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Generic Name: Deflazacort
Class: Adrenals
Chemical Name: (11β,16β)-21-(Acetyloxy)-11-hydroxy-2′-methyl-5′H-pregna-1,4-dieno[17,16-d]oxazole-3,20-dione
Molecular Formula: C25H31NO6
CAS Number: 14484-47-0

Medically reviewed by Last updated on Mar 30, 2020.


Synthetic corticosteroid.1 3 4 15 20

Uses for Emflaza

Duchenne Muscular Dystrophy

Management of Duchenne muscular dystrophy (designated an orphan drug by FDA for use in this condition).1 2 3 4 15

Current standard of care for patients with Duchenne muscular dystrophy includes the use of corticosteroids for improving muscle function and strength.3 15 16 26 The American Academy of Neurology recommends prednisone or deflazacort to improve muscle strength, pulmonary function, and possibly also slow the development of scoliosis and need for surgery.16

Emflaza Dosage and Administration


  • Patients receiving corticosteroid therapy may require higher dosages of corticosteroids when subjected to stress (e.g., infection, surgery, trauma).1 29

  • When discontinuing deflazacort therapy after the drug has been given for more than a few days, taper dosage gradually to minimize potential for adrenal insufficiency.1 (See Adrenal Insufficiency under Cautions.)


Oral Administration

Administer orally (as tablets or oral suspension) once daily without regard to food.1

Oral suspension is bioequivalent to the tablets.1 32

Oral Suspension

Shake well prior to administration.1

Administer only with the dosing device supplied by manufacturer.1 Withdraw appropriate dose and slowly add to 3–4 ounces of juice or milk; do not use grapefruit juice.1 Mix well and administer immediately.1


Swallow tablets whole, or crush and mix with applesauce immediately before administration.1


Pediatric Patients

Duchenne Muscular Dystrophy

Children ≥5 years of age: Approximately 0.9 mg/kg daily.1

If the tablets are used, round up to the nearest 6-mg increment and use any combination of tablet strengths to achieve the required dose.1 If the oral suspension is used, round up to the nearest 0.1 mL.1

Dosage Modification for Concomitant Use with Drugs Affecting Hepatic Microsomal Enzymes

If used concomitantly with moderate or potent CYP3A4 inhibitors, reduce dosage to one-third of the recommended dosage (e.g., reduce dosage of 36 mg daily to 12 mg daily).1 (See Drugs Affecting Hepatic Microsomal Enzymes under Interactions.)


Duchenne Muscular Dystrophy

Approximately 0.9 mg/kg daily.1

If the tablets are used, round up to the nearest 6-mg increment and use any combination of tablet strengths to achieve the required dose.1 If the oral suspension is used, round up to the nearest 0.1 mL.1

Dosage Modification for Concomitant Use with Drugs Affecting Hepatic Microsomal Enzymes

If used concomitantly with moderate or potent CYP3A4 inhibitors, reduce dosage to one-third of the recommended dosage (e.g., reduce dosage of 36 mg daily to 12 mg daily).1 (See Drugs Affecting Hepatic Microsomal Enzymes under Interactions.)

Special Populations

Hepatic Impairment

Mild or moderate hepatic impairment: Dosage adjustments not needed.1

Severe hepatic impairment: Dosage recommendations not available; safety and efficacy not established.1

Renal Impairment

Mild, moderate, or severe renal impairment: Dosage adjustments not needed.1

Geriatric Patients

No specific dosage recommendations at this time.1

Cautions for Emflaza


  • Known hypersensitivity to deflazacort or any ingredient in the formulation.1


General Precautions

Deflazacort shares the toxic potentials of other corticosteroids, and the usual cautions, precautions, and contraindications associated with these drugs should be observed.29

Endocrine and Metabolic Effects

Corticosteroids, including deflazacort, can cause serious and life-threatening endocrine effects, especially when administered over prolonged periods.1

Adrenal Insufficiency

May cause hypothalamic-pituitary-adrenal (HPA) axis suppression with potential for developing secondary adrenal insufficiency following corticosteroid withdrawal.1

The degree and duration of adrenal insufficiency is highly variable among patients and depends on the dose, frequency and time of administration, and duration of therapy.1 Adrenal suppression may persist for months after discontinuance of prolonged therapy.1

Acute adrenal insufficiency, sometimes fatal, may occur when corticosteroids are withdrawn abruptly.1

Monitor patients for HPA-axis suppression.1 If discontinuance of therapy is necessary, withdraw gradually.1 (See General under Dosage and Administration.)

