PREDNISONE-prednisone tablet
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`Watson Pharma, Inc.
`
`Prednisone Tablets USP
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`Revised: April 2008
`Rx only 2000260-01
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`Rx only
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`DESCRIPTION
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`Prednisone tablets contain prednisone which is a glucocorticoid. Glucocorticoids are adrenocortical
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`steroids, both naturally occurring and synthetic, which are readily absorbed from the gastrointestinal
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`tract. The chemical name for prednisone is pregna-1,4-diene-3,11,20-trione monohydrate, 17,21-
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`dihydroxy-. The structural formula is represented below:
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`Prednisone is a white to practically white, odorless, crystalline powder. It is very slightly soluble in
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`water; slightly soluble in alcohol, chloroform, dioxane, and methanol.
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`Each tablet, for oral administration, contains 5 mg, 10 mg or 20 mg of prednisone USP (anhydrous). In
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`addition, each tablet contains the following inactive ingredients: anhydrous lactose, colloidal silicon
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`dioxide, crospovidone, docusate sodium, magnesium stearate and sodium benzoate.
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`Prednisone Tablets USP 20 mg also contain FD&C Yellow No. 6.
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`CLINICAL PHARMACOLOGY
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`Naturally occurring glucocorticoids (hydrocortisone and cortisone), which also have salt-retaining
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`properties, are used as replacement therapy in adrenocortical deficiency states. Their synthetic analogs
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`are primarily used for their potent antiinflammatory effects in disorders of many organ systems.
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`Glucocorticoids cause profound and varied metabolic effects. In addition, they modify the body's
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`immune responses to diverse stimuli.
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`INDICATIONS AND USAGE
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`Prednisone tablets are indicated in the following conditions:
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`Endocrine disorders:
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`primary or secondary adrenocortical insufficiency (hydrocortisone or cortisone
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`AVENTIS EXHIBIT 2146
`Mylan v. Aventis, IPR2016-00712
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`1-10
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`

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`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; hypercalcemia associated with cancer; nonsuppurative thyroiditis.
`Rheumatic disorders: as adjunctive therapy for short-term administration (to tide the patient over an
`acute episode or exacerbation) in: psoriatic arthritis, rheumatoid arthritis, including juvenile rheumatoid
`arthritis (selected cases may require low-dose maintenance therapy), ankylosing spondylitis, acute and
`subacute bursitis, acute nonspecific tenosynovitis, acute gouty arthritis, post-traumatic osteoarthritis,
`synovitis of osteoarthritis, epicondylitis.
`Collagen diseases: during an exacerbation or as maintenance therapy in selected cases of: systemic
`lupus erythematosus, systemic dermatomyositis (polymyositis), acute rheumatic carditis.
`Dermatologic diseases: pemphigus; bullous dermatitis herpetiformis; severe erythema multiforme
`(Stevens-Johnson syndrome); exfoliative dermatitis; mycosis fungoides; severe psoriasis; severe
`seborrheic dermatitis.
`Allergic states: control of severe or incapacitating allergic conditions intractable to adequate trials of
`conventional treatment: seasonal or perennial allergic rhinitis; bronchial asthma; contact dermatitis;
`atopic dermatitis; serum sickness; drug hypersensitivity reactions.
`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, sympathetic ophthalmia, allergic conjunctivitis,
`keratitis, chorioretinitis, optic neuritis, iritis and iridocyclitis.
`Respiratory diseases: symptomatic sarcoidosis; Loeffler’s syndrome not manageable by other means;
`berylliosis; fulminating or disseminated pulmonary tuberculosis when used concurrently with
`appropriate antituberculous chemotherapy; aspiration pneumonitis.
`Hematologic disorders: idiopathic thrombocytopenic purpura in adults; secondary thrombocytopenia
`in adults; acquired (autoimmune) hemolytic anemia; erythroblastopenia (RBC anemia); congenital
`(erythroid) hypoplastic anemia.
`Neoplastic diseases: for palliative management of: leukemias and lymphomas in adults, acute leukemia
`of childhood.
`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.
`Gastrointestinal diseases: to tide the patient over a critical period of the disease in: ulcerative colitis,
`regional enteritis.
`Nervous system: acute exacerbations of multiple sclerosis.
