b9-a929c18fdeab | 1 | 2026-01-08 |
Every source-derived product name is available through these pages.
| Product NDC | Package NDC |
|---|---|
| 74157-010 | 74157-010-30 |
| 74157-019 | 74157-019-30 |
Every source-derived ingredient row is available through these pages.
All distinct exact application/product contexts derived from this label’s complete NDC list are paginated below.
| Application-product | Trade name | Ingredient | Strength | Dosage form / route | TE codes | RLD / RS | Approval date |
|---|---|---|---|---|---|---|---|
| A219477-001 | PREDNISONE | PREDNISONE | 1MG | TABLET, DELAYED RELEASE / ORAL | 2025-10-01 | ||
| A219477-002 | PREDNISONE | PREDNISONE | 2MG | TABLET, DELAYED RELEASE / ORAL | 2025-10-01 |
Observed FDA ZIP history: Each table is queried independently by exact application/product key from successfully parsed Orange Book snapshots. Capture times identify archived source observations; absence or a change between snapshots is not inferred. FDA publication files that were not recoverable as structured ZIP data are not represented as states.
| Captured | Edition | Application-product | Trade name | Strength | Dosage form / route | Product TE source text | RLD / RS | Approval date | Source SHA-256 |
|---|---|---|---|---|---|---|---|---|---|
| 2026-09-14 22:38:34 | 2026-08 | A219477-001 | PREDNISONE | 1MG | TABLET, DELAYED RELEASE / ORAL | 2025-10-01 | 84e616aacf4f… | ||
| 2026-09-14 22:38:34 | 2026-08 | A219477-002 | PREDNISONE | 2MG | TABLET, DELAYED RELEASE / ORAL | 2025-10-01 | 84e616aacf4f… | ||
| 2026-08-18 06:07:40 | 2026-07 | A219477-001 | PREDNISONE | 1MG | TABLET, DELAYED RELEASE / ORAL | 2025-10-01 | caaa826d4ba7… | ||
| 2026-08-18 06:07:40 | 2026-07 | A219477-002 | PREDNISONE | 2MG | TABLET, DELAYED RELEASE / ORAL | 2025-10-01 | caaa826d4ba7… | ||
| 2026-02-19 14:30 UTC | 2026-02 | A219477-001 | PREDNISONE | 1MG | TABLET, DELAYED RELEASE / ORAL | RS | 2025-10-01 | 011fe1cb6892… | |
| 2026-02-19 14:30 UTC | 2026-02 | A219477-002 | PREDNISONE | 2MG | TABLET, DELAYED RELEASE / ORAL | 2025-10-01 | 011fe1cb6892… | ||
| 2025-12-14 10:44 UTC · 2 captures of this ZIP | 2025-12 | A219477-001 | PREDNISONE | 1MG | TABLET, DELAYED RELEASE / ORAL | RS | 2025-10-01 | 31067a03dcf5… | |
| 2025-12-14 10:44 UTC · 2 captures of this ZIP | 2025-12 | A219477-002 | PREDNISONE | 2MG | TABLET, DELAYED RELEASE / ORAL | 2025-10-01 | 31067a03dcf5… | ||
| 2026-07-26 02:55 UTC · 3 captures of this ZIP | 2026-06 | A219477-001 | PREDNISONE | 1MG | TABLET, DELAYED RELEASE / ORAL | 2025-10-01 | a50c72e98297… | ||
| 2026-07-26 02:55 UTC · 3 captures of this ZIP | 2026-06 | A219477-002 | PREDNISONE | 2MG | TABLET, DELAYED RELEASE / ORAL | 2025-10-01 | a50c72e98297… |
OpenFDA label data provides additional search and identifier links. DailyMed’s Structured Product Label is the canonical label on FDA.report. Matching records are deduplicated before they are shown below.
| Brand | Generic | Manufacturer | SPL set ID | Effective date | Available safety fields | Join |
|---|---|---|---|---|---|---|
| Prednisone delayed release | PREDNISONE | INA Pharmaceutics Inc | 463c7cd2-c973-5c6c-e063-6394a90a09a0 | 2025-12-17 | Warnings, Adverse reactions | 74157-010-30 74157-019-30 74157-019 74157-010 74157001930 74157001030 463c5b39-7eb2-d396-e063-6394a90aa451 463c7cd2-c973-5c6c-e063-6394a90a09a0 |
Adverse event summaries are temporarily unavailable. Other product information remains available.
