Label: PREDNISOLONE SODIUM PHOSPHATE solution

Prednisolone Sodium Phosphate Oral Solution is a dye free, colorless to light strawcolored,
raspberry flavored solution. Each 5 mL (teaspoonful) of Prednisolone Sodium
Phosphate Oral Solution contains 6.7 mg prednisolone sodium phosphate (5 mg prednisolone
base) in a palatable, aqueous vehicle. Prednisolone Sodium Phosphate Oral Solution also
contains dibasic sodium phosphate, edetate disodium, methylparaben, purified water,
sodium biphosphate, sorbitol, natural and artificial raspberry flavor.

Prednisolone sodium phosphate occurs as white or slightly yellow, friable granules or powder.
It is freely soluble in water; soluble in methanol; slightly soluble in alcohol and in chloroform;
and very slightly soluble in acetone and in dioxane. The chemical name of prednisolone sodium
phosphate is: pregna-1,4-diene-3,20-dione,11,17-dihydroxy-21-(phosphonooxy)-,disodium
salt,(11β)-. The empirical formula is C21H27Na2O8P; the molecular weight is 484.39.

The chemical structure is: 

Pharmacological Category: Glucocorticoid

Naturally occurring glucocorticoids (hydrocortisone), which also have salt-retaining
properties, are used as replacement therapy in adrenocortical deficiency states. Their
synthetic analogs are primarily used for their potent anti-inflammatory effects in disorders
of many organ systems.

Prednisolone is a synthetic adrenocortical steroid drug with predominantly glucocorticoid
properties. Some of these properties reproduce the physiological actions of endogenous
glucocorticosteroids, but others do not necessarily reflect any of the adrenal hormones’
normal functions; they are seen only after administration of large therapeutic doses of the
drug. The pharmacological effects of prednisolone which are due to its glucocorticoid
properties include: promotion of gluconeogenesis; increased deposition of glycogen in the
liver; inhibition of the utilization of glucose; anti-insulin activity; increased catabolism of
protein; increased lipolysis; stimulation of fat synthesis and storage; increased glomerular
filtration rate and resulting increase in urinary excretion of urate (creatinine excretion remains
unchanged); and increased calcium excretion.

Depressed production of eosinophils and lymphocytes occurs, but erythropoiesis and
production of polymorphonuclear leukocytes are stimulated. Inflammatory processes
(edema, fibrin deposition, capillary dilatation, migration of leukocytes and phagocytosis)
and the later stages of wound healing (capillary proliferation, deposition of collagen,
cicatrization) are inhibited.

Prednisolone can stimulate secretion of various components of gastric juice. Suppression
of the production of corticotropin may lead to suppression of endogenous corticosteroids.
Prednisolone has slight mineralocorticoid activity, whereby entry of sodium into cells and
loss of intracellular potassium is stimulated. This is particularly evident in the kidney, where
rapid ion exchange leads to sodium retention and hypertension.

Prednisolone is rapidly and well absorbed from the gastrointestinal tract following oral
administration. Prednisolone Sodium Phosphate Oral Solution produces a 14% higher peak
plasma level of prednisolone which occurs 20% faster than that seen with tablets.
Prednisolone is 70-90% protein-bound in the plasma and it is eliminated from the plasma
with a half-life of 2 to 4 hours. It is metabolized mainly in the liver and excreted in the urine
as sulfate and glucuronide conjugates.

The systemic availability, metabolism and elimination of prednisolone after administration of
single weight-based doses (0.8 mg/kg) of intravenous (IV) prednisolone and oral prednisone
were reported in a small study of 19 young (23 to 34 years) and 12 elderly (65 to 89 years)
subjects. Results showed that the systemic availability of total and unbound prednisolone, as
well as interconversion between prednisolone and prednisone were independent of age. The
mean unbound fraction of prednisolone was higher, and the steady-state volume of distribution
(Vss) of unbound prednisolone was reduced in elderly patients. Plasma prednisolone
concentrations were higher in elderly subjects, and the higher AUCs of total and unbound
prednisolone were most likely reflective of an impaired metabolic clearance, evidenced by
reduced fractional urinary clearance of 6b-hydroxyprednisolone. Despite these findings of higher
total and unbound prednisolone concentrations, elderly subjects had higher AUCs of cortisol,
suggesting that the elderly population is less sensitive to suppression of endogenous cortisol
or their capacity for hepatic inactivation of cortisol is diminished.

