A wide range of conditions may sometimes need treatment with glucocorticoids. The indications
include: Anaphylaxis, asthma, severe hypersensitivity reactions Rheumatoid arthritis, juvenile chronic
arthritis, polymyalgia rheumatica Systemic lupus erythematosus, dermatomyositis, mixed connective
tissue disease (other than systemic sclerosis), polyarteritis nodosa, sarcoidosis Pemphigus, bullous
pemphigoid, pyoderma gangrenosum Minimal change nephrotic syndrome, acute interstitial nephritis
Rheumatic carditis Ulcerative colitis, Crohn's disease Uveitis, optic neuritis Autoimmune haemolytic
anaemia, idiopathic throئئئئئmbocytopenic purpura Acute and lymphatic leukaemia, malignant lymphoma, multiple myeloma Immune suppression in transplantation.

Dose:
The initial dose varies from 6 to 120 mg/day for adults, and 0.25 to 1.5 mg/kg for children, depending
on the severity and progression of the disorder in each case. This initial dose may be maintained or
modified, until the required clinical response is obtained.
The maintenance dose should always be the minimum dose required to control symptoms. Reductions
in the dose should be applied gradually, to allow for the recovery of the hypothalamus-pituitaryadrenal axis function.
Adults
For acute disorders, it may be necessary to administer up to 120 mg/day of deflazacort initially.
Maintenance doses in most disorders are within the range of 3 to 18 mg/day. The following regimens
are for guidance only.
Rheumatoid arthritis: The maintenance dose is usually within the range of 3 to 18 mg/day.
The smallest effective dose should be used and increased if necessary.
Bronchial asthma: In the treatment of an acute attack, high doses of 48–72 mg/day may be necessary,
depending on the severity. They are then gradually reduced once the attack has been controlled. For
maintenance in chronic asthma, doses should be adjusted to the lowest dose that controls symptoms.
Other conditions: The dose of deflazacort depends on clinical requirements, adjusting to the lowest
effective dose for maintenance. The initial doses can be estimated on the basis of the ratio of
5 mg of prednisone or prednisolone to 6 mg of deflazacort.
Hepatic impairment
In patients with hepatic impairment, blood levels of deflazacort may increase.
Therefore, the dose of deflazacort should be carefully controlled and adjusted to the minimum
effective dose.
Renal impairment
In patients with renal impairment, no special precautions need to be taken, apart from those usually
adopted in patients receiving glucocorticoid therapy.
Elderly patients
In elderly patients, no special precautions are necessary beyond those usually taken in patients
receiving glucocorticoid therapy. The common adverse effects of systemic corticosteroids may be
associated with more serious consequences in elderly patients (see Warnings and Precautions).
Paediatric population
Exposure of children to deflazacort in clinical trials has been limited.
In children, the indications for glucocorticoids are the same as for adults, but it is
important to use the lowest effective dose. Alternate day administration should be considered (see
Warnings and Precautions).
Doses of deflazacort are usually in the range of 0.25–1.5 mg/kg/day. The following ranges provide
general guidance:
Juvenile idiopathic arthritis: The usual maintenance dose is from 0.25 to 1.0 mg/kg/day.
Nephrotic syndrome: The initial dose is usually 1.5 mg/kg/day, followed by a downward adjustment
according to clinical requirements.
Bronchial asthma: Based on the potency ratio, the initial dose should be
0.25 to 1.0 mg/kg of deflazacort every other day.
Withdrawal of deflazacort
When taken for period of over 3 weeks, higher than physiological doses of systemic corticosteroids
(approximately 9 mg per day or equivalent) should not be discontinued suddenly. How to reduce the
dose of systemic corticosteroids depends largely on the likelihood of disease recurrence when
reducing the dose. Clinical evaluation of disease progression during withdrawal may be necessary.
If the disease is unlikely to relapse when systemic corticosteroids are discontinued but there is
uncertainty about HPA suppression, the dose of systemic corticosteroids can rapidly be reduced to
physiological doses. Once a daily dose equivalent to 9 mg of deflazacort is reached, the dose reduction
should be slower to allow recovery of the HPA axis.
Sudden withdrawal of systemic corticosteroid therapy that has lasted for up to 3 weeks is appropriate
if the disease is considered unlikely to relapse. In most patients, sudden withdrawal of doses of up to
48 mg daily of deflazacort or its equivalent for 3 weeks is unlikely to result in clinically relevant HPA
axis suppression.
In the following groups of patients, the gradual withdrawal of systemic corticosteroid treatment
should be considered even after cycles lasting 3 weeks or less:
 Patients who have received repeated courses of systemic corticosteroids, particularly if taken
for more than 3 weeks.
 When a short course has been prescribed within one year after discontinuing long-term
therapy (months or years).
 Patients who may have reasons for adrenal insufficiency other than exogenous corticosteroid
therapy.
 Patients receiving systemic corticosteroid doses greater than 48 mg daily of deflazacort (or
equivalent).
 Patients who take repeated doses at night.
Method of administration:
For oral use.

