ORUDIS® ORUDIS® E ORUDIS® SR
Anti-inflammatory – Analgesic
Action And Clinical Pharmacology: Animal pharmacological studies have shown that ketoprofen is a NSAID that possesses anti-inflammatory, analgesic and antipyretic properties. The anti-inflammatory action is not mediated through the pituitary adrenal axis.
Its therapeutic effectiveness has been demonstrated by a reduction in joint swelling, pain and duration of morning stiffness, and by increased grip strength and an improvement in functional capacity.
Clinical trials in rheumatoid arthritis have shown that the antiarthritic activity of ketoprofen 200 mg/day was similar to that of ASA 3.6 g/day.
Ketoprofen 200 mg daily induced less gastrointestinal bleeding than ASA 4 g daily.
The effectiveness of ketoprofen as a general purpose analgesic has been studied in standard pain models which have shown the effectiveness of doses of 25 to 150 mg. Doses of 25 mg were superior to placebo. Larger doses than 25 mg generally could not be shown significantly more effective but there was a tendency toward faster onset and greater duration of action with 50 mg and, in the case of dysmenorrhea, a significantly greater effect overall with 75 mg. Doses greater than 50 to 75 mg did not have increased analgesic effect.
Pharmacokinetics: In man, ketoprofen is rapidly and almost completely absorbed from the gastrointestinal tract. Maximum plasma levels are reached within 0.5 to 2 hours after administration of capsules or suppositories; however, peak plasma levels are delayed by a further 1 to 2 hours with enteric coated tablets and by 5 to 6 hours with sustained-release tablets. The biotransformation of ketoprofen is characterized by 2 main processes: hydroxylation and conjugation, the latter being the main metabolic pathway in man. The drug is 99% bound to plasma proteins, mainly to the albumin fraction. Metabolites as well as the unchanged drug are excreted mainly in the urine. Fecal excretion is negligible.
Following the administration of capsules or enteric coated tablets in man, 25% to 90% of the drug is excreted in the urine within 24 hours, with the major portion being excreted during the first 6 hours. The elimination half-life is approximately 2 hours. Following administration of slow release ketoprofen, absorption is gradual reaching a plateau during which plasma levels remain steady from the fifth to twelfth hour after ingestion and decrease with an apparent half-life of 3 to 4 hours. No accumulation of ketoprofen was found following repeated once daily administration of ketoprofen sustained-release tablets. Repeated administration of the drug, in both animals and man, caused no induction of liver enzymes.
When ketoprofen capsules are administered with food, the total bioavailability (AUC) is not altered; however, the rate of absorption is slowed resulting in delayed and reduced peak concentrations (Cmax). Following a single 50 mg dose of ketoprofen while fasting, the mean Cmax was 4.1 mg/L (at 1.1 hours); when administered after food, it decreased to 2.4 mg/L (at 2.0 hours).
The composition of the diet slightly but significantly alters the extent of absorption of ketoprofen from sustained-release tablets: a high-fat/high-calorie meal (3 000 cal/day) was associated with lower ketoprofen bioavailability values (about 20%) than a low low-fat/low-calorie content (Â£1 200 cal/day). Mean trough ketoprofen plasma concentrations were similar after high or low fat meals.
To date, studies of the effects of age and renal-function impairment have been small, generally involving 5 to 8 subjects per group, but they indicate modest decrease in clearance in the elderly and in patients with impaired renal function. In normal elderly volunteers (mean age 73 years), the plasma and renal clearance and protein-binding were reduced while the Vd increased when compared to a younger normal population (mean age 27 years). (Plasma clearance and Vd were 0.05 L/kg/h and 0.4 L/kg in elderly and 0.06 L/kg/h and 0.3 L/kg in young subjects, respectively). The mean half-life of ketoprofen in this normal geriatric population, as well as in a rheumatoid elderly population (mean age 64 years), was about 5 hours as compared to 3 hours in the younger population.
Patients with impaired renal function (mean age 44 years) also demonstrate decreases in plasma clearance (0.04 L/kg/h) of drug, with the mean half-life increasing to about 3.5 hours.
Indications And Clinical Uses: In the treatment of rheumatoid arthritis, ankylosing spondylitis and osteoarthritis.
