Prednisone is a synthetic corticosteroid taken by mouth. It is an anti-inflammatory and immune-suppressing drug, labeled for conditions from asthma flares and allergic reactions to rheumatoid arthritis, lupus, inflammatory bowel disease and some blood cancers. It is a generic, FDA-approved prescription drug.
Despite the shared word “steroid,” prednisone is not an anabolic steroid. It mimics cortisol, the body’s own stress hormone, and one of its labeled effects is increased breakdown of protein. In other words, it pushes muscle in the opposite direction from testosterone and its derivatives. Long or high-dose courses also suppress the body’s own cortisol production, which is why longer courses are tapered rather than stopped abruptly.
This page summarizes what the FDA labels, clinical guidelines and large cohort studies report. It is for education only and is not medical advice.
| Property | Detail |
|---|---|
| Drug class | Synthetic glucocorticoid (corticosteroid); not an anabolic-androgenic steroid |
| Brands | Deltasone (NDA 009986) and Rayos delayed-release (NDA 202020) are both discontinued; generics are marketed |
| Route | Oral (immediate-release tablets, delayed-release tablets, oral solution) |
| Example strengths | 5, 10 and 20 mg immediate-release tablets; 1 and 2 mg delayed-release tablets |
| Labeled starting dose | 5–60 mg/day, individualized to the disease and response |
| Activation | Prodrug, completely converted to prednisolone; prednisolone exposure is 4–6× that of prednisone |
| Half-life | Terminal half-life 2–3 h (label); biological (tissue) effect 12–36 h (guideline) |
| Potency | 5 mg prednisone ≈ 20 mg hydrocortisone ≈ 0.75 mg dexamethasone (label) |
| US status | Prescription only (Rx); no DEA schedule |
| WADA status | S9 glucocorticoid: prohibited in-competition by oral, injectable or rectal route; Specified Substance |
What it is
Prednisone is pregna-1,4-diene-3,11,20-trione, 17,21-dihydroxy-, formula C₂₁H₂₆O₅, molecular weight 358.4 g/mol (Mylan prednisone label; PubChem). It is a 21-carbon (pregnane) steroid and a synthetic analog of the natural adrenal glucocorticoids hydrocortisone (cortisol) and cortisone.
The label describes it as an adrenocortical steroid with “predominantly corticosteroid properties.” Its labeled pharmacologic effects include (prednisone delayed-release label):
- more glucose production by the liver (gluconeogenesis) and anti-insulin activity;
- increased breakdown (catabolism) of protein;
- increased fat breakdown and, at the same time, fat synthesis and storage;
- increased calcium excretion;
- depressed production of eosinophils and lymphocytes (two types of white blood cell), and inhibition of inflammation and the later stages of wound healing;
- slight mineralocorticoid (salt-retaining) activity, with sodium retention and potassium loss.
It also suppresses corticotropin (ACTH) from the pituitary, which in turn shuts down the adrenal glands’ own cortisol output.
Corticosteroid vs anabolic-androgenic steroid
Both are steroid hormones, but they mimic different natural hormones and have opposite effects on muscle protein.
| Feature | Corticosteroid (prednisone) | Anabolic-androgenic steroid (e.g. testosterone) |
|---|---|---|
| Natural hormone it mimics | Cortisol (adrenal cortex) | Testosterone (testes) |
| Main medical use | Suppressing inflammation and the immune system | Treating low testosterone (hypogonadism) |
| Effect on muscle | Increased protein catabolism; loss of muscle mass and steroid myopathy on the label | Increases fat-free mass, muscle size and strength in trials |
| Effect on own hormone axis | Suppresses ACTH and adrenal cortisol | Suppresses LH and the body’s own testosterone; at large doses FSH and sperm production |
| US controlled substance | No | Yes, Schedule III |
| WADA class | S9, in-competition only (route-dependent) | S1.1, prohibited at all times |
The prednisone column is from its labels. The testosterone column is from the Depo-Testosterone label and a 10-week trial of 600 mg/week testosterone enanthate in 43 men (Bhasin et al., NEJM 1996). For more on the anabolic side, see testosterone cypionate and oxandrolone. The WADA classes are from the WADA 2026 Prohibited List; the anabolic steroid schedule is in 21 CFR 1308.13.