- Hypersensitivity to the active substance deflazacort or to any of the excipients listed in section 6.1. - Patients receiving live virus immunisation. - Systemic infection, unless specific anti-infective therapy is used. - The use of corticosteroids for longer than the duration of replacement treatment or short-term emergency therapy is contraindicated in the following cases: Peptic ulcer, bacterial and viral infections, active tuberculosis, ocular herpes simplex, herpes zoster (viraemic phase), varicella, systemic mycotic infections; and in pre- and postvaccination periods

One 6 mg tablet of Disflax is therapeutically equivalent to approximately 5 mg of prednisone.
However, it should be considered that corticosteroid requirements vary and, therefore, dosages must
be set individually, taking the patient’s condition and response to therapy into account.
Undesirable effects can be minimised by using the lowest effective dose for the shortest possible time
and administering the daily requirement as a single morning dose or, whenever possible, in a single
morning dose on alternate days. The patient will need to be examined regularly in order to adjust the
dose to the progression of the disease (see section 4.2).
Adrenal suppression
Adrenal cortical atrophy develops during prolonged treatment and may persist for years
after discontinuation of treatment. Discontinuation of corticosteroids after prolonged treatment should
always be gradual to avoid acute adrenal insufficiency, which could be fatal. During prolonged
treatment, any intercurrent illness, trauma or surgical procedure will require a temporary increase in
dosage; if corticosteroids have been discontinued after prolonged treatment, it may be necessary to
reintroduce them temporarily.
Patients should carry “Corticosteroid Treatment” cards, which provide clear guidance on precautions
to be taken to minimise risk and provide details on the prescriber, drug, dosage and duration of
treatment.
Anti-inflammatory/immunosuppressive effects and infection
Suppression of the inflammatory response and immune function increases susceptibility to and
severity of infections. The clinical manifestation may often be atypical, and serious infections, such as
septicaemia and tuberculosis, may be masked and may reach an advanced stage before being
recognised.
Varicella is of particular concern, as this normally minor disease can be fatal in immunocompromised
patients. Patients (or parents of children) who do not have a clear history of varicella should avoid
personal contact with varicella or herpes zoster and, in case of exposure, should seek urgent medical
attention. Passive immunisation with varicella zoster immune globulin (VZIG) is required for nonimmune exposed patients who are receiving systemic corticosteroids or have used them within the
previous 3 months; it should be administered within 10 days of varicella exposure. If the diagnosis of
varicella is confirmed, the disease will require specialised care and urgent treatment. Corticosteroids
should not be discontinued and it may be necessary to increase the dose.
Patients should be advised to take special care to avoid exposure to measles and to
seek medical attention immediately in case of exposure. Prophylaxis with intramuscular normal
immunoglobulin may be necessary.
Live vaccines should not be administered to persons with impaired response. Antibody response to
other vaccines may be diminished.
Anticoagulants
The effect of corticosteroids on anticoagulants is variable. There are reports of enhanced as well as
diminished effects of anticoagulants when given concurrently with corticosteroids. Therefore,
coagulation indices should be monitored to maintain the desired anticoagulant effects (see section 4.5).
Gastrointestinal ulcers
Care should be taken when deflazacort is prescribed in combination with non-steroidal
antiinflammatory drugs (NSAIDs) due to increased risk of gastrointestinal ulcers (see section 4.5).
Severe cutaneous adverse reactions
Deflazacort may cause severe cutaneous adverse reactions such as toxic epidermal necrolysis (TEN)
and Stevens-Johnson syndrome (SJS) (see section 4.8). If severe cutaneous adverse reactions occur,
deflazacort should be discontinued and appropriate therapy and/or measures should be taken.
Special precautions
Special care should be taken in the following cases before deciding to initiate treatment with
glucocorticoids:
- Heart disease or congestive heart failure (except in the presence of active rheumatic carditis),
hypertension, thromboembolic diseases.
Glucocorticoids can cause salt and water retention and increased potassium excretion. Dietary
salt restriction and potassium supplementation may be necessary.
- Gastritis or oesophagitis, diverticulitis, ulcerative colitis if there is a risk of perforation or
pyogenic infection, recent intestinal anastomosis, active or latent peptic ulcer.
