DEFLAZACORT
Clinical safety rating: caution
Comprehensive clinical and safety monograph for DEFLAZACORT (DEFLAZACORT).
Deflazacort is a glucocorticoid prodrug that is metabolized to its active form, 21-desacetyldeflazacort. It binds to glucocorticoid receptors, leading to anti-inflammatory and immunosuppressive effects by inhibiting phospholipase A2, reducing prostaglandin and leukotriene synthesis, and modulating cytokine production.
| Metabolism | Primarily metabolized via ester hydrolysis to active metabolite 21-desacetyldeflazacort; further metabolism mainly by CYP3A4. |
| Excretion | Renal (approximately 70% as metabolites, <5% unchanged); biliary/fecal (approximately 30%) |
| Half-life | Terminal half-life of the active metabolite Δ6-deflazacort is 1.1–1.9 hours; parent drug half-life is approximately 1–2 hours. Clinical glucocorticoid effect persists for 12–24 hours due to receptor binding. |
| Protein binding | Approximately 40% bound to albumin; minimal binding to corticosteroid-binding globulin (CBG). |
| Volume of Distribution | 1.1–1.4 L/kg (distributes into total body water; not extensively tissue-bound). |
| Bioavailability | Oral: approximately 70% (as active metabolite Δ6-deflazacort); rectal: not established (not a standard route). |
| Onset of Action | Oral: 1–2 hours (peak effect on glucocorticoid activity); IV: not applicable (oral only). |
| Duration of Action | 12–24 hours (anti-inflammatory and immunosuppressive effects persist beyond plasma half-life). |
| Molecular Weight | 441.52 |
6-90 mg orally once daily; initial dose typically 6-30 mg/day, maintenance as lowest effective dose; taper gradually upon discontinuation.
| Dosage form | SUSPENSION |
| Renal impairment | No dose adjustment required for renal impairment; not removed by hemodialysis. |
| Liver impairment | Severe hepatic impairment (Child-Pugh class C): reduce dose by 50%; monitor for adverse effects. |
| Pediatric use | 0.25-1.5 mg/kg orally per day in divided doses; maximum 90 mg/day; use lowest effective dose. |
| Geriatric use | Start at lower end of dosing range (6-15 mg/day); monitor for osteoporosis, hyperglycemia, and increased susceptibility to infections. |
| 1st trimester | Corticosteroids including deflazacort cross the placenta. Use only if potential benefit justifies risk. Associated with oral clefts in animal studies, but human data limited. Use lowest effective dose for shortest duration. |
| 2nd trimester | Use with caution. Prolonged use may increase risk of intrauterine growth restriction (IUGR). Monitor fetal growth and amniotic fluid volume with prolonged therapy. |
| 3rd trimester | Use with caution. Chronic use may suppress fetal adrenal function leading to neonatal adrenal insufficiency. Risk of preterm birth and reduced birth weight. Monitor neonatal adrenal function if maternal use continues to term. |
Clinical note
Comprehensive clinical and safety monograph for DEFLAZACORT (DEFLAZACORT).
| Placental transfer | Deflazacort crosses the placenta. Its active metabolite 21-desacetyldeflazacort also crosses. The extent of transfer is considered moderate, with fetal concentrations approximately 10-15% of maternal serum levels. |
| Breastfeeding |
■ FDA Black Box Warning
No black box warning.
| Serious Effects |
Hypersensitivity to deflazacort or any excipientsSystemic fungal infectionsConcurrent live or attenuated virus vaccines (in immunocompromised patients)
| Precautions | Immunosuppression and increased infection risk, Adrenal suppression with long-term use, Cushing's syndrome with prolonged therapy, Osteoporosis, Growth retardation in children, Ocular effects (cataracts, glaucoma), Psychiatric disturbances, Gastrointestinal perforation risk |
| Food/Dietary | Grapefruit juice may increase deflazacort levels; avoid concurrent use. High-sodium foods should be limited due to potential fluid retention. Avoid excessive potassium depletion; consider potassium-rich foods or supplements if needed. |
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| Deflazacort and its active metabolite (21-desacetyldeflazacort) are excreted into breast milk in small amounts. Milk-to-plasma ratio is approximately 0.25. Very low doses are considered compatible with breastfeeding. However, high maternal doses (e.g., >40 mg/day) could theoretically affect infant adrenal function. Monitor infant for growth and adrenal suppression if maternal use is prolonged or high-dose. |
| Lactation Rating | L2 (Limited data - probably compatible) |
| Teratogenic Risk | Deflazacort is a corticosteroid. First trimester: Increased risk of cleft palate (approximately 3.5-fold increase). Second and third trimesters: Risk of fetal adrenal suppression, intrauterine growth restriction, and preterm birth. Chronic use may cause neonatal adrenal insufficiency. |
| Fetal Monitoring | Monitor maternal blood glucose, blood pressure, signs of infection. Monitor fetal growth via ultrasound. Assess neonatal adrenal function after delivery if maternal use prolonged. |
| Fertility Effects | No specific data on deflazacort. Corticosteroids may alter menstrual cycle and reduce fertility at high doses. Effects likely reversible upon dose reduction or discontinuation. |
| Clinical Pearls | Deflazacort is a glucocorticoid with a bone-sparing advantage; consider in patients at high risk for osteoporosis. Monitor for growth suppression in children. Taper dose when discontinuing after prolonged use to avoid adrenal insufficiency. Adjust dose in hepatic impairment. Avoid live vaccines during therapy. |
| Patient Advice | Take with food to reduce gastrointestinal discomfort. · Do not stop taking this medicine suddenly; the dose must be reduced gradually. · Inform any healthcare provider that you are taking deflazacort before surgery or vaccinations. · Report any signs of infection (fever, sore throat) or unusual weight gain promptly. · Avoid alcohol consumption while on this medication. |