Prednisolone Sodium Phosphate Oral Solution is indicated in the following conditions:

1. Allergic States
Control of severe or incapacitating allergic conditions intractable to adequate trials of
conventional treatment in adult and pediatric populations with: seasonal or perennial
allergic rhinitis; asthma; contact dermatitis; atopic dermatitis; serum sickness; drug
hypersensitivity reactions.
2. Dermatologic Diseases
Pemphigus; bullous dermatitis herpetiformis; severe erythema multiforme (Stevens-Johnson
syndrome); exfoliative erythroderma; mycosis fungoides.
3. Edematous States
To induce diuresis or remission of proteinuria in nephrotic syndrome in adults with lupus
erythematosus and in adults and pediatric populations, with idiopathic nephrotic syndrome,
without uremia.
4. 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; hypercalcemia associated with cancer; nonsuppurative thyroiditis.
5. Gastrointestinal Diseases
To tide the patient over a critical period of the disease in: ulcerative colitis; regional enteritis.
6. Hematologic Disorders
Idiopathic thrombocytopenic purpura in adults; selected cases of secondary thrombocytopenia;
acquired (autoimmune) hemolytic anemia; pure red cell aplasia; Diamond-Blackfan anemia.
7. Neoplastic Diseases
For the treatment of acute leukemia and aggressive lymphomas in adults and children.
8. Nervous System
Acute exacerbations of multiple sclerosis.
9. Ophthalmic Diseases
Uveitis and ocular inflammatory conditions unresponsive to topical corticosteroids; temporal
arteritis; sympathetic ophthalmia.
10. Respiratory Diseases
Symptomatic sarcoidosis; idiopathic eosinophilic pneumonias; fulminating or disseminated
pulmonary tuberculosis when used concurrently with appropriate antituberculous
chemotherapy; asthma (as distinct from allergic asthma listed above under “Allergic States”),
hypersensitivity pneumonitis, idiopathic pulmonary fibrosis, acute exacerbations of chronic
obstructive pulmonary disease (COPD), and Pneumocystis carinii pneumonia (PCP)
associated with hypoxemia occurring in an HIV (+) individual who is also under treatment
with appropriate anti- PCP antibiotics. Studies support the efficacy of systemic corticosteroids
for the treatment of these conditions: allergic bronchopulmonary aspergillosis, idiopathic
bronchiolitis obliterans with organizing pneumonia.
11. 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;
epicondylitis. For the treatment of systemic lupus erythematosus, dermatomyositis
(polymyositis), polymyalgia rheumatica, Sjogren’s syndrome, relapsing polychondritis, and
certain cases of vasculitis.
12. Miscellaneous
Tuberculous meningitis with subarachnoid block or impending block, tuberculosis with
enlarged mediastinal lymph nodes causing respiratory difficulty, and tuberculosis with pleural
or pericardial effusion (appropriate antituberculous chemotherapy must be used concurrently
when treating any tuberculosis complications); Trichinosis with neurologic or myocardial
involvement; acute or chronic solid organ rejection (with or without other agents).

Systemic fungal infections. Hypersensitivity to the drug or any of its components.

General
In patients on corticosteroid therapy subjected to unusual stress, increased dosage of rapidly
acting corticosteroids before, during and after the stressful situation is indicated.

Cardio-renal
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.

Endocrine
Corticosteroids can produce reversible hypothalamic-pituitary adrenal (HPA) axis suppression
with the potential for glucocorticosteroid insufficiency after withdrawal of treatment.
Metabolic clearance of corticosteroids is decreased in hypothyroid patients and increased
in hyperthyroid patients. Changes in thyroid status of the patient may necessitate adjustment
in dosage.

Immunosuppression and Increased Risk of Infection
Corticosteroids, including Prednisolone Sodium Phosphate Oral Solution, suppress the
immune system and increase the risk of infection with any pathogen, including viral,
bacterial, fungal, protozoan, or helminthic pathogens. Corticosteroids can:
• Reduce resistance to new infections
• Exacerbate existing infections
• Increase the risk of disseminated infections
• Increase the risk of reactivation or exacerbation of latent infections
• Mask some signs of infection
Corticosteroid-associated infections can be mild but can be severe and at times fatal. The
rate of infectious complications increases with increasing corticosteroid dosages.
Monitor for the development of infection and consider Prednisolone Sodium Phosphate Oral
Solution withdrawal or dosage reduction as needed.