- Diabetes mellitus (including family history), osteoporosis, myasthenia gravis, renal
impairment.
- Emotional instability or psychotic tendency, epilepsy.
- Prior corticosteroid-induced myopathy.
- Hepatic impairment.
- Hypothyroidism and cirrhosis, which can increase the effect of glucocorticoids.
- Ocular herpes simplex due to possible perforation of the cornea.
Patients and/or caregivers should be warned that potentially serious psychiatric adverse reactions may
occur with systemic steroids (see section 4.8). Symptoms usually appear within days or weeks of
starting treatment. Risks may be greater with high doses/systemic exposure (see also section 4.5
pharmacokinetic interactions that may increase the risk of side effects), although dose levels do not
allow us to predict the occurrence, type, severity or duration of reactions. Most reactions resolve after
the dose is reduced or discontinued, although specific treatment may be necessary.
Patients/caregivers should be advised to see a doctor if any worrying psychological symptoms occur,
especially if depressive mood or suicidal ideation is suspected.
Patients/caregivers should also be alert to possible psychiatric disturbances that may occur during or
immediately after reduction/discontinuation of the dose of systemic steroids,
although such reactions have been reported infrequently.
Special care should be taken when considering the use of systemic corticosteroids in patients with a
prior or current history of severe affective disorders in themselves or their first-degree relatives. These
include depressive or manic-depressive disorders and psychosis prior to steroids.
Glucocorticoids are known to cause irregular menstruation and leukocytosis, so special care should be
taken in the use of deflazacort.
Paediatric population
Exposure to Corticosteroids in infancy, childhood and adolescence may cause irreversible growth
retardation.
Hypertrophic cardiomyopathy has been reported following systemic administration of glucocorticoids
in premature infants. In infants receiving systemic glucocorticoid administration, echocardiograms
should be performed to monitor myocardial structure and function (see section 4.8).
Use in the elderly
Common adverse effects of systemic corticosteroids may be associated with more serious
consequences in old age, especially osteoporosis, hypertension, hypokalaemia, diabetes, susceptibility
to infections and thinning of the skin. Close clinical supervision is required to avoid life-threatening
reactions.
Since the complications of glucocorticoid therapy are dose and duration dependent, the lowest possible
dose should be administered and a risk/benefit decision should be made as to whether intermittent
therapy should be used.
Doses may need to be increased in stressful situations, such as infections, injuries or surgery.
Over prolonged treatment and at high doses, the electrolyte balance should be monitored and, if
necessary, sodium and potassium intake adjusted.
Visual disturbances
Visual disturbances can occur with topical and systemic corticosteroids. If a patient experiences
symptoms such as blurred vision or other visual disturbances, an ophthalmologist should be consulted
to assess the possible causes, including cataracts, glaucoma or rare diseases such as central serous
chorioretinopathy (CSCR), which has been reported after use of systemic and topical corticosteroids.
Prolonged use of glucocorticoids may cause posterior subcapsular cataracts, glaucoma with possible
optic nerve damage, and may increase the likelikhood of secondary fungal or viral ocular infections.
Use in active tuberculosis should be limited to cases of fulminant tuberculosis and disseminated
tuberculosis in which deflazacort is part of the management plan. If glucocorticoids are indicated in
patients with latent tuberculosis or tuberculin reactivity, close observation is necessary as reactivation
of the disease may occur. Patients receiving prolonged glucocorticoid therapy should be given
chemoprophylaxis.
Tendinitis and tendon rupture are known class effects of glucocorticoids. The risk of these reactions
may increase with co-administration of quinolones (see section 4.8).
Pheochromocytoma crises, which can be fatal, have been reported after administration of systemic
corticosteroids. Corticosteroids should only be administered to patients with suspected or identified
pheochromocytoma after an adequate risk/benefit assessment (see section 4.8).
Prolonged use of glucocorticoids in children may inhibit growth and development.
Warnings about excipients
6 mg and 30 mg tablets:
Contains lactose. Patients with hereditary galactose intolerance, total lactase deficiency or glucose or
galactose absorption problems should not take this medicinal product.
Use by athletes
This medicine contains deflazacort, which may test positive in doping controls. 