Monitor for adrenal insufficiency following discontinuance of deflazacort therapy.1 Reinstitute corticosteroid therapy if stress-inducing situations occur during period of discontinuance.1 For patients already taking corticosteroids, dosage increase may be necessary during times of stress.1

A steroid withdrawal syndrome seemingly unrelated to adrenocortical insufficiency also reported following abrupt corticosteroid withdrawal.1

Cushing Syndrome

Cushing syndrome (hypercortisolism) may occur with prolonged use of corticosteroids.1 Manifestations include hypertension, truncal obesity and thinning of the limbs, purple striae, facial rounding, facial plethora, muscle weakness, easy and frequent bruising with thin fragile skin, posterior neck fat deposition, osteopenia, acne, amenorrhea, hirsutism, and psychiatric abnormalities.1

Monitor patients for Cushing syndrome.1


Corticosteroids can decrease glucose tolerance, produce hyperglycemia, and worsen or precipitate diabetes mellitus, particularly when administered over prolonged periods.1 Efficacy of antidiabetic agents also may be reduced.1

Monitor blood glucose concentrations at regular intervals; initiate or adjust antidiabetic therapy as necessary.1

Effects in Patients with Altered Thyroid Function

Metabolic clearance of corticosteroids may be decreased in hypothyroidism and increased in hyperthyroidism.1 Changes in thyroid status may necessitate adjustment of corticosteroid dosage.1 (See Specific Drugs and Foods under Interactions.)

Pheochromocytoma Crisis

Pheochromocytoma crisis, sometimes fatal, reported.1 Prior to use, consider risk of pheochromocytoma crisis in patients with suspected or confirmed pheochromocytoma.1

Increased Susceptibility to Infection

Corticosteroids suppress the immune system and can mask signs and symptoms of infection.1 Immunosuppressive effects can reduce resistance to new infections, exacerbate existing infections, increase risk of disseminated infections, or reactivate latent infections (e.g., HBV infection, amebiasis).1 Risk of infections with any pathogen (e.g., viral, bacterial, fungal, protozoan, helminthic) is increased.1

Monitor patients for infections.1 Consider withdrawal of therapy or dosage reduction as needed.1

Some infections (e.g., varicella [chickenpox], measles) can have a more serious or even fatal outcome, particularly in children.1 Avoid exposure to these infections in children and adults who have not been previously exposed.1 If exposure to varicella or measles occurs in susceptible patients, treat appropriately (e.g., with varicella zoster immune globulin [VZIG], immune globulin, or antiviral agent).1

Use with great care in patients with known or suspected Strongyloides (threadworm) infection.1 Immunosuppression may lead to Strongyloides hyperinfection and dissemination with widespread larval migration, often accompanied by severe enterocolitis and potentially fatal gram-negative septicemia.1 22

Do not use in patients with systemic fungal infections due to potential for exacerbation of infection.1

Can reactivate latent amebiasis.1 Exclude possible amebiasis in any patient who has been in the tropics or who has unexplained diarrhea prior to initiating therapy.1

Fluid, Electrolyte, Cardiovascular, and Renal Effects

Sodium and water retention, increased BP, and increased potassium and calcium excretion may occur.1 Use with caution in patients with heart failure, hypertension, renal insufficiency, or recent MI.1

Monitor BP and serum electrolytes, and assess patients for manifestations of volume overload; dietary salt restriction and potassium supplementation may be necessary.1

Use with extreme caution in patients with recent MI since an association between use of glucocorticoids and left ventricular free wall rupture has been suggested.1