Tuberculosis
If Prednisolone Sodium Phosphate Oral Solution is used to treat a condition in patients with
latent tuberculosis or tuberculin reactivity, reactivation of the disease may occur. Closely
monitor such patients for reactivation. During prolonged Prednisolone Sodium Phosphate
Oral Solution therapy, patients with latent tuberculosis or tuberculin reactivity should receive
chemoprophylaxis.

Varicella Zoster and Measles Viral Infections
Varicella and measles can have a serious or even fatal course in non-immune patients taking
corticosteroids, including Prednisolone Sodium Phosphate Oral Solution. In corticosteroid-
treated patients who have not had these diseases or are non-immune, particular care should
be taken to avoid exposure to varicella and measles:
• If a Prednisolone Sodium Phosphate Oral Solution-treated patient is exposed to
varicella, prophylaxis with varicella zoster immune globulin (VZIG) may be indicated.
If varicella develops, treatment with antiviral agents may be considered.
•If a Prednisolone Sodium Phosphate Oral Solution-treated patient is exposed to
measles, prophylaxis with immunoglobulin (IG) may be indicated.

Hepatitis B Virus Reactivation
Hepatitis B virus reactivation can occur in patients who are hepatitis B carriers treated with
immunosuppressive dosages of corticosteroids, including Prednisolone Sodium Phosphate
Oral Solution. Reactivation can also occur infrequently in corticosteroid-treated patients who
appear to have resolved hepatitis B infection.
Screen patients for hepatitis B infection before initiating immunosuppressive (e.g.,
prolonged) treatment with Prednisolone Sodium Phosphate Oral Solution. For patients who
show evidence of hepatitis B infection, recommend consultation with physicians with
expertise in managing hepatitis B regarding monitoring and consideration for hepatitis B
antiviral therapy.

Fungal Infections
Corticosteroids, including Prednisolone Sodium Phosphate Oral Solution, may exacerbate
systemic fungal infections; therefore, avoid Prednisolone Sodium Phosphate Oral Solution
use in the presence of such infections unless Prednisolone Sodium Phosphate Oral Solution
is needed to control drug reactions. For patients on chronic Prednisolone Sodium Phosphate
Oral Solution therapy who develop systemic fungal infections, Prednisolone Sodium
Phosphate Oral Solution withdrawal or dosage reduction is recommended.

Amebiasis
Corticosteroids, including Prednisolone Sodium Phosphate Oral Solution, may activate latent
amebiasis. Therefore, it is recommended that latent amebiasis or active amebiasis be ruled
out before initiating Prednisolone Sodium Phosphate Oral Solution in patients who have
spent time in the tropics or patients with unexplained diarrhea.

Strongyloides Infestation
Corticosteroids, including Prednisolone Sodium Phosphate Oral Solution, 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.

Cerebral Malaria
Avoid corticosteroids, including Prednisolone Sodium Phosphate Oral Solution, in patients
with cerebral malaria.

Ophthalmic
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 bacteria, fungi or viruses. The use of oral corticosteroids is not
recommended in the treatment of optic neuritis and may lead to an increase in the risk of
new episodes. Corticosteroids should not be used in active ocular herpes simplex.

Kaposi’s Sarcoma
Kaposi’s sarcoma has been reported to occur in patients receiving corticosteroid therapy,
most often for chronic conditions. Discontinuation of corticosteroids may result in clinical
improvement of Kaposi’s sarcoma.

Vaccination
Administration of live or live, attenuated vaccines is contraindicated in patients receiving
immunosuppressive doses of corticosteroids. Killed or inactivated vaccines may be
administered, however, the response to such vaccines cannot be predicted. Immunization
procedures may be undertaken in patients who are receiving corticosteroids as replacement
therapy, e.g., for Addison’s disease.

(listed alphabetically under each subsection):

Cardiovascular: Hypertrophic cardiomyopathy in premature infants.

Dermatologic: Facial erythema; increased sweating; impaired wound healing; may suppress
reactions to skin tests; petechiae and ecchymoses; thin fragile skin; urticaria; edema.

Endocrine: Decreased carbohydrate tolerance; development of cushingoid state; hirsutism;
increased requirements for insulin or oral hypoglycemic agents in diabetic patients;
manifestations of latent diabetes mellitus; menstrual irregularities; secondary adrenocortical
and pituitary unresponsiveness, particularly in times of stress, as in trauma, surgery or
illness; suppression of growth in children.

Fluid and Electrolyte Disturbances: Congestive heart failure in susceptible patients; fluid
retention; hypertension; hypokalemic alkalosis; potassium loss; sodium retention.