Concomitant administration of this medicine with non-steroid anti-inflammatory drugs may increase
the risk of gastrointestinal ulcers.
Levels of salicylates in the blood may drop due to increased renal clearance when using
glucocorticoids, and rise spontaneously to toxic levels when treatment is interrupted.
Potassium depleting diuretics may enhance the hypokalaemic action of glucocorticoids, while digitalis
drugs can increase the possibility of hypokalaemia-associated arrhythmia. It may be necessary to
increase the dose of anti-diabetic drugs.
The desired effects of hypoglycaemic agents (including insulin), antihypertensives and diuretics are
antagonised by corticosteroids and the hypokalaemic effects of acetazolamide, loop diuretics, thiazide
diuretics, beta agonists, xanthines and carbenoxolone.
Deflazacort is metabolised in the liver. The maintenance dose of deflazacort should be increased if
liver enzyme inducing drugs, e.g. rifampicin, rifabutin, carbamazepine, phenobarbital, phenytoin,
primidone and aminoglutethimide, are co-administered. In the case of hepatic enzyme inhibitors, e.g.
ketoconazole, it may be possible to reduce the maintenance dose of deflazacort.
In patients taking oestrogens, corticosteroid requirements may be reduced.
Rifampicin, barbiturates and phenytoin may accelerate glucocorticoid metabolism. Accordingly,
addiction to or withdrawal from said drugs may require an adjustment to the corticosteroid dose.
In patients with myasthenia gravis, anticholinesterases may interact with glucocorticoids and lead to
severe muscular fatigue.
In patients under treatment with systemic corticosteroids, the use of non-depolarising muscle relaxants
may lead to prolonged relaxation and acute myopathy. Risk factors for this situation are prolonged and
high-dose corticosteroid treatment and prolonged duration of muscle paralysis. This interaction is
more likely after prolonged ventilation (as in UTI).
Glucocorticoids decrease the immunological response to vaccines and toxoids and may also enhance
germ growth in attenuated live vaccines.
Patients with hypoprothrombinaemia are advised to be careful when associating acetylsalicylic acid
and corticosteroids.
Levels of protein-linked iodine and thyroxine (T4) in plasma may decrease, as may I131 uptake.
Corticosteroids may increase or decrease the effects of anti-coagulants.
The efficacy of coumarin anticoagulants may be enhanced by concurrent treatment with
corticosteroids, and close monitoring of INR or prothrombin time is required to avoid spontaneous
bleeding.
Since glucocorticoids can suppress the body’s normal responses to attack by microorganisms, it is
important to ensure that any anti-infective treatment is effective, and close monitoring of patients is
recommended. Concomitant use of glucocorticoids and oral contraceptives should be closely
monitored, as plasma levels of glucocorticoids may increase. This effect may be due to a change in
metabolism or binding to serum proteins.
Antacids may reduce bioavailability; wait at least 2 hours between taking deflazacort and antacids.
Concomitant treatment with CYP3A inhibitors, including cobicistat-containing drugs, is expected to
increase the risk of systemic adverse reactions. This combination should be avoided unless the benefit
outweighs the increased risk of systemic corticosteroid-related adverse reactions, in which case
patients should be monitored for systemic corticosteroid reactions.

Pregnancy:
The ability of corticosteroids to cross the placenta varies between drugs; however, deflazacort does cross the placenta. Corticosteroids have been observed to cause foetal abnormalities in animals, including cleft palate, intrauterine growth retardation and effects on brain growth and development. There is no evidence that corticosteroids cause an increased incidence of congenital anomalies such as cleft palate/lip in humans. However, when administered for prolonged periods or repeatedly during pregnancy, corticosteroids may increase the risk of intrauterine growth retardation. Hypoadrenalism can theoretically occur in the neonate after prenatal corticosteroid exposure, but it usually resolves spontaneously after birth and is rarely clinically significant. As with all medications, corticosteroids should only be prescribed when the benefits to the mother and child outweigh the risks. However, when corticosteroid treatment is essential, patients with normal pregnancies can be treated as if they were not pregnant.
Breastfeeding:
Glucocorticoids are excreted in breast milk, although no data are available for deflazacort.
Daily doses of up to 50 mg of deflazacort are unlikely to cause systemic effects in the infant. Infants of mothers taking higher doses than these may have some degree of adrenal suppression, but the benefits of breastfeeding are likely to outweigh any theoretical risk.
Fertility
There are no available data on Deflazacort and its effects on fertility.

