United States - English - NLM (National Library of Medicine)
PREDNISONE- prednisone tablet
Prednisone is a glucocorticoid. Glucocorticoids are adrenocortical steroids, both naturally occurring
and synthetic, which are readily absorbed from the gastrointestinal tract. Prednisone is a white to
practically white, odorless, crystalline powder. It is very slightly soluble in water; slightly soluble in
alcohol, in chloroform, in dioxane, and in methanol. The chemical name for prednisone is pregna-1, 4-
diene-3, 11, 20-trione, 17, 21-dihydroxy-
The structural formula is represented below:
Molecular weight: 358.44
Prednisone Tablets, USP are available in three strengths: 5 mg, 10 mg, and 20 mg. In addition, each
tablet contains the following Inactive Ingredients: Lactose Monohydrate, Magnesium Stearate,
Pregelatinized Starch, Sodium Lauryl Sulfate and Sodium Starch Glycolate. Also Prednisone Tablets
USP, 20 mg contains FD & C yellow #6 aluminum lake HT 15-18%.
Prednisone Tablets, USP are indicated in the following conditions:
1. Endocrine Disorders
Primary or secondary adrenocortical insufficiency (hydrocortisone or cortisone is the first choice;
synthetic analogs may be used in conjunction with mineralocorticoids where applicable; in infancy
mineralocorticoid supplementation is of particular importance)
Congenital adrenal hyperplasia
2. Rheumatic Disorders
As adjunctive therapy for short-term administration (to tide the patient over an acute episode or
Rheumatoid arthritis, including juvenile rheumatoid arthritis (selected cases may require low-dose
Acute and subacute bursitis
Acute nonspecific tenosynovitis
Acute gouty arthritis
Synovitis of osteoarthritis
3. Collagen Diseases
During an exacerbation or as maintenance therapy in selected cases of:
Systemic lupus erythematosus
Systemic derznatomyositis (polymyositis)
Acute rheumatic carditis
4. Dermatologic Diseases
Bullous dermatitis herpetiformis
Severe erythema multiforme (Stevens-Johnson syndrome)
Severe seborrheic dermatitis
5. Allergic States
Control of severe or incapacitating allergic conditions intractable to adequate trials of conventional
Seasonal or perennial allergic rhinitis
Drug hypersensitivity reactions
6. Ophthalmic Diseases
Severe acute and chronic allergic and inflammatory processes involving the eye and its adnexa such as:
Allergic corneal marginal ulcers
Herpes zoster ophthalmicus
Anterior segment inflammation
Diffuse posterior uveitis and choroiditis
Iritis and iridocyclitis
7. Respiratory Diseases
Loeffler’s syndrome not manageable by other means
Fulminating or disseminated pulmonary tuberculosis when used concurrently with appropriate
8. Hematologic Disorders
Idiopathic thrombocytopenic purpura in adults
Secondary thrombocytopenia in adults
Acquired (autoimmune) hemolytic anemia
Erythroblastopenia (RBC anemia)
Congenital (erythroid) hypoplastic anemia
9. Neoplastic Diseases
For palliative management of:
Leukemias and lymphomas in adults
Acute leukemia of childhood
10. Edematous States
To induce a diuresis or remission of proteinuria in the nephrotic syndrome, without uremia, of the
idiopathic type or that due to lupus erythematosus
11. Gastrointestinal Diseases
To tide the patient over a critical period of the disease in:
12. Nervous System
Acute exacerbations of multiple sclerosis
Tuberculous meningitis with subarachnoid block or, impending block when used concurrently with
appropriate antituberculous chemotherapy
Trichinosis with neurologic or myocardial involvement
Systemic fungal infections and known hypersensitivity to components.
In patients on corticosteroid therapy subjected to unusual stress, increased dosage of rapidly acting
corticosteroids before, during, and after the stressful situation is indicated.
Corticosteroids may mask some signs of infection, and new infections may appear during their use.
There may be decreased resistance and inability to localize infection when corticosteroids are used.
Prolonged use of corticosteroids may produce posterior subcapsular cataracts, glaucoma with possible
damage to the optic nerves, and may enhance the establishment of secondary ocular infections due to
fungi or viruses.
Usage in pregnancy: Since adequate human reproduction studies have not been done with
corticosteroids, the use of these drugs in pregnancy, nursing mothers or women of childbearing
potential requires that the possible benefits of the drug be weighed against the potential hazards to the
mother and embryo or fetus. Infants born of mothers who have received substantial doses of
corticosteroids during pregnancy, should be carefully observed for signs of hypoadrenalism.
Average and large doses of hydrocortisone or cortisone can cause elevation of blood pressure, salt and
water retention, and increased excretion of potassium. These effects are less likely to occur with the
synthetic derivatives except when used in large doses. Dietary salt restriction and potassium
supplementation may be necessary. All corticosteroids increase calcium excretion.