For the treatment of primary dysmenorrhea as well as for the relief of mild to moderate acute pain associated with musculotendinous trauma (sprains and strains), postoperative (including dental surgery) or postpartum pain.
Contra-Indications: In patients with active peptic ulcers, a history of recurrent ulceration or active inflammatory diseases of the gastrointestinal tract; suppositories should not be used in patients with any inflammatory lesions of rectum or anus and in patients with a recent history of rectal or anal bleeding.
In patients with known or suspected hypersensitivity to the drug or other NSAIDs. Because of cross-sensitivity, ketoprofen should not be given to patients with the complete or partial syndrome of nasal polyps, or asthma, anaphylaxis, rhinitis or urticaria. Fatal anaphylactoid reactions have occurred in such individuals.
Significant hepatic impairment or active liver disease.
Severely impaired or deteriorating renal function (creatinine clearance
Ketoprofen is not recommended for use with other NSAIDs because of the absence of any evidence demonstrating synergistic benefits and the potential for additive side effects.
Manufacturers’ Warnings In Clinical States: Gastrointestinal: Serious gastrointestinal toxicity, such as peptic ulceration, perforation and gastrointestinal bleeding, sometimes severe and occasionally fatal can occur at any time, with or without symptoms in patients treated with NSAIDs including ketoprofen. Unlike most adverse reactions, which usually manifest themselves in the first month if they are going to occur in an individual, new peptic ulcers keep appearing in patients under treatment with ketoprofen at a rate of greater than 1% per year.
Minor upper gastrointestinal problems, such as dyspepsia, are common, usually developing early in therapy. Physicians should remain alert for ulceration and bleeding in patients treated with NSAIDs, even in the absence of previous gastrointestinal tract symptoms.
In patients observed in clinical trials of such agents, symptomatic upper gastrointestinal ulcers, gross bleeding, or perforation appear to occur in approximately 1% of patients treated for 3 to 6 months and in about 2 to 4% of patients treated for 1 year. The risk continues beyond 1 year and possibly increases.
The incidence of these complications increases with increasing dose.
Ketoprofen should be given under close medical supervision to patients prone to gastrointestinal tract irritation particularly those with a history of peptic ulcer, diverticulosis or other inflammatory disease of the gastrointestinal tract such as ulcerative colitis and Crohn’s disease. In these cases the physician must weigh the benefits of treatment against the possible hazards.
Physicians should inform patients about the signs and/or symptoms of serious gastrointestinal toxicity and instruct them to contact a physician immediately if they experience persistent dyspepsia or other symptoms or signs suggestive of gastrointestinal ulceration or bleeding.
Because serious gastrointestinal tract ulceration and bleeding can occur without warning symptoms, physicians should follow chronically treated patients by checking their hemoglobin periodically and by being vigilant for the signs and symptoms of ulceration and bleeding and should inform the patients of the importance of this follow-up. If ulceration is suspected or confirmed, or if gastrointestinal bleeding occurs, ketoprofen should be discontinued immediately, appropriate treatment instituted and the patients monitored closely.
No studies, to date, have identified any group of patients not at risk of developing ulceration and bleeding. A prior history of serious gastrointestinal events and other factors such as excess alcohol intake, smoking, age, female gender and concomitant oral steroid and anticoagulant use have been associated with increased risk.
Studies to date show that all NSAIDs can cause gastrointestinal tract adverse events. Although existing data does not clearly identify differences in risk between various NSAIDs, this may be shown in the future.
Geriatrics: Patients older than 65 years and frail or debilitated patients are most susceptible to a variety of adverse reactions from NSAIDs. The incidence of the adverse reactions increases with dose and duration of treatment. In addition, these patients are less tolerant to ulceration and bleeding. Most reports of fatal gastrointestinal events are in this population. Older patients are also at risk of lower esophageal ulceration and bleeding.
For such patients, consideration should be given to a starting dose lower than the one usually recommended, with individual adjustment when necessary and under close supervision (see Precautions).
Cross-sensitivity: Patients sensitive to any one of the NSAIDs may be sensitive to any of the other NSAIDs also.