Pharmacokinetics
Prednisone itself is inactive until the liver converts it. According to the delayed-release label, prednisone is completely converted to prednisolone, which is then metabolized mainly in the liver and excreted in urine as sulfate and glucuronide conjugates (delayed-release label).
| Parameter | Value | Source |
|---|---|---|
| Time to peak, immediate-release | Median 2.0 h | Delayed-release label (comparator arm) |
| Time to peak, delayed-release | Median 6.0–6.5 h (about a 4 h lag) | Delayed-release label, 27 healthy men |
| Prednisolone vs prednisone exposure | 4–6× higher | Delayed-release label |
| Terminal half-life (prednisone and prednisolone) | 2–3 h | Delayed-release label |
| Plasma half-life (prednisone) | About 60 min | ESE/Endocrine Society guideline, Table 1 |
| Biological half-life (duration of effect) | 12–36 h | ESE/Endocrine Society guideline, Table 1 |
In other words, the drug’s effect lasts much longer than the drug itself stays in the blood (Beuschlein et al., JCEM 2024). The guideline classes prednisone as intermediate-acting with 4 times the glucocorticoid potency of hydrocortisone. Dexamethasone, by comparison, is long-acting, with a biological half-life of 36–72 h.
A pharmacokinetic review found that conversion of prednisone to prednisolone is not a limiting step, even in severe liver impairment. Free (unbound) prednisolone levels are higher in older adults, in liver or kidney failure, with estrogen-containing contraceptives and with ketoconazole. They are lower with liver enzyme-inducing drugs and in hyperthyroidism (Frey and Frey, Clin Pharmacokinet 1990).
Approved medical use
The immediate-release label lists a very wide range of indications, grouped by organ system (Mylan prednisone label):
| Category | Examples from the label |
|---|---|
| Endocrine | Adrenal insufficiency (hydrocortisone or cortisone preferred), congenital adrenal hyperplasia, cancer-related hypercalcemia |
| Rheumatic | Short-term add-on in rheumatoid, psoriatic and gouty arthritis, ankylosing spondylitis, bursitis |
| Collagen diseases | Systemic lupus erythematosus, dermatomyositis, acute rheumatic carditis |
| Dermatologic | Pemphigus, Stevens-Johnson syndrome, severe psoriasis |
| Allergic | Severe asthma, allergic rhinitis, contact and atopic dermatitis, drug reactions, when conventional treatment fails |
| Ophthalmic | Uveitis, optic neuritis, allergic and inflammatory eye disease |
| Respiratory | Sarcoidosis, aspiration pneumonitis, some forms of tuberculosis with anti-TB drugs |
| Hematologic | Immune thrombocytopenia, autoimmune hemolytic anemia |
| Neoplastic | Palliative care in leukemias and lymphomas |
| Renal, GI, other | Nephrotic syndrome, ulcerative colitis, Crohn’s disease, tuberculous meningitis, trichinosis |
The only contraindications on the immediate-release label are systemic fungal infections and known hypersensitivity to its components.
Labeled dosing principles
The label does not give a fixed dose. It states:
- the initial dose may vary from 5 mg to 60 mg per day depending on the disease;
- dosage must be individualized to the disease and the patient’s response;
- after a response, the dose should be lowered in small steps to the lowest dose that maintains control;
- if there is no satisfactory response after a reasonable time, prednisone should be stopped and other therapy used;
- a single daily dose is best taken in the morning before 9 am, when it suppresses the adrenal axis the least;
- after long-term therapy, it should be withdrawn gradually rather than abruptly.
The label also describes alternate-day therapy (twice the daily dose every other morning) for patients who need long-term treatment. The aim is to reduce adrenal suppression, Cushing-like changes and growth suppression in children. Prednisone qualifies because a single dose suppresses the adrenal axis for only about 1¼–1½ days.