While on corticosteroid therapy patients should not be vaccinated against smallpox. Other immunization
procedures should not be undertaken in patients who are on corticosteroids, especially on high dose,
because of possible hazards of neurological complications and a lack of antibody response.
The use of Prednisone Tablets, USP in active tuberculosis should be restricted to those cases of
fulminating or disseminated tuberculosis in which the corticosteroid is used for the management of the
disease in conjunction with an appropriate anti-tuberculous regimen.
If corticosteroids are indicated in patients with latent tuberculosis or tuberculin reactivity, close
observation is necessary as reactivation of the disease may occur. During prolonged corticosteroid
therapy, these patients should receive chemoprophylaxis.
Persons who are on drugs which suppress the immune system are more susceptible to infections than
healthy individuals. Chickenpox and measles, for example, can have a more serious or even fatal course
in non-immune children or adults on corticosteroids. In such children or adults who have not had these
diseases, particular care should be taken to avoid exposure. How the dose, route and duration of
corticosteroid administration affects the risk of developing a disseminated infection is not known. The
contribution of the underlying disease and/or prior corticosteroid treatment to the risk is also not known.
If exposed to chickenpox, prophylaxis with varicella-zoster immune globulin (VZIG) may be indicated.
If exposed to measles, prophylaxis with pooled intramuscular immunoglobulin (IG) may be indicated.
(See the respective package inserts for complete VZIG and IG prescribing information.) If chickenpox
develops, treatment with antiviral agents may be considered.
Drug-induced secondary adrenocortical insufficiency may be minimized by gradual reduction of
dosage. This type of relative insufficiency may persist for months after discontinuation of therapy;
therefore, in any situation of stress occurring during that period, hormone therapy should be
reinstituted. Since mineralocorticoid secretion may be impaired, salt and/or a mineralocorticoid should
be administered concurrently.
There is an enhanced effect of corticosteroids on patients with hypothyroidism and in those with
Corticosteroids should be used cautiously in patients with ocular herpes simplex because of possible
The lowest possible dose of corticosteroid should be used to control the condition under treatment, and
when reduction in dosage is possible, the reduction should be gradual.
Psychic derangements may appear when corticosteroids are used, ranging from euphoria, insomnia,
mood swings, personality changes, and severe depression, to frank psychotic manifestations. Also,
existing emotional instability or psychotic tendencies may be aggravated by corticosteroids.
Aspirin should be used cautiously in conjunction with corticosteroids in hypoprothrombinemia.
Steroids should be used with caution in nonspecific ulcerative colitis, if there is a probability of
impending perforation, abscess or other pyogenic infection; diverticulitis; fresh intestinal anastomoses;
active or latent peptic ulcer; renal insufficiency; hypertension; osteoporosis; and myasthenia gravis.
Growth and development of infants and children on prolonged corticosteroid therapy should be
Although controlled clinical trials have shown corticosteroids to be effective in speeding the
resolution of acute exacerbations of multiple sclerosis, they do not show that corticosteroids affect the
ultimate outcome or natural history of the disease. The studies do show that relatively high doses of
corticosteroids are necessary to demonstrate a significant effect. (See DOSAGE AND
Since complications of treatment with glucocorticoids are dependent on the size of the dose and the
duration of treatment, a risk/benefit decision must be made in each individual case as to dose and
duration of treatment and as to whether daily or intermittent therapy should be used.
Convulsions have been reported with concurrent use of methylprednisolone and cyclosporine. Since
concurrent use of these agents results in a mutual inhibition of metabolism, it is possible that adverse
events associated with the individual use of either drug may be more apt to occur.
Information for patients
Persons who are on immunosuppressant doses of corticosteroids should be warned to avoid exposure
to chickenpox or measles. Patients should also be advised that if they are exposed, medical advice
should be sought without delay.
Fluid and Electrolyte Disturbances
Congestive heart failure in susceptible patients
Loss of muscle mass
Vertebral compression fractures
Aseptic necrosis of femoral and humeral heads
Pathologic fracture of long bones
Peptic ulcer with possible perforation and hemorrhage
Impaired wound healing
Thin fragile skin
Petechiae and ecchymoses
May suppress reactions to skin tests
Negative nitrogen balance due to protein catabolism
Increased intracranial pressure with papilledema (pseudo-tumor cerebri) usually after treatment
Development of Cushingoid state
Secondary adrenocortical and pituitary unresponsiveness, particularly in times of stress, as in trauma,
surgery or illness
Suppression of growth in children
Decreased carbohydrate tolerance
Manifestations of latent diabetes melliltus
Increased requirements for insulin or oral hypoglycemic agents in diabetics
Posterior subcapsular cataracts
Increased intraocular pressure
Urticaria and other allergic, anaphylactic or hypersensitivity reactions.
