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). |
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 | Consult provider |
| 2nd trimester | Consult provider |
| 3rd trimester | Consult provider |
Clinical note
Comprehensive clinical and safety monograph for DEFLAZACORT (DEFLAZACORT).
| Breastfeeding | Deflazacort is excreted into breast milk in low amounts. Estimated infant dose <1% of maternal weight-adjusted dose. M/P ratio not reported. No adverse effects observed in breastfed infants. Use with caution. |
| 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. |
■ FDA Black Box Warning
No black box warning.
| Serious Effects |
["Hypersensitivity to deflazacort or any component","Systemic fungal infections","Live vaccine administration"]
| 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"] |
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| 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. |