Aseptic Meningitis: In occasional cases, with some NSAIDs, the symptoms of aseptic meningitis (stiff neck, severe headaches, nausea and vomiting, fever or clouding of consciousness) have been observed. Patients with autoimmune disorders (systemic lupus erythematosus, mixed connective tissues diseases, etc.) seem to be predisposed. Therefore, in such patients, the physician must be vigilant to the development of this complication.
Pregnancy: The safety of ketoprofen when administered to pregnant or nursing women has not been determined and therefore such use is not recommended. Pregnant rats who received ketoprofen 6 and 9 mg/kg/day orally from day 15 of gestation, showed dystocia and increased pup mortality.
Lactation: In rats, ketoprofen at doses of 9 mg/kg (approximately 1.5 times the maximum human therapeutic dose) did not affect perinatal development. Upon administration to lactating dogs, the milk concentration of ketoprofen was found to be 4 to 5% of the plasma drug level. Data on secretion in human milk after ingestion of ketoprofen do not exist. As with other drugs that are excreted in milk, ketoprofen is not recommended for use in nursing mothers.
Children: The conditions for safe and effective use of ketoprofen in children under 12 years of age have not been established and the drug is therefore not recommended in this age group.
Precautions: Gastrointestinal: There is no definitive evidence that the concomitant administration of histamine H2-receptor antagonists and/or antacids will either prevent the occurrence of gastrointestinal side effects or allow the continuation of ketoprofen therapy when and if these adverse reactions appear.
Suppositories should be given with caution to patients with any rectal or anal pathology.
Renal Function: Long-term administration of NSAIDs to animals has resulted in renal papillary necrosis and other abnormal renal pathology. In humans, there have been reports of acute interstitial nephritis with hematuria, proteinuria, and occasionally nephrotic syndrome.
A second form of renal toxicity has been seen in patients with prerenal conditions leading to the reduction in renal blood flow or blood volume, where the renal prostaglandins have a supportive role in the maintenance of renal perfusion. In these patients, administration of a NSAID may cause a dose-dependent reduction in prostaglandin formation and may precipitate overt renal decompensation. Patients at greatest risk of this reaction are those with impaired renal function, heart failure, liver dysfunction, those taking diuretics, and the elderly. Discontinuation of nonsteroidal anti-inflammatory therapy is usually followed by recovery to the pretreatment state.
Ketoprofen and its metabolites are eliminated primarily by the kidneys, therefore the drug should be used with great caution in patients with impaired renal function. In these cases, utilization of lower doses of ketoprofen should be considered and patients carefully monitored.
During long-term therapy kidney function should be monitored periodically.
Genitourinary: Some NSAIDs are known to cause persistent urinary symptoms (bladder pain, dysuria, urinary frequency), hematuria or cystitis. The onset of these symptoms may occur at any time after the initiation of therapy with a NSAID. Some cases have become severe on continued treatment. Should urinary symptoms occur, treatment with ketoprofen must be stopped immediately to obtain recovery. This should be done before any urological investigations or treatments are carried out.
Hepatic Function: As with other NSAIDs, borderline elevations of one or more liver function tests may occur in up to 15% of patients. These abnormalities may progress, may remain essentially unchanged, or may be transient with continued therapy. Meaningful (3 times the upper limit of normal) elevations of ALT or AST occurred in controlled clinical trials in less than 1% of patients. A patient with symptoms and/or signs suggesting liver dysfunction, or in whom an abnormal liver test has occurred, should be evaluated for evidence of the development of more severe hepatic reaction while on therapy with this drug. Severe hepatic reactions including jaundice and cases of fatal hepatitis have been reported with NSAIDs. Although such reactions are rare, if abnormal liver tests persist or worsen, if clinical signs and symptoms consistent with liver disease develop, or if systemic manifestations occur (e.g., eosinophilia, rash, etc.), this drug should be discontinued.
During long-term therapy, liver function tests should be monitored periodically. If there is a need to prescribe this drug in the presence of impaired liver function, it must be done under strict observation.
Fluid and Electrolyte Balance: Fluid retention and edema have been observed in approximately 2% of patients treated with ketoprofen. Therefore, as with many other NSAIDs, the possibility of precipitating congestive heart failure in elderly patients or those with compromised cardiac function should be borne in mind. Ketoprofen should be used with caution in patients with heart failure, hypertension or other conditions predisposing to fluid retention.