GI Effects

Patients with certain GI disorders (e.g., active or latent peptic ulcers, diverticulitis, recent intestinal anastomoses, nonspecific ulcerative colitis) are at increased risk of GI perforation with corticosteroid use.1 Corticosteroids may mask signs of GI perforation (e.g., peritoneal irritation).1

Avoid use in patients with increased likelihood of impending perforation, abscess, other pyogenic infection, diverticulitis, recent intestinal anastomoses, or active or latent peptic ulcer.1

Behavioral and Mood Disturbances

Systemic corticosteroid therapy may precipitate potentially severe psychiatric effects, including hypomanic, manic, or depressive symptoms.1 3 4 Abnormal behavior, irritability, hostility, personality changes, labile affect, or psychosis also may occur.1 15

Inform patients of potential for behavioral and mood changes and closely monitor for such effects.1 (See Advice to Patients.) Dosage reduction or withdrawal of therapy may result in symptom improvement, but pharmacologic treatment may be necessary.1

Musculoskeletal Effects

Corticosteroids decrease bone formation and increase bone resorption, potentially leading to inhibited bone growth in pediatric patients and bone loss in patients of all ages.1 29 Patients with such bone loss may be predisposed to vertebral and long-bone fractures.1 4 6 27

Monitor bone mineral density (BMD) during chronic therapy.1 Assess patients for their risk of osteoporosis prior to initiating therapy.1 Consider preventative measures (e.g., calcium and vitamin D supplementation, bisphosphonate therapy) in patients with moderate-to-high risk of fractures.27

Although risk is not known with deflazacort, corticosteroids also may cause avascular necrosis.1

Acute myopathy observed with use of glucocorticoids, particularly in patients with disorders of neuromuscular transmission (e.g., myasthenia gravis) or receiving concomitant therapy with neuromuscular blocking agents.1 29 (See Specific Drugs and Foods under Interactions.) Resolution or clinical improvement may occur weeks to years after discontinuance of corticosteroid therapy.1

Ocular Effects

Corticosteroids may produce posterior subcapsular cataracts and glaucoma (with possible damage to the optic nerves).1 3 5 16 Some clinicians suggest periodic ophthalmologic examinations in children receiving long-term treatment.5

If therapy is continued for >6 weeks, monitor IOP.1

May increase susceptibility to secondary ocular infections; do not use in patients with active ocular herpes infection.1

Altered Response to Vaccines

Do not administer live or live attenuated vaccines to patients receiving immunosuppressive dosages of corticosteroids.1

Although killed or inactivated vaccines may be administered, expected response may not be obtained.1 (See Specific Drugs and Foods under Interactions.)

Dermatologic Effects

Toxic epidermal necrolysis reported.1 7 8 17 Discontinue deflazacort at first sign of a rash unless it is clearly not drug related.1

Kaposi’s sarcoma reported; discontinuance of corticosteroid therapy may result in clinical improvement.1

Benzyl Alcohol Toxicity

Deflazacort oral suspension contains benzyl alcohol, which has been associated with serious and potentially fatal adverse reactions (e.g., neonatal gasping syndrome) in neonates and low-birthweight infants.1 (See Pediatric Use under Cautions.)

Deflazacort tablets do not contain benzyl alcohol.1

Thromboembolic Events

Increased risk of thromboembolism, particularly with higher cumulative doses of corticosteroids, noted in observational studies.1 Use with caution in patients who have, or who may be at increased risk of, thromboembolic disorders.1

Sensitivity Reactions

Hypersensitivity reactions, including rare cases of anaphylaxis, reported.1 17 24 (See Contraindications under Cautions.)