Gastrointestinal: Abdominal distention; elevation in serum liver enzyme levels (usually
reversible upon discontinuation); pancreatitis; peptic ulcer with possible perforation and
hemorrhage; ulcerative esophagitis.

Metabolic: Negative nitrogen balance due to protein catabolism.

Musculoskeletal: Aseptic necrosis of femoral and humeral heads; loss of muscle mass;
muscle weakness; osteoporosis; pathologic fracture of long bones; steroid myopathy; tendon
rupture; vertebral compression fractures.

Neurological: Convulsions; headache; increased intracranial pressure with papilledema
(pseudotumor cerebri) usually following discontinuation of treatment; psychic disorders; vertigo.

Ophthalmic: Exophthalmos; glaucoma; increased intraocular pressure; posterior
subcapsular cataracts.

Other: Increased appetite; malaise; nausea; weight gain.

To report SUSPECTED ADVERSE REACTIONS, contact PAI Pharma at 1-800-845-8210 or FDA at
1-800-FDA-1088 or www.fda.gov/medwatch.

The effects of accidental ingestion of large quantities of prednisolone over a very short period
of time have not been reported, but prolonged use of the drug can produce mental
symptoms, moon face, abnormal fat deposits, fluid retention, excessive appetite, weight
gain, hypertrichosis, acne, striae, ecchymosis, increased sweating, pigmentation, dry scaly
skin, thinning scalp hair, increased blood pressure, tachycardia, thrombophlebitis, decreased
resistance to infection, negative nitrogen balance with delayed bone and wound healing,
headache, weakness, menstrual disorders, accentuated menopausal symptoms, neuropathy,
fractures, osteoporosis, peptic ulcer, decreased glucose tolerance, hypokalemia, and adrenal
insufficiency. Hepatomegaly and abdominal distention have been observed in children.

Treatment of acute overdosage is by immediate gastric lavage or emesis followed by
supportive and symptomatic therapy. For chronic overdosage in the face of severe disease
requiring continuous steroid therapy the dosage of prednisolone may be reduced only
temporarily, or alternate day treatment may be introduced.

The initial dosage of Prednisolone Sodium Phosphate Oral Solution may vary from 5 mL to
60 mL (5 to 60 mg prednisolone base) 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, Prednisolone Sodium Phosphate Oral Solution should
be discontinued and the patient placed on 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 Prednisolone Sodium Phosphate
Oral Solution 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 or 4 to 8 mg dexamethasone
every other day for one month have been shown to be effective.

In pediatric patients, the initial dose of Prednisolone Sodium Phosphate Oral Solution
may vary depending on the specific disease entity being treated. The range of initial doses
is 0.14 to 2 mg/kg/day in three or four divided doses (4 to 60 mg/m2bsa/day).

The standard regimen used to treat nephrotic syndrome in pediatric patients is 60 mg/m2/day
given in three divided doses for 4 weeks, followed by 4 weeks of single dose alternate-day
therapy at 40 mg/m2/day.

The National Heart, Lung, and Blood Institute (NHLBI) recommended dosing for systemic
prednisone, prednisolone or methylprednisolone in children whose asthma is uncontrolled
by inhaled corticosteroids and long-acting bronchodilators is 1-2 mg/kg/day in single or
divided doses. It is further recommended that short course, or “burst” therapy, be continued
until a child achieves a peak expiratory flow rate of 80% of his or her personal best or
symptoms resolve. This usually requires 3 to 10 days of treatment, although it can take
longer. There is no evidence that tapering the dose after improvement will prevent a relapse.

For the purpose of comparison, the following is the equivalent milligram dosage of the
various glucocorticoids:

Prednisolone Sodium Phosphate Oral Solution is a colorless to light straw-colored, raspberry
flavored solution containing 6.7 mg prednisolone sodium phosphate (5 mg prednisolone
base) per 5 mL (teaspoonful).

NDC 0121-1100-04
120 mL bottle

Storage and Handling
Store at 4°-25°C (39°-77°F). May be refrigerated. Keep tightly closed and out of the
reach of children.

Distributed by:
PAI Pharma
Greenville, SC 29605
www.paipharma.com

Code 1231C00
Rev. 03/2026

NDC 0121-1100-04
PrednisoLONE Sodium Phosphate Oral Solution,
5 mg/5 mL
NONALCOHOLIC, DYE FREE, SUGAR FREE
Rx only
120 mL
PAI Pharma