With nonsteroidal anti-inflammatory treatment there is a potential risk of hyperkalemia, particularly in patients with conditions such as diabetes mellitus or renal failure; in elderly patients; or in patients receiving concomitant therapy with b-adrenergic blockers, angiotensin converting enzyme inhibitors or some diuretics. Serum electrolytes should be monitored periodically during long-term therapy, especially in those patients who are at risk.
Hematology: Drugs inhibiting prostaglandin biosynthesis do interfere with platelet function to varying degrees; therefore, patients who may be adversely affected by such an action should be carefully observed when ketoprofen is administered.
Blood dyscrasias (such as neutropenia, leukopenia, thrombocytopenia, aplastic anemia and agranulocytosis) associated with the use of NSAIDs are rare, but could be with severe consequences.
Anemia is commonly observed in rheumatoid arthritis and is sometimes aggravated by NSAIDs, which may produce fluid retention or minor gastrointestinal blood loss in some patients. Therefore, patients with initial hemoglobin values of 10 g/dL or less who are to receive long-term therapy should have hemoglobin values determined frequently.
Infection: In common with other anti-inflammatory drugs, ketoprofen may mask the usual signs of infection.
Ophthalmology: Blurred and/or diminished vision has been reported with the use of ketoprofen and other NSAIDs. If such symptoms develop this drug should be discontinued and an ophthalmologic examination performed; ophthalmic examination should be carried out at periodic intervals in any patient receiving this drug for an extended period of time.
CNS: Some patients may experience drowsiness, dizziness, vertigo, insomnia or depression with the use of ketoprofen. If patients experience these side effects, they should exercise caution in carrying out activities that require alertness.
Drug Interactions: Methotrexate: The concomitant administration of ketoprofen and high-dose methotrexate has been associated with prolonged and marked enhancement of serum methotrexate levels resulting in severe methotrexate toxicity. This may also apply to some other NSAIDs. There were no abnormalities in methotrexate kinetics or evidence of toxicity when ketoprofen was given at least 12 hours after completion of high-dose methotrexate infusion. Ketoprofen should not be used in patients receiving high-dose methotrexate.
The potential for severe toxicity should be kept in mind when prescribing ketoprofen and low-dose methotrexate concurrently. Ketoprofen should not be administered within 12 hours of methotrexate infusion.
ASA or other NSAIDs: Concurrent administration of ASA decreased ketoprofen protein binding and increased its plasma clearance. The overall result was a 40% reduction in the AUC of ketoprofen. Ketoprofen does not alter ASA absorption.
The use of ketoprofen in addition to any other NSAID, including those over-the-counter ones (such as ASA and ibuprofen) is not recommended due to the possibility of additive side effects. Concurrent therapy may increase the risk of gastrointestinal toxicity, including ulceration or hemorrhage, without providing additional symptomatic relief. Concurrent use of ASA with other NSAIDs may also increase the risk of bleeding at sites other than the gastrointestinal tract because of additive inhibition of platelet aggregation.
Oral Anticoagulants: Ketoprofen has been shown to depress platelet aggregation and it can prolong bleeding time by approximately 3 to 4 minutes from baseline values. However, a study conducted in 20 patients undergoing therapy with coumarin and simultaneously receiving ketoprofen, failed to demonstrate potentiation of anticoagulant effect. Nevertheless, close monitoring of patients is recommended when ketoprofen is given concomitantly with anticoagulants.
Numerous studies have shown that the concomitant use of NSAIDs and anticoagulants increases the risk of gastrointestinal adverse events such as ulceration and bleeding.
Diuretics: Hydrochlorothiazide, given concomitantly with ketoprofen, produces a reduction in urinary potassium and chloride excretion compared to hydrochlorothiazide alone. Patients taking diuretics are at greater risk of developing renal failure secondary to a decrease in renal blood flow caused by prostaglandin inhibition. Concurrent use of a potassium-sparing diuretic with some NSAIDs may increase the risk of hyperkalemia.