`Miscellaneous: tuberculous meningitis with subarachnoid block or impending block when used
`concurrently with appropriate antituberculous chemotherapy; trichinosis with neurologic or myocardial
`involvement.
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`CONTRAINDICATIONS
`Prednisone tablets are contraindicated in systemic fungal infections and known hypersensitivity to
`components.
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`WARNINGS
`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.
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`2-10
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`Infections with any pathogen including viral, bacterial, fungal, protozoan or helminthic infections, in any
`location of the body, may be associated with the use of corticosteroids alone or in combination with
`other immunosuppressive agents that affect cellular immunity, humoral immunity, or neutrophil
`1
`function.
`These infections may be mild, but can be severe and at times fatal. With increasing doses of
`2
`corticosteroids, the rate of occurrence of infectious complications increases. 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.
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`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.
`Administration of live or live, attenuated vaccines is contraindicated in patients receiving
`immunosuppressive doses of corticosteroids. Killed or inactivated vaccines may be administered to
`patients receiving immunosuppressive doses of corticosteroids; however, the response to such
`vaccines may be diminished. Indicated immunization procedures may be undertaken in patients receiving
`nonimmunosuppressive doses of corticosteroids. The use of prednisone tablets 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
`antituberculous 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. Chicken pox 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 chicken pox, 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 chicken pox
`develops, treatment with antiviral agents may be considered. Similarly, corticosteroids should be used
`with great care in patients with known or suspected Strongyloides (threadworm) infestation. In such
`patients, corticosteroid- induced immunosuppression may lead to Strongyloides hyperinfection and
`dissemination with widespread larval migration, often accompanied by severe enterocolitis and
`potentially fatal gram-negative septicemia.
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`PRECAUTIONS
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`General Precautions
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`3-10
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`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
`cirrhosis.
`Corticosteroids should be used cautiously in patients with ocular herpes simplex because of possible
`corneal perforation.
`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.
`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
`carefully observed.
`Kaposi’s sarcoma has been reported to occur in patients receiving corticosteroid therapy.
`Discontinuation of corticosteroids may result in clinical remission.
`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. (SeeDOSAGE AND
`ADMINISTRATION.)
`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 cyclosporin. 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.
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`Drug Interactions
`The pharmacokinetic interactions listed below are potentially clinically important. Drugs that induce
`hepatic enzymes such as phenobarbital, phenytoin and rifampin may increase the clearance of
`corticosteroids and may require increases in corticosteroid dose to achieve the desired response.
`Drugs such as troleandomycin and ketoconazole may inhibit the metabolism of corticosteroids and thus
`decrease their clearance. Therefore, the dose of corticosteroid should be titrated to avoid steroid
`toxicity. Corticosteroids may increase the clearance of chronic high dose aspirin. This could lead to
`decreased salicylate serum levels or increase the risk of salicylate toxicity when corticosteroid is
`withdrawn. Aspirin should be used cautiously in conjunction with corticosteroids in patients suffering
`from hypoprothrombinemia. The effect of corticosteroids on oral 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 effect.
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`Information for Patients
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`4-10
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`Patients who are on immunosuppressant doses of corticosteroids should be warned to avoid exposure
`to chicken pox or measles. Patients should also be advised that if they are exposed, medical advice
`should be sought without delay.
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`ADVERSE REACTIONS
`Fluid and electrolyte disturbances: sodium retention; fluid retention; congestive heart failure in
`susceptible patients; potassium loss; hypokalemic alkalosis; hypertension.
`Musculoskeletal: muscle weakness; steroid myopathy; loss of muscle mass; osteoporosis; tendon
`rupture, particularly of the Achilles tendon; vertebral compression fractures; aseptic necrosis of
`femoral and humeral heads; pathologic fracture of long bones.
`Gastrointestinal: peptic ulcer with possible perforation and hemorrhage; pancreatitis; abdominal
`distention; ulcerative esophagitis; increases in alanine transaminase (ALT, SGPT), aspartate
`transaminase (AST, SGOT) and alkaline phosphatase have been observed following corticosteroid
`treatment. These changes are usually small, not associated with any clinical syndrome and are reversible
`upon discontinuation.
`Dermatologic: impaired wound healing; thin fragile skin; petechiae and ecchymoses; facial erythema;
`increased sweating; may suppress reactions to skin tests.