Specific Populations


No adequate and well-controlled studies in pregnant women.1 Use during pregnancy only if potential benefits justify potential risks to fetus.1

Monitor infants born to women who received substantial doses of corticosteroids during pregnancy for symptoms of adrenal insufficiency.1


Distributed into human milk.1 Can suppress growth, interfere with endogenous corticosteroid production, or cause other adverse effects in nursing infants.1 Effects of the drug on milk production unknown.1

Consider benefits of breast-feeding along with woman’s clinical need for deflazacort; also consider potential adverse effects on the breast-fed infant from the drug.1

Pediatric Use

Safety and efficacy not established in pediatric patients <5 years of age.1

Adverse effects on growth and development reported in children, particularly after long-term use.1 3 20 27 (See Musculoskeletal Effects under Cautions.) Monitor growth and development in children if prolonged therapy is necessary.29

Each mL of deflazacort oral suspension contains 10.45 mg of benzyl alcohol as a preservative.1 Large amounts (i.e., 100–400 mg/kg daily) of benzyl alcohol have been associated with toxicity (fatal “gasping syndrome”) in neonates.9 10 11 12 13 14 (See Benzyl Alcohol Toxicity under Cautions.) The lower limit for benzyl alcohol toxicity is unknown.1 Do not use oral suspension in pediatric patients <5 years of age.1

Geriatric Use

No experience in geriatric patients; Duchenne muscular dystrophy is generally a disease of children and young adults.1

Hepatic Impairment

Pharmacokinetics not affected by moderate hepatic impairment (Child-Pugh class B).1 (See Special Populations under Pharmacokinetics.)

Not studied in patients with severe hepatic impairment.1

Renal Impairment

Pharmacokinetics not affected by end-stage renal disease (Clcr <15 mL/minute).1 (See Special Populations under Pharmacokinetics.)

Common Adverse Effects

Cushingoid appearance,1 3 4 weight gain,1 3 increased appetite,1 3 4 upper respiratory tract infection,1 3 cough,1 3 pollakiuria,1 3 nasopharyngitis,1 3 hirsutism,1 3 4 central obesity,1 3 erythema,1 3 irritability,1 rhinorrhea,1 abdominal discomfort.1 3

Interactions for Emflaza

Active metabolite of deflazacort is a substrate of CYP3A4.1

Active metabolite does not inhibit CYP1A2, 2C9, 2C19, 3A4, UGT1A1, 1A4, 1A6, 1A9, or 2B7; exhibits weak inhibition of CYP2B6, 2C8, 2D6, 3A4, UGT1A3 and 2B15, but clinically important effects unlikely.1 Does not induce CYP1A2, 2B6, or 3A4 to a clinically important extent.1

Deflazacort and its active metabolite are substrates of P-glycoprotein (P-gp), but do not inhibit P-gp.1 Active metabolite is not a substrate of breast cancer resistance protein (BCRP); neither deflazacort nor its active metabolite inhibit BCRP.1 Active metabolite is not a substrate or inhibitor of organic anion-transporting protein (OATP) 1B1 or 1B3, and is not an inhibitor of organic anion transporter (OAT) 1 or 3 or organic cation transporter (OCT) 2.1

Drugs Affecting Hepatic Microsomal Enzymes

Moderate or potent CYP3A4 inhibitors: Reduce deflazacort dosage.1 (See Dosage Modification for Concomitant Use with Drugs Affecting Hepatic Microsomal Enzymes under Dosage and Administration.)

Moderate or potent CYP3A4 inducers: Avoid concomitant use.1

Specific Drugs and Foods




Anticonvulsants (e.g., carbamazepine, phenytoin)

Possible decreased exposure of active deflazacort metabolite1

Avoid concomitant use1

Antidiabetic agents

Corticosteroids may reduce efficacy of antidiabetic agents1

Calcium-channel blocking agents, nondihydropyridine (e.g., diltiazem, verapamil)

Possible increased exposure of active deflazacort metabolite1

Reduce deflazacort dosage to one-third of the recommended dosage1


Increased exposure of active deflazacort metabolite by approximately threefold1

Reduce deflazacort dosage to one-third of the recommended dosage1


Possible decreased exposure of active deflazacort metabolite1

Avoid concomitant use1


Possible increased exposure of active deflazacort metabolite1

Reduce deflazacort dosage to one-third of the recommended dosage1

Grapefruit juice

Possible increased exposure of active deflazacort metabolite1

Reduce deflazacort dosage to one-third of the recommended dosage1


Possible increased risk of adrenal crisis1

Initiate deflazacort prior to levothyroxine therapy1

Neuromuscular blocking agents (e.g., pancuronium)