No studies have been performed on the effects of deflazacort on the ability to drive or operate machinery

The incidence of predictable adverse effects, including hypothalamic-pituitary-adrenal axis suppression, correlates with relative drug potency, dose, dose pattern, timing of administration and duration of treatment (see section 4.4).
The following frequency classification is used: Very common (≥1/10); common (≥1/100 to <1/10); uncommon (≥1/1,000 to <1/100); rare (≥1/10,000 to <1/1,000); very rare (<1/10,000); frequency not known (cannot be estimated from the available data).

System organ class	Frequency according to MedDRA convention
Common (≥1/100 to <1/10)	Uncommon (≥1/1,000 to <1/100)	Rare (≥1/10,000 to <1/1,000)	Not known (cannot be estimated from the available data)
Immune system disorders	Cases of hypersensitivity, including anaphylaxis, have been reported
Blood and lymphatic system disorders	Leukocytosis
Vascular disorders	Thromboembolism in particular in patients with underlying conditions associated with increased thrombotic tendency, rare incidence of benign intracranial hypertension
Gastrointestinal disorders:	Dyspepsia, peptic ulcer, haemorrhage, nausea
Nervous system disorders	Headache, vertigo.	Restlessness, increased intracranial pressure with papilloedema in children (pseudotumor cerebri), aggravation of epilepsy (usually after withdrawal of treatment).
Psychiatric disorders1	Depressed and labile mood. Behavioural changes.	Irritability, euphoria, suicidal thoughts, mania, delusions, hallucinations, aggravation of schizophrenia. Anxiety, sleep disorders and cognitive dysfunction, including confusion and amnesia.
Eye disorders	Blurred vision (see section 4.4), increased intraocular pressure, glaucoma, papilloedema, posterior subcapsular cataracts, especially in children, chorioretinopathy (see section 4.4), corneal or scleral thinning, exacerbation of ophthalmic viral or fungal diseases.
Skin and subcutaneous tissue	Hirsutism, stretch marks, acne.	Bruising.	Severe cutaneous

Peptic ulcer
perforation, acute
pancreatitis (especially
in children),
candidiasis.
 

disorders	adverse reactions (SCARs) such as Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN), skin atrophy, telangiectasia
Cardiac disorders
Endocrine disorders	Hypothalamic pituitary-adrenal (HPA) axis suppression, which may persist up to 1 year after stopping treatment, cushingoid facies (moon face)	Growth suppression in infancy, childhood and adolescence, steroid withdrawal syndrome (see section 4.4)
Metabolism and nutrition disorders	Weight gain.	Altered carbohydrate tolerance with increased need for antidiabetic therapy, sodium and water retention with hypertension, potassium loss and hypokalaemic alkalosis when co-administered with beta agonists and xanthines.	Negative protein and calcium balance, increased appetite.
Infections and infestations	Increased susceptibility to and severity of infections with suppression of clinical signs and symptoms, opportunistic infections, recurrence of latent tuberculosis (see section 4.4).	Candidiasis
Musculoskeletal and connective tissue disorders	Osteoporosis, vertebral and long-bone fractures	Avascular osteonecrosis, tendinitis and tendon rupture when co-administered with quinolones (see

Heart failure,
hypertrophic
cardiomyopathy in
preterm infants
Loss of
muscle mass
 

section 4.4), myopathy, acute myopathy may be precipitated by non depolarising muscle relaxants (see section 4.5), negative nitrogen balance.
Reproductive system and breast disorders	Menstrual irregularity.
General disorders and administration site conditions.2	Oedema.	Impaired healing. Too rapid a reduction in corticosteroid dose after prolonged treatment may lead to acute adrenal insufficiency, hypotension and death (see section 4.4).

1 Reactions are common and can occur in both adults and children. In adults, the frequency of severe reactions has been estimated at 5–6%. Psychological effects have been reported on withdrawal of corticosteroids; the frequency is unknown.