Glucocorticoids: Numerous studies have shown that the concomitant use of NSAIDs and oral glucocorticoids increases the gastrointestinal side effects such as ulceration and bleeding. This is especially the case in older (>65 years of age) individuals.
Antacids: Concomitant administration of magnesium hydroxide and aluminum hydroxide does not interfere with the rate or extent of the absorption of ketoprofen.
Lithium: NSAIDs have been reported to increase steady-state plasma lithium levels. It is recommended that plasma lithium levels be monitored when ketoprofen is coadministered with lithium.
Probenecid: Concurrent administration of probenecid increases both free and bound ketoprofen through reducing the plasma clearance of ketoprofen to about one-third as well as decreasing its protein binding. Ketoprofen is not recommended in association with probenecid.
Ketoprofen is extensively (99%) protein bound to human serum albumin and may compete for binding sites with drugs such as sulfonamides, oral hypoglycemic agents, phenytoin or lithium. Although no significant interaction has been documented, patients with such combination therapy should be monitored.
Clinical Laboratory Test: The presence of ketoprofen and its metabolites in urine has been shown to interfere with certain tests which are used to detect albumin, bile salts, 17-ketosteroids or 17-hydroxycorticosteroids in urine and which rely upon acid precipitation as an end point or upon color reactions for carbonyl groups. No interference was seen in the tests for proteinuria using Albustix, Hema-Combistix or Labstix Reagent Strips.
Ketoprofen decreases platelet adhesion and aggregation. Therefore, it can prolong bleeding time by approximately 3 to 4 minutes from baseline values. There is no significant change in platelet count, prothrombin time, partial thromboplastin time, or thrombin time.
The following interactions have not been documented with every NSAID. However, they have been reported with several of these medications and should be considered potential precautions to the use of any NSAID, especially with chronic administration.
Acetaminophen: Prolonged concurrent use of acetaminophen with a NSAID may increase the risk of adverse renal effects; it is recommended that patients be under close medical supervision while receiving such combined therapy.
Alcohol: Concurrent use of alcohol with an NSAID may increase the risk of gastrointestinal side effects, including ulceration or hemorrhage.
Colchicine: Concurrent use of colchicine with a NSAID may increase the risk of gastrointestinal ulceration or hemorrhage. Inhibition of platelet aggregation by NSAIDs, added to colchicine’s effects on blood clotting mechanisms, may increase the risk of bleeding at sites other than the gastrointestinal tract.
Cyclosporine: Inhibition of renal prostaglandin by NSAIDs may increase the plasma concentration of cyclosporine and the risk of cyclosporine-induced nephrotoxicity. Patients should be carefully monitored during concurrent use.
Digoxin: The possibility should be considered that some NSAIDs may increase digoxin concentrations, leading to an increased risk of digitalis toxicity. Increased monitoring and dosage adjustments of digoxin may be necessary during and following concurrent NSAID therapy. However, ketoprofen may have no effect on digoxin concentrations.
Oral Antidiabetic Agents: NSAIDs may increase the hypoglycemic effect of oral antidiabetic agents because prostaglandins are directly involved in regulatory mechanisms of glucose metabolism and possibly because of displacement of the oral antidiabetic from serum proteins. Dosage adjustments of the antidiabetic agent may be necessary.
Potassium Supplements: Concurrent use of potassium supplements may increase the risk of gastrointestinal side effects, including ulceration or hemorrhage.
Valproic Acid: Valproic acid may cause hypoprothrombinemia. In addition, it may inhibit platelet aggregation. Concurrent use with a NSAID may increase the risk of bleeding because of additive interference with platelet function and the potential occurrence of NSAID-induced gastrointestinal ulceration or hemorrhage.
Adverse Reactions: The most common adverse reactions encountered with NSAIDs are gastrointestinal, of which peptic ulcer, with or without bleeding, is the most severe. Fatalities have occurred on occasion, particularly in the elderly.
In clinical trials involving 1 542 patients, the most common side effects reported were gastrointestinal (22%). The most severe were peptic ulcer or gastrointestinal bleeding which occurred in controlled clinical trials in less than 1% of 1 076 patients; however, in open label continuation studies in 1 292 patients, the rate was greater than 2%.