Possible increased risk of acute myopathy1


Substantially decreased exposure of active deflazacort metabolite1

Avoid concomitant use1

Vaccines and Toxoids

May cause a diminished response to toxoids and live or inactivated vaccines1 28

May potentiate replication of some organisms contained in live, attenuated vaccines1 28

Live or live attenuated vaccines not recommended in individuals receiving immunosuppressive dosages of corticosteroids1 28

Expected serum antibody response may not be obtained if killed or inactivated vaccines are administered1 28

Emflaza Pharmacokinetics



Prodrug; following oral administration, rapidly absorbed and subsequently hydrolyzed to its active form (21-desacetyldeflazacort; 21-desDFZ).1 15 18 19 20 21 23

Following administration of tablets or oral suspension in the fasted state, median time to peak plasma concentration is about 1 hour (0.25–2 hours).1

Oral biovailability is about 70% in healthy adults.19

Bioavailability of tablets is similar to that of oral suspension.1

Exhibits dose proportional pharmacokinetics over dose range of 3–36 mg.18 23


Administration of tablets with a high-fat meal decreased peak plasma concentration by about 30% and delayed time to peak plasma concentration by about 1 hour; however, extent of absorption not affected.1 21

Administration with food or of tablets crushed in applesauce did not affect absorption or bioavailability.1

Special Populations

In one study, pharmacokinetic profile of deflazacort in pediatric patients with chronic renal failure was similar to that in individuals with normal renal function.19

Exposure similar between patients with moderate hepatic impairment (Child-Pugh class B) and healthy individuals.1

Exposure similar between patients with end-stage renal disease (Clcr <15 mL/minute) and healthy individuals.1

Pharmacokinetics not affected by gender or race.1 23



Only a small portion of the deflazacort active metabolite crosses blood-brain barrier.20

Corticosteroids readily cross the placenta and are distributed into milk.1

Plasma Protein Binding

Active metabolite: Approximately 40%.1



Deflazacort is a prodrug that is rapidly converted to the active moiety by plasma esterases.1 15 18 19 20 21 23

Active metabolite further metabolized by CYP3A4 to several other inactive metabolites.1

Elimination Route

Principally renal (about 68%);1 20 active metabolite accounts for 18% of eliminated drug in urine.1


Active metabolite: 1.5–2 hours.18 19





20–25°C (may be exposed to 15–30°C).1


20–25°C (may be exposed to 15–30°C).1 Discard bottle 1 month after first opening.1


  • Oxazoline derivative of prednisolone;1 3 4 15 18 19 20 synthetic corticosteroid prodrug.1 15 18 20

  • Active metabolite binds with high affinity to tissue glucocorticoid receptors to exert potent anti-inflammatory and immunosuppressive effects.1 15 20

  • Effects are predominantly glucocorticoid in nature26 with little to no effect on sodium retention.20

  • Exact mechanism of action in Duchenne muscular dystrophy unknown;1 26 may decrease inflammation and fibrosis in muscles affected by the disease.15

Advice to Patients

  • Importance of patients or caregivers reading the manufacturer’s patient information and instructions for use when deflazacort oral suspension is prescribed.1

  • Importance of not discontinuing deflazacort therapy abruptly or without first consulting a clinician since there may be a need for gradual dosage reduction to minimize the risk of adrenal insufficiency.1

  • Importance of patients taking the tablets and oral suspension as directed by the manufacturer.1 (See Administration under Dosage and Administration.)