`Metabolic: negative nitrogen balance due to protein catabolism.
`Neurological: increased intracranial pressure with papilledema (pseudo-tumor cerebri) usually after
`treatment; convulsions; vertigo; headache.
`Endocrine: menstrual irregularities; 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 mellitus;
`increased requirements for insulin or oral hypoglycemic agents in diabetics.
`Ophthalmic: posterior subcapsular cataracts; increased intraocular pressure; glaucoma; exophthalmos.
`Additional Reactions: urticaria and other allergic, anaphylactic or hypersensitivity reactions.
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`DOSAGE AND ADMINISTRATION
`The initial dosage of prednisone tablets may vary from 5 mg to 60 mg 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.
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`Multiple Sclerosis
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`5-10
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`

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`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.)
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`Alternate Day Therapy
`Alternate day therapy 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 antiinflammatory 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 1¼ to 1½ 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 alternate
`day therapy should not encourage the indiscriminate use of steroids.
`2. Alternate day therapy 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 alternate day therapy. More severe disease states usually will require daily
`divided high dose therapy for initial control of the disease process. The initial suppressive dose
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`6-10
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`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 alternate day therapy 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 alternate day therapy, it may be desirable to try patients on this form of
`therapy who have been on daily corticoids for long periods of time (e.g., patients with rheumatoid
`arthritis). Since these patients may already have a suppressed HPA axis, establishing them on
`alternate day therapy 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 (e.g., 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 alternate day therapy 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 alternate day therapy will help the patient to understand and tolerate the
`possible flare-up in symptoms which may occur in the latter part of the offsteroid 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 reinstituted.
`9. Although many of the undesirable features of corticosteroid therapy can be minimized by alternate
`day therapy, as in any therapeutic situation, the physician must carefully weigh the benefit-risk ratio
`for each patient in whom corticoid therapy is being considered.
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`HOW SUPPLIED
`Prednisone Tablets USP 5 mg are scored, round, white tablets imprinted DAN DAN and 5052 supplied
`in bottles of 100 and 1000.
`Prednisone Tablets USP 10 mg are scored, round, white tablets imprinted DAN DAN and 5442 supplied
`in bottles of 100, 500 and 1000.
`Prednisone Tablets USP 20 mg are scored, round, peach tablets imprinted DAN DAN and 5443
`supplied in bottles of 100, 500 and 1000.
`Dispense in a well-closed container with child-resistant closure.
`Store at 20°-25°C (68°-77°F). [See USP controlled room temperature.]
`
`REFERENCES
` Fekety R. Infections associated with corticosteroids and immunosuppressive therapy. In: Gorbach SL,
`Bartlett JG, Blacklow NR, eds. Infectious Diseases. Philadelphia: WBSaunders Company 1992: 1050-1.
`
`1 2
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`7-10
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`2
` Stuck AE, Minder CE, Frey FJ. Risk of infectious complications in patients taking glucocorticoids.
`Rev Infect Dis 1989:11(6):954-63.
`Manufactured by:
`Watson Pharma Private Ltd.
`Verna, Goa INDIA
`Distributed By:
`Watson Pharma, Inc.