The delayed-release tablet (formerly Rayos) is taken daily with food and must not be broken or chewed; it releases the drug about 4 hours after it is taken. Its 12-week trial in 350 people with active rheumatoid arthritis compared 5 mg at 10 pm with placebo (delayed-release label):
| ACR response at 12 weeks | Prednisone DR 5 mg (n = 231) | Placebo (n = 119) | Difference (95% CI) |
|---|---|---|---|
| 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 label notes that its efficacy relative to immediate-release prednisone has not been established.
Adrenal suppression and tapering
This is the main reason prednisone cannot simply be stopped after a long course.
The labels state that corticosteroids can cause reversible suppression of the hypothalamic-pituitary-adrenal (HPA) axis, the hormone chain that controls the body’s own cortisol. Stopping too quickly can cause adrenal insufficiency. This relative insufficiency may persist for up to 12 months after high doses for long periods, so steroid cover may be needed again during illness, surgery or trauma in that window (Mylan prednisone label). After prolonged therapy, withdrawal can also cause a withdrawal syndrome with muscle pain, joint pain and malaise.
How common is it? A meta-analysis of 74 studies with 3,753 adult corticosteroid users found adrenal insufficiency in 2.4% (95% CI 0.6–9.3) with low doses and 21.5% (95% CI 12.0–35.5) with high doses. The authors concluded that no route, dose or duration rules it out with certainty (Broersen et al., JCEM 2015).
The 2024 joint guideline from the European Society of Endocrinology and the Endocrine Society sets these working thresholds and principles (Beuschlein et al., JCEM 2024):
| Guideline point | What it says |
|---|---|
| Physiologic daily dose | About 4–6 mg prednisone (equal to 15–25 mg hydrocortisone) |
| Exposure that poses risk | Over 3–4 weeks of oral therapy at doses above the physiologic range |
| Short courses (under 3–4 weeks) | Can be stopped without a taper or testing, irrespective of dose |
| Long-term therapy | Taper only once the disease is controlled; taper faster in the supraphysiologic range, then slower with smaller steps near 4–6 mg/day |
| Withdrawal syndrome | If severe, temporarily return to the last tolerated dose and lengthen the taper |
| Testing | Not routinely while still on supraphysiologic doses; test only once near a physiologic dose |
| Long-acting steroids | Switch dexamethasone or betamethasone to a shorter-acting one such as prednisone when no longer needed |
Side effects and risks
Prednisone has no boxed warning. The labels list a long set of adverse reactions that rise with dose and duration. The delayed-release label names the most common as fluid retention, altered glucose tolerance, raised blood pressure, behavioral and mood changes, and increased appetite and weight gain (delayed-release label).
Even short courses carry measurable risk. In a US claims cohort of 1,548,945 adults aged 18–64, 21.1% received at least one oral corticosteroid course under 30 days over three years. In the 30 days after starting, rates rose as follows (Waljee et al., BMJ 2017):
| Outcome | Incidence rate ratio, days 0–30 (95% CI) | At under 20 mg/day prednisone equivalent |
|---|---|---|
| Sepsis | 5.30 (3.80–7.41) | 4.02 |
| Venous thromboembolism | 3.33 (2.78–3.99) | 3.61 |
| Fracture | 1.87 (1.69–2.07) | 1.83 |
These risks fell over the following 31–90 days. This was an observational study, so the conditions being treated may account for part of the increase.
Bone loss and fractures
The label explains that corticosteroids reduce bone formation, increase bone resorption, lower calcium absorption, raise calcium excretion and inhibit osteoblasts (bone-building cells). This can cause osteoporosis at any age and slow bone growth in children (Mylan prednisone label). The label cites recommendations to start bone-protective measures in anyone expected to take at least the equivalent of 5 mg prednisone for at least 3 months. These include calcium, vitamin D, weight-bearing exercise and, where indicated, a bisphosphonate.