  • Risk of infection, sometimes severe and/or fatal.1 Importance of patients informing their clinician of recent or ongoing infections, recent vaccinations, or exposure to chickenpox or measles.1 Advise patients or caregivers to seek immediate medical attention if fever or other signs of infection are present.1

  • Risk of increased BP and water retention.1 Importance of advising patients or caregivers that dietary sodium restriction and potassium supplementation may be required.1

  • Importance of advising patients or caregivers that severe behavioral and mood changes may occur with deflazacort therapy.1 Advise patients or caregivers to seek medical attention if any psychiatric symptoms develop, especially if depressed mood or suicidal ideation is suspected.1

  • Importance of advising patients that prolonged use of deflazacort can increase the risk of osteoporosis and related fractures.1

  • Risk of cataracts or glaucoma.1 Importance of advising patients or caregivers that monitoring is recommended if deflazacort therapy is continued for >6 weeks.1

  • Importance of advising patients or caregivers that administration of live or live attenuated vaccines is not recommended during therapy with deflazacort.1 Killed or inactivated vaccines may be administered; however, response cannot be predicted.1

  • Importance of advising patients or caregivers to seek immediate medical attention at the first sign of a rash.1

  • Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs, vitamins, and herbal supplements, as well as any concomitant illnesses (e.g., osteoporosis, infections).1

  • Importance of women informing clinicians if they are or plan to become pregnant or plan to breast-feed.1

  • Importance of advising patients of other important precautionary information.1 (See Cautions.)


Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.

Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.



Dosage Forms


Brand Names




22.75 mg/mL


Marathon Pharmaceuticals


6 mg


Marathon Pharmaceuticals

18 mg


Marathon Pharmaceuticals

30 mg


Marathon Pharmaceuticals

36 mg


Marathon Pharmaceuticals

AHFS DI Essentials™. © Copyright 2020, Selected Revisions April 9, 2018. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, Maryland 20814.


1. Marathon Pharmaceuticals, LLC. Emflaza (deflazacort) tablets and oral suspension prescribing information. Northbrook, IL; 2017 Feb.

2. Food and Drug Administration. Search Orphan Drug Designations and Approvals. Silver Spring, MD. From FDA website. Accessed 2017 Mar 8.

3. Griggs RC, Miller JP, Greenberg CR et al. Efficacy and safety of deflazacort vs prednisone and placebo for Duchenne muscular dystrophy. Neurology. 2016; 87:2123-2131.

4. Angelini C, Pegoraro E, Turella E et al. Deflazacort in Duchenne dystrophy: study of long-term effect. Muscle Nerve. 1994; 17:386-91.

5. Krmar RT, Ramirez JA, Torres CG et al. Posterior subcapsular cataracts associated with deflazacort therapy. Clin Nephrol. 1997; 47:205.

6. Singh A, Schaeffer EK, Reilly CW. Vertebral Fractures in Duchenne Muscular Dystrophy Patients Managed With Deflazacort. J Pediatr Orthop. 2016; :.

7. Lee EC, Kim GA, Koo JW. Toxic epidermal necrolysis associated with deflazacort therapy with nephrotic syndrome. Kidney Res Clin Pract. 2014; 33:222-5.

8. Lim MH, Bae HJ, Park SY et al. Two cases of toxic epidermal necrolysis associated with deflazacort therapy in nephrotic syndrome: successfully treated with cyclosporine A. Child Kidney Dis. 2016; 20:97-100.

9. American Academy of Pediatrics Committee on Fetus and Newborn and Committee on Drugs. Benzyl alcohol: toxic agent in neonatal units. Pediatrics. 1983; 72:356-8.

10. Anon. Benzyl alcohol may be toxic to newborns. FDA Drug Bull. 1982; 12:10-11.

11. Centers for Disease Control (CDC). Neonatal deaths associated with use of benzyl alcohol--United States. MMWR Morb Mortal Wkly Rep. 1982; 31:290-1.

12. Gershanik J, Boecler B, Ensley H et al. The gasping syndrome and benzyl alcohol poisoning. N Engl J Med. 1982; 307:1384-8.

13. Menon PA, Thach BT, Smith CH et al. Benzyl alcohol toxicity in a neonatal intensive care unit. Incidence, symptomatology, and mortality. Am J Perinatol. 1984; 1:288-92.