The initial dosage of prednisone Tablets, USP may vary from 5 mg to 60 mg prednisone per day
depending on the specific disease entity being treated. In situations of less severity lower doses will
generally suffice while in selected patients higher initial doses may be required. The initial dosage
should be maintained or adjusted until a satisfactory response is noted. If after a reasonable period of
time there is a lack of satisfactory clinical response, Prednisone should be discontinued and the patient
transferred to other appropriate therapy. IT SHOULD BE EMPHASIZED THAT DOSAGE
REQUIREMENTS ARE VARIABLE AND MUST BE INDIVIDUALIZED ON THE BASIS OF THE
DISEASE UNDER TREATMENT AND THE RESPONSE OF THE PATIENT. After a favorable
response is noted, the proper maintenance dosage should be determined by decreasing the initial drug
dosage in small decrements at appropriate time intervals until the lowest dosage which will maintain an
adequate clinical response is reached. It should be kept in mind that constant monitoring is needed in
regard to drug dosage. Included in the situations which may make dosage adjustments necessary are
changes in clinical status secondary to remissions or exacerbations in the disease process, the patient’s
individual drug responsiveness, and the effect of patient exposure to stressful situations not directly
related to the disease entity under treatment; in this latter situation it may be necessary to increase the
dosage of Prednisone for a period of time consistent with the patient’s condition. If after long-term
therapy the drug is to be stopped, it is recommended that it be withdrawn gradually rather than abruptly.
In the treatment of acute exacerbations of multiple sclerosis daily doses of 200 mg of prednisolone for
a week followed by 80 mg every other day for 1 month have been shown to be effective. (Dosage range
is the same for prednisone and prednisolone.)
ADT ® (Alternate Day Therapy)
ADT is a corticosteroid dosing regimen in which twice the usual daily dose of corticoid is
administered every other morning. The purpose of this mode of therapy is to provide the patient
requiring long-term pharmacologic dose treatment with the beneficial effects of corticoids while
minimizing certain undesirable effects, including pituitary-adrenal suppression, the Cushingoid state,
corticoid withdrawal symptoms, and growth suppression in children. The rationale for this treatment
schedule is based on two major premises: (a) the anti-inflammatory or therapeutic effect of corticoids
persists longer than their physical presence and metabolic effects and (b) administration of the
corticosteroid every other morning allows for re-establishment of more nearly normal hypothalamic-
pituitary-adrenal (HPA) activity on the off-steroid day.
A brief review of the HPA physiology may be helpful in understanding this rationale. Acting primarily
through the hypothalamus a fall in free cortisol stimulates the pituitary gland to produce increasing
amounts of corticotropin (ACTH) while a rise in free cortisol inhibits ACTH secretion. Normally the
HPA system is characterized by diurnal (circadian) rhythm. Serum levels of ACTH rise from a low
point about 10 pm to a peak level about 6 am. Increasing levels of ACTH stimulate adrenocortical
activity resulting in a rise in plasma cortisol with maximal levels occurring between 2 am and 8 am. This
rise in cortisol dampens ACTH production and in turn adrenocortical activity. There is a gradual fall in
plasma corticoids during the day with lowest levels occurring about midnight.
The diurnal rhythm of the HPA axis is lost in Cushing’s disease, a syndrome of adrenocortical
hyperfunction characterized by obesity with centripetal fat distribution, thinning of the skin with easy
bruisability, muscle wasting with weakness, hypertension, latent diabetes, osteoporosis, electrolyte
imbalance, etc. The same clinical findings of hyperadrenocorticism may be noted during long-term
pharmacologic dose corticoid therapy administered in conventional daily divided doses. It would
appear, then, that a disturbance in the diurnal cycle with maintenance of elevated corticoid values during
the night may play a significant role in the development of undesirable corticoid effects. Escape from
these constantly elevated plasma levels for even short periods of time may be instrumental in protecting
against undesirable pharmacologic effects.
During conventional pharmacologic dose corticosteroid therapy, ACTH production is inhibited with
subsequent suppression of cortisol production by the adrenal cortex. Recovery time for normal HPA
activity is variable depending upon the dose and duration of treatment. During this time the patient is
vulnerable to any stressful situation. Although it has been shown that there is considerably less adrenal
suppression following a single morning dose of prednisolone (10 mg) as opposed to a quarter of that
dose administered every 6 hours, there is evidence that some suppressive effect on adrenal activity may
be carried over into the following day when pharmacologic doses are used. Further, it has been shown
that a single dose of certain corticosteroids will produce adrenocortical suppression for two or more
days. Other corticoids, including methylprednisolone, hydrocortisone, prednisone, and prednisolone,
are considered to be short acting (producing adrenocortical suppression for 1 ¼ to 1 ½ days following
a single dose) and thus are recommended for alternate day therapy.