A UK cohort of 244,235 oral corticosteroid users and the same number of matched controls quantified the dose response (van Staa et al., J Bone Miner Res 2000):
| Daily dose (prednisolone equivalent) | Hip fracture, relative rate (95% CI) | Vertebral fracture, relative rate (95% CI) |
|---|---|---|
| Under 2.5 mg | 0.99 (0.82–1.20) | 1.55 (1.20–2.01) |
| 2.5–7.5 mg | 1.77 (1.55–2.02) | 2.59 (2.16–3.10) |
| 7.5 mg or more | 2.27 (1.94–2.66) | 5.18 (4.25–6.31) |
Fracture risk declined toward baseline rapidly after stopping. The labels also list osteonecrosis (bone death) of the femoral and humeral heads and tendon rupture, especially of the Achilles tendon. The tendon risk is higher with fluoroquinolone antibiotics.
Hyperglycemia and diabetes
Prednisone raises blood glucose through more liver glucose output and anti-insulin effects. The labels list new or worsened diabetes and higher insulin or oral drug requirements in people with diabetes. In a meta-analysis of 13 mostly observational studies of people without diabetes on systemic glucocorticoids, 32.3% developed hyperglycemia and 18.6% developed diabetes (Liu et al., Ann Nutr Metab 2014).
Infection
The label warns that corticosteroids raise the risk of infection with any pathogen, can reactivate latent infections and can mask signs of infection. Specific warnings cover tuberculosis, hepatitis B reactivation, fungal infections, Strongyloides (threadworm) and chickenpox or measles in people who are not immune. Live vaccines are contraindicated at immunosuppressive doses (Mylan prednisone label).
A pooled analysis of 71 controlled trials found infections in 12.7% of 2,111 patients on systemic corticosteroids vs 8.0% of 2,087 controls (relative risk 1.6, 95% CI 1.3–1.9). The rate was not increased at under 10 mg/day or a cumulative dose under 700 mg of prednisone (Stuck et al., Rev Infect Dis 1989).
Mood and psychiatric effects
The label describes effects ranging from euphoria, insomnia, mood swings and personality changes to severe depression and psychosis, and notes that existing conditions may worsen. In a UK primary care cohort of 372,696 adults given oral glucocorticoids, compared with people with the same underlying disease who did not receive them (Fardet et al., Am J Psychiatry 2012):
| Outcome | Hazard ratio (95% CI) |
|---|---|
| Suicide or suicide attempt | 6.89 (4.52–10.50) |
| Delirium, confusion or disorientation | 5.14 (4.54–5.82) |
| Mania | 4.35 (3.67–5.16) |
| Depression | 1.83 (1.72–1.94) |
| Panic disorder | 1.45 (1.15–1.85) |
Higher doses and a past psychiatric history increased the risk.
Muscle wasting and steroid myopathy
The labels list loss of muscle mass, muscle weakness, steroid myopathy and negative nitrogen balance from protein catabolism. They also describe an acute myopathy at high doses, most often in myasthenia gravis or with neuromuscular-blocking drugs. It can involve the breathing and eye muscles, cause weakness of all four limbs, and take weeks to years to recover from (delayed-release label).
Animal and cell studies point to two mechanisms: more muscle protein breakdown through the ubiquitin-proteasome and lysosomal systems, and less protein synthesis through inhibition of the mTOR pathway, with roles for IGF-1 and myostatin (Schakman et al., Int J Biochem Cell Biol 2013).
Short human studies show how this may start. In two small randomized, double-blind crossover trials in healthy volunteers taking 6 days of prednisone or placebo:
- at 0.5 mg/kg/day (n = 6), fasting muscle protein synthesis, breakdown and strength were unchanged, but leg blood flow fell by 25% and fasting glucose and insulin rose (Short et al., JCEM 2004);
- at 0.8 mg/kg/day (n = 7), insulin’s stimulation of leg glucose uptake was 65% lower, and the insulin-driven gain in muscle protein balance was 45–140% lower than on placebo (Short et al., Am J Physiol 2009).
The authors concluded that prednisone makes muscle resistant to insulin’s anabolic effect, which could lead to atrophy with continued use.
Other labeled risks
- Cardiovascular and fluid: high blood pressure, salt and water retention and low potassium; caution in heart failure and kidney disease.
- Gastrointestinal: peptic ulcer and perforation, with signs that may be masked; higher risk with NSAIDs.
- Eyes: cataracts and glaucoma; the label advises monitoring eye pressure if treatment continues beyond 6 weeks.