`Corona, CA 92880 USA
`200026-01 0408B
`
`PREDNISONE
`prednisone tablet
`
`Product Information
`Product T ype
`
`HUMAN PRESCRIPTION DRUG
`
`Ite m Code (Source )
`
`NDC:0 9 51-50 52
`
`Route of Administration
`
`ORAL
`
`Active Ingredient/Active Moiety
`Ingredient Name
`Predniso ne (UNII: VB0 R9 6 1HZT) (Predniso ne - UNII:VB0 R9 6 1HZT)
`
`Basis of Strength
`
`Strength
`5 mg
`
`Inactive Ingredients
`
`Ingredient Name
`
`Strength
`
`a nhydro us la cto se (UNII: 3SY5LH9 PMK)
`co llo idio l silico n dio xide ()
`cro spo vido ne (UNII: 6 8 40 19 6 0 MK)
`do cusa te so dium (UNII: F0 5Q2T2JA0 )
`ma g nesium stea ra te (UNII: 70 0 9 7M6 I30 )
`so dium benzo a te (UNII: OJ245FE5EU)
`
`Product Characteristics
`Color
`white
`Shape
`ROUND
`Flavor
`Contains
`Coating
`
`
`false
`
`Score
`Siz e
`Imprint Code
`
`Symbol
`
`Packaging
`#
`Item Code
`1 NDC:0 9 51-50 52-0 1
`2 NDC:0 9 51-50 52-10
`
`Package Description
`10 0 in 1 BOTTLE
`10 0 0 in 1 BOTTLE
`
`
`
`
`
`
`
`
`2 pieces
`6 mm
`DAN;DAN;50 52
`
`false
`
`Marketing Start Date
`
`Marketing End Date
`
`8-10
`
`

`
`PREDNISONE
`prednisone tablet
`
`Product Information
`Product T ype
`
`HUMAN PRESCRIPTION DRUG
`
`Ite m Code (Source )
`
`NDC:0 9 51-5442
`
`Route of Administration
`
`ORAL
`
`Active Ingredient/Active Moiety
`Ingredient Name
`Predniso ne (UNII: VB0 R9 6 1HZT) (Predniso ne - UNII:VB0 R9 6 1HZT)
`
`Basis of Strength
`
`Strength
`10 mg
`
`Inactive Ingredients
`
`Ingredient Name
`
`Strength
`
`a nhydro us la cto se (UNII: 3SY5LH9 PMK)
`co llo idio l silico n dio xide ()
`cro spo vido ne (UNII: 6 8 40 19 6 0 MK)
`do cusa te so dium (UNII: F0 5Q2T2JA0 )
`ma g nesium stea ra te (UNII: 70 0 9 7M6 I30 )
`so dium benzo a te (UNII: OJ245FE5EU)
`
`Product Characteristics
`Color
`white
`Shape
`ROUND
`Flavor
`Contains
`Coating
`
`
`false
`
`Score
`Siz e
`Imprint Code
`
`Symbol
`
`Packaging
`#
`Item Code
`1 NDC:0 9 51-5442-0 1
`2 NDC:0 9 51-5442-0 5
`3 NDC:0 9 51-5442-10
`
`Package Description
`10 0 in 1 BOTTLE
`50 0 in 1 BOTTLE
`10 0 0 in 1 BOTTLE
`
`
`
`
`
`
`
`
`2 pieces
`9 mm
`DAN;DAN;5442
`
`false
`
`Marketing Start Date
`
`Marketing End Date
`
`PREDNISONE
`prednisone tablet
`
`Product Information
`Product T ype
`
`HUMAN PRESCRIPTION DRUG
`
`Ite m Code (Source )
`
`NDC:0 9 51-5443
`
`Route of Administration
`
`ORAL
`
`9-10
`
`

`
`Active Ingredient/Active Moiety
`Ingredient Name
`Predniso ne (UNII: VB0 R9 6 1HZT) (Predniso ne - UNII:VB0 R9 6 1HZT)
`
`Basis of Strength
`
`Strength
`20 mg
`
`Inactive Ingredients
`
`Ingredient Name
`
`Strength
`
`a nhydro us la cto se (UNII: 3SY5LH9 PMK)
`co llo idio l silico n dio xide ()
`cro spo vido ne (UNII: 6 8 40 19 6 0 MK)
`do cusa te so dium (UNII: F0 5Q2T2JA0 )
`ma g nesium stea ra te (UNII: 70 0 9 7M6 I30 )
`so dium benzo a te (UNII: OJ245FE5EU)
`FD & C Yello w #6 ()
`
`Product Characteristics
`Color
`o range (Peach)
`Shape
`ROUND
`Flavor
`Contains
`Coating
`
`
`false
`
`Packaging
`#
`Item Code
`1 NDC:0 9 51-5443-0 1
`2 NDC:0 9 51-5443-0 5
`3 NDC:0 9 51-5443-10
`
`Package Description
`10 0 in 1 BOTTLE
`50 0 in 1 BOTTLE
`10 0 0 in 1 BOTTLE
`
`Labeler - Watson Pharma, Inc.
`
`Revised: 1/2009
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`Score
`Siz e
`Imprint Code
`
`2 pieces
`10 mm
`DAN;DAN;5443
`
`Symbol
`
`false
`
`Marketing Start Date
`
`Marketing End Date
`
`Watson Pharma, Inc.
`
`10-10