14. Anderson CW, Ng KJ, Andresen B et al. Benzyl alcohol poisoning in a premature newborn infant. Am J Obstet Gynecol. 1984; 148:344-6.

15. US Food and Drug Administration. Center for Drug Evaluation and Research. Application number 208684Orig1s000, 208685Orig1s000: Medical review(s). From FDA website.,208685Orig1s000MedR.pdf

16. Gloss D, Moxley RT, Ashwal S et al. Practice guideline update summary: Corticosteroid treatment of Duchenne muscular dystrophy: Report of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology. 2016; 86:465-72.

17. Bianchi L, Hansel K, Antonelli E et al. Deflazacort hypersensitivity: a difficult-to-manage case of systemic allergic dermatitis and literature review. Contact Dermatitis. 2016; 75:54-6.

18. Rao N, Bhargava VO, Reynolds DL et al. An investigation of the dose proportionality of deflazacort pharmacokinetics. Biopharm Drug Dispos. 1996; 17:753-60.

19. Ferraris J, Krmar R, Flores D et al. Pharmacokinetics of deflazacort in renal transplanted and hemodialyzed children. Clin Nephrol. 1998; 50:172-7.

20. Parente L. Deflazacort: therapeutic index, relative potency and equivalent doses versus other corticosteroids. BMC Pharmacol Toxicol. 2017; 18:1.

21. Rao N, Eller M, Arumugham T et al. The effect of food on the relative bioavailability of deflazacort. Eur J Drug Metab Pharmacokinet. 1996 Jul-Sep; 21:241-5.

22. Altintop L, Cakar B, Hokelek M et al. Strongyloides stercoralis hyperinfection in a patient with rheumatoid arthritis and bronchial asthma: a case report. Ann Clin Microbiol Antimicrob. 2010; 9:27.

23. Ding W, Ding L, Li WB et al. [Pharmacokinetics of deflazacort tablets in healthy Chinese volunteers]. Yao Xue Xue Bao. 2014; 49:921-6.

24. Pacheco D, Travassos AR, Antunes J et al. Allergic hypersensitivity to Deflazacort. Allergol Immunopathol (Madr). 2013 Sep-Oct; 41:352-4.

25. Joshi N, Rajeshwari K. Deflazacort. J Postgrad Med. 2009 Oct-Dec; 55:296-300.

26. Matthews E, Brassington R, Kuntzer T et al. Corticosteroids for the treatment of Duchenne muscular dystrophy. Cochrane Database Syst Rev. 2016; :CD003725.

27. Buckley L, Guyatt G, Fink HA et al. 2017 American College of Rheumatology Guideline for the Prevention and Treatment of Glucocorticoid-Induced Osteoporosis. Arthritis Rheumatol. 2017; 69:1521-1537.

28. Kroger AT, Duchin J, Vazquez M. General best practice guidelines for immunization: best practices guidance of the advisory committee on immunization practices (ACIP). From website. Accessed on October 6, 2017.

29. AHFS drug information 2018. McEvoy GK, ed. Corticosteroids general statement. Bethesda, MD: American Society of Health-System Pharmacists; 2018.

30. Ferraris JR, Pasqualini T, Legal S et al. Effect of deflazacort versus methylprednisone on growth, body composition, lipid profile, and bone mass after renal transplantation. The Deflazacort Study Group. Pediatr Nephrol. 2000; 14:682-8.

31. Loftus J, Allen R, Hesp R et al. Randomized, double-blind trial of deflazacort versus prednisone in juvenile chronic (or rheumatoid) arthritis: a relatively bone-sparing effect of deflazacort. Pediatrics. 1991; 88:428-36.

32. US Food and Drug Administration. Center for Drug Evaluation and Research. Application number 208684Orig1s000, 208685Orig1s000: Clinical pharmacology and biopharmaceutitcs review(s). From FDA website.,208685Orig1s000ClinPharmR.pdf

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