- Cushing-like features: moon face, abnormal fat deposits, thin skin, easy bruising, acne and striae.
- Growth in children: slowed growth, even at low doses.
- Pregnancy: the delayed-release label cites a small, inconsistent increase in orofacial clefts with first-trimester use.
Key interactions
From the immediate-release label:
| Interacting drug | Effect |
|---|---|
| CYP3A4 inducers (rifampin, phenytoin, carbamazepine, barbiturates) | Lower corticosteroid levels; dose may need to rise |
| CYP3A4 inhibitors (ketoconazole, itraconazole, ritonavir, macrolides) | Higher corticosteroid levels; ketoconazole can cut metabolism by up to 60% |
| Warfarin | Usually reduced anticoagulant response; monitor coagulation |
| Diabetes medicines | Doses may need adjustment because glucose rises |
| Potassium-depleting diuretics, amphotericin B | Risk of low potassium |
| NSAIDs and aspirin | More gastrointestinal side effects |
| Fluoroquinolones | Higher risk of tendon rupture, especially in older adults |
| Estrogens and oral contraceptives | Slower corticosteroid metabolism, stronger effect |
| Live vaccines | Contraindicated at immunosuppressive doses |
Anti-doping status
Glucocorticoids, including prednisone and prednisolone by name, are in class S9 of the WADA 2026 Prohibited List. The rules are route-specific:
- Prohibited in-competition when given by any injectable, oral (including buccal, gingival and sublingual) or rectal route. Prednisone tablets fall here.
- Not prohibited by other routes (inhaled, skin, nasal, eye, ear, perianal and dental-intracanal) when used within licensed doses and indications.
- Not prohibited out-of-competition. The in-competition period normally runs from 11:59 p.m. the day before a competition until the end of the competition and sample collection.
- All S9 substances are Specified Substances, a category for substances more likely to have been taken for a non-doping reason. WADA notes this does not make them less important.
Because the list bans oral use only in-competition, the timing of a course relative to an event matters. The 2026 list does not give a washout period for prednisone, so this page does not state one.
Key takeaways
- A corticosteroid, not an anabolic. Prednisone mimics cortisol. Its labeled effects include protein catabolism, loss of muscle mass and steroid myopathy, the opposite of testosterone-type steroids.
- A prodrug with a long tail of effect. It is fully converted to prednisolone. Plasma half-life is 2–3 hours, but the biological effect lasts 12–36 hours.
- Dose is individualized. The label gives 5–60 mg/day to start, then the lowest dose that controls the disease, ideally as a single morning dose.
- Long courses suppress the adrenal glands. After more than 3–4 weeks above about 4–6 mg/day, guidelines call for a gradual taper. Suppression can last up to 12 months.
- Risks scale with dose and time, but short courses are not risk-free. Bone loss and fractures, high blood sugar, infections, mood changes and muscle weakness are the major concerns.
- WADA S9, in-competition and route-dependent. Oral, injectable and rectal use is prohibited in-competition; inhaled and topical use within licensed doses is not.
Sources
- Mylan Pharmaceuticals Inc. Prednisone tablets USP, prescribing information (revised 9/2026). DailyMed.
- Dr. Reddy’s Laboratories Inc. Prednisone delayed-release tablets, prescribing information (revised 11/2025). DailyMed.
- US Food and Drug Administration. Drugs@FDA: Rayos (prednisone) delayed-release tablets, NDA 202020; Deltasone (prednisone), NDA 009986. FDA, NDA 202020; FDA, NDA 009986.
- Pfizer. Depo-Testosterone (testosterone cypionate) injection, prescribing information. DailyMed.
- Bhasin S, Storer TW, Berman N, et al. The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men. N Engl J Med. 1996;335(1):1–7. PubMed.
- National Center for Biotechnology Information. Prednisone, PubChem CID 5865. PubChem.
- World Anti-Doping Agency. The 2026 Prohibited List, International Standard. Valid 1 January 2026. WADA 2026 Prohibited List.
- Code of Federal Regulations. 21 CFR 1308.13, Schedule III. 21 CFR 1308.13.
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