2A “withdrawal syndrome” may also occur, including fever, myalgia, arthralgia, rhinitis, conjunctivitis, painful itchy skin nodules and weight loss. This can occur in patients even without evidence of adrenal insufficiency. Class effect
Pheochromocytoma crisis has been reported with other systemic corticosteroids and is a known class effect (see section 4.4).
Reporting of suspected adverse reactions
Reporting suspected adverse reactions after authorisation of the medicinal product is important. It allows continued monitoring of the benefit/risk balance of the medicinal product. Healthcare professionals are asked to report any suspected adverse reactions via the Spanish Pharmacovigilance System for Medicinal Products for Human Use: www.notificaRAM.es and the National
Pharmacovigilance (NPC)-SFDA.

Call Center: 19999

- E-mail: npc.drug@sfda.gov.sa

- Website: http://ade.sfda.gov.sa

No cases of intoxication have been described with Disflax; in any case, symptomatic treatment is advised.
High doses of corticosteroids, taken orally over a prolonged period of time, may suppress hypothalamus-pituitary-adrenal axis function.

Pharmacotherapeutic group: systemic corticosteroids, ATC code: H02AB13.
Disflax (deflazacort) is a synthetic glucocorticoid. It is similar to other corticosteroids in that it
possesses anti-inflammatory properties, but has a different safety profile due to its reduced activity on bone and hydrocarbon metabolism.
When the physiological dose is exceeded, all glucocorticoids lead to negativisation of the calcium balance by reducing intestinal absorption and/or increasing urinary elimination: this initially results in a gradual loss of bone mass, which may progress to the final stage of osteopenia, osteoporosis.
In dual-photon absorptiometry and iliac crest biopsy studies carried out on humans, in comparison with other glucocorticoids Disflax was observed to interfere less with calcium absorption and urinary excretion of calcium, with the subsequent effect on bone reabsorption shown by a less marked reduction in the volume of the trabecular bone and bone mineral content. Moreover, in 3 clinical studies carried out on 143 children under treatment up to 26 months, Disflax was observed to interfere less with their growth. On the other hand, natural and synthetic corticosteroids tend to decrease glucose tolerance and clinically unmask latent diabetes mellitus, requiring treatment for diabetes to be instituted, or to exacerbate already clinical diabetes, consequently requiring an increase in the habitual dose of diabetes drugs. In comparative studies, the interference of Disflax on glucid metabolism has been observed to be significantly lower than other glucocorticoids, with better metabolic control and better glucose tolerance in diabetic patients.

Deflazacort taken orally is absorbed well and immediately transformed by plasma esterases into its active metabolite deflazacort 21-OH. This metabolite reaches maximum plasma concentrations in 1.5–2 hours. The metabolite, 40% of which is bound to plasma proteins, has no affinity for transcortin. The average plasma half-life of deflazacort 21-OH is 1.1–1.9 hours. It is eliminated mainly through the kidneys, 70% of the compound being excreted within 8 hours of being taken. The remaining 30% is eliminated via faeces. Deflazacort 21-OH is extensively metabolised, only 5% of urinary excretion consisting of 21-OH deflazacort, while deflazacort 6-beta-OH metabolites account for a third of urinary excretion.

Acute and chronic toxicology studies show findings similar to those found for other corticosteroids at equivalent anti-inflammatory doses. The teratogenic effects observed in laboratory animals are those observed for other corticosteroids.
Doses of DL50 (4000–5200 mg/kg) given to mice, rats and dogs were 3000–4000 times higher than the maximum daily clinical doses given to humans. Two full toxicity studies on oral doses repeated over 12 months, carried out on rats and cynomolgus monkeys and backed up by short-term studies, showed changes related with the typical treatment of glucocorticoids.
As with other glucocorticoids, deflazacort showed dose-dependent teratogenic effects in rats and
rabbits at very high doses, with no genotoxic effects being observed throughout an extensive battery of mutagenic tests in vivo and in vitro. Deflazacort was not observed to induce or stimulate the development of tumours in mice.

Lactose monohydrate,
Corn starch,
Microcrystalline cellulose,
Magnesium stearate

None reported.
 

5 years

Store below 30^oC
 

Packaged in PVC-Aluminium blister packs.
Disflax 6 mg tablets: packs containing 20 or 500 tablets.
Disflax 30 mg tablets: packs containing 10 or 500 tablets

Any unused medicinal product or waste material should be disposed of in accordance with local
requirements.