The following should be kept in mind when considering alternate day therapy:
1) Basic principles and indications for corticosteroid therapy should apply. The benefits of ADT
should not encourage the indiscriminate use of steroids.
2) ADT is a therapeutic technique primarily designed for patients in whom long-term pharmacologic
corticoid therapy is anticipated.
3) In less severe disease processes in which corticoid therapy is indicated, it may be possible to initiate
treatment with ADT. More severe disease states usually will require daily divided high dose therapy
for initial control of the disease process. The initial suppressive dose level should be continued until
satisfactory clinical response is obtained, usually four to ten days in the case of many allergic and
collagen diseases. It is important to keep the period of initial suppressive dose as brief as possible
particularly when subsequent use of alternate day therapy is intended.
Once control has been established, two courses are available: (a) change to ADT and then gradually
reduce the amount of corticoid given every other day or (b) following control of the disease process
reduce the daily dose of corticoid to the lowest effective level as rapidly as possible and then change
over to an alternate day schedule. Theoretically, course (a) may be preferable.
4) Because of the advantages of ADT, it may be desirable to try patients on this form of therapy who
have been on daily corticoids for long periods of time (eg, patients with rheumatoid arthritis). Since
these patients may already have a suppressed HPA axis, establishing them on ADT may be difficult and
not always successful. However, it is recommended that regular attempts be made to change them over.
It may be helpful to triple or even quadruple the daily maintenance dose and administer this every other
day rather than just doubling the daily dose if difficulty is encountered. Once the patient is again
controlled, an attempt should be made to reduce this dose to a minimum.
5) As indicated above, certain corticosteroids, because of their prolonged suppressive effect on
adrenal activity, are not recommended for alternate day therapy (eg; dexamethasone and betamethasone).
6) The maximal activity of the adrenal cortex is between 2 am and 8 am, and it is minimal between 4 pm
and midnight. Exogenous corticosteroids suppress adrenocortical activity the least, when given at the
time of maximal activity (am).
7) In using ADT it is important, as in all therapeutic situations to individualize and tailor the therapy to
each patient. Complete control of symptoms will not be possible in all patients. An explanation of the
benefits of ADT will help the patient to understand and tolerate the possible flare-up in symptoms which
may occur in the latter part of the off-steroid day. Other symptomatic therapy may be added or increased
at this time if needed.
8) In the event of an acute flare-up of the disease process, it may be necessary to return to a full
suppressive daily divided corticoid dose for control. Once control is again established alternate day
therapy may be re-instituted.
9) Although many of the undesirable features of corticosteroid therapy can be minimized by ADT, as in
any therapeutic situation, the physician must carefully weigh the benefit-risk ratio for each patient in
whom corticoid therapy is being considered.
Prednisone Tablets, USP are available in the following strengths and package sizes:
5 mg (White, round tablets debossed with "TL 172" on one side and scored on the other side)
Bottles of 100
Bottles of 1000
10 mg (White, round tablets debossed with "TL 173" on one side and scored on the other side)
Bottles of 100
Bottles of 500
Bottles of 1000
20mg (Peach, round tablets debossed with "TL 175" on one side and scored on the other side)
Bottles of 100
Bottles of 500
Bottles of 1000
Store at 20° to 25° C (68° to 77° F) [See USP Room Temperature].
Jubilant Cadista Pharmaceuticals Inc.
Salisbury, MD 21801, USA.
Product T ype
HUMAN PRESCRIPTION DRUG
Ite m Code (Source )
NDC:6 19 19 -235(NDC:59 746 -173)
Route of Administration
Active Ingredient/Active Moiety
Basis of Strength
Stre ng th
PREDNISO NE (UNII: VB0 R9 6 1HZT) (PREDNISONE - UNII:VB0 R9 6 1HZT)
Stre ng th
LACTO SE MO NO HYDRATE (UNII: EWQ57Q8 I5X)
MAGNESIUM STEARATE (UNII: 70 0 9 7M6 I30 )
STARCH, PO TATO (UNII: 8 I0 8 9 SAH3T)
SO DIUM LAURYL SULFATE (UNII: 36 8 GB5141J)
STARCH, CO RN (UNII: O8 232NY3SJ)
S hap e
S iz e
Marketing Start Date
Marketing End Date
NDC:6 19 19 -235-40
40 in 1 BOTTLE; Type 0 : No t a Co mbinatio n Pro duct
0 8 /29 /20 19
NDC:6 19 19 -235-15
15 in 1 BOTTLE; Type 0 : No t a Co mbinatio n Pro duct
0 8 /29 /20 19
Marke ting Cate gory
Application Numbe r or Monograph Citation
Marke ting Start Date
Marke ting End Date
ANDA0 40 36 2
0 8 /29 /20 19
Ad d re s s
Busine ss Ope rations
Dire c t_Rx
0 79 254320
re pa c k(6 19 19 -235)