The detailed breakdown of side effects with their corresponding frequencies (not indicated when
Gastrointestinal (22%): dyspepsia (12.8%), nausea (4.0%), indigestion and flatulence (2.8%), vomiting (2.0%), constipation (2.0%), diarrhea (1.4%), anorexia, ulcer, gastrointestinal bleeding and perforation, melena, hematemesis, stomatitis.
Rectal administration was associated with a lower incidence of upper gastrointestinal reactions (12%) with the exception of ulceration, the incidence of which was the same. However, ano-rectal reactions presenting as local pain, burning, pruritus, tenesmus and rare instances of rectal bleeding occurred in 16.5% of patients. Five percent of patients discontinued rectal therapy because of these local reactions.
CNS (3 to 5%): headache (1.7%), fatigue (1%), dizziness, tension, anxiety, depression, drowsiness, impotence, vertigo, migraine, paresthesia.
Body as a Whole: angioedema, asthma, life threatening bronchospasm, anaphylaxis.
Cardiovascular: peripheral edema (2%), palpitation, congestive heart failure, hypertension.
Special Senses: tinnitus, hearing impairment, visual disturbance, conjunctivitis, conjunctivitis sicca, taste perversion.
Hematologic: hypocoagulability, agranulocytosis, anemia, hemolysis, purpura, thrombocytopenia.
Renal: interstitial nephritis, hematuria, nephrotic syndrome, impairment of renal function, acute renal failure.
Hepatic: hepatic dysfunction, jaundice.
Laboratory Tests: Abnormal alkaline phosphatase, lactic dehydrogenase, AST and BUN values were found in some patients receiving ketoprofen therapy. The abnormalities did not lead to discontinuation of treatment and, in some cases, returned to normal while the drug was continued. There have been sporadic reports of decreased hematocrit and hemoglobin values without progressive deterioration on prolonged administration of the drug.
Symptoms And Treatment Of Overdose: Symptoms: Of 20 cases of overdosage (up to 5 000 mg) reported in Great Britain (5 children, 14 adolescents or young adults, and 1 elderly), only 4 had mild symptoms (vomiting in 3, drowsiness in 1 child).
Treatment: Administer gastric lavage or an emetic and treat symptomatically: compensate for dehydration, monitor urinary excretion and correct acidosis if present.
The drug is dialyzable; therefore, hemodialysis may be useful to remove circulating drug and to assist in case of renal failure.
Dosage And Administration: Adults: Rheumatoid arthritis and osteoarthritis: Oral: The usual dosage of ketoprofen capsules or enteric coated tablets is 150 to 200 mg/day in 3 or 4 divided doses.
Once the maintenance dosage has been established, patients may be tried on a twice daily dosing regimen. Clinical trials, however, show that some rheumatoid arthritis patients respond better to more frequent dosing. The usual maintenance dose is 100 mg twice daily.
Patients with rheumatoid arthritis or osteoarthritis on a maintenance dose of 200 mg/day may be changed to a once daily dose of Orudis SR tablets administered in the morning or evening. Orudis SR should be swallowed whole.
Orudis E tablets and Orudis SR provide alternative presentations for those who may prefer these dosage forms. No difference in toxicity profile was documented.
Rectal: Suppositories offer an alternative route of administration for those patients who prefer it. Administer 1 suppository morning and evening or 1 suppository at bedtime supplemented as needed by divided oral doses.
The total daily dose of ketoprofen capsules, tablets and suppositories should not exceed 200 mg/day. When the patient’s response warrants it, the dose may be decreased to the minimum effective level.
In severe cases, during a flare-up of rheumatic activity or if a satisfactory response cannot be obtained with the lower dose, a daily dosage in excess of 200 mg may be used. However, a dose of 300 mg/day should not be exceeded.
Primary dysmenorrhea and mild to moderate pain: Oral: The usual dose for ketoprofen is 25 to 50 mg 3 or 4 times daily as necessary.
A larger dose may be tried if the patient’s response to a previous dose was less than satisfactory, but individual doses above 50 mg have not been shown to give added analgesia. The total daily dose should not exceed 300 mg. In most types of acute pain, a course of 3 to 7 days has been shown to be sufficient.
Elderly and Debilitated Patients: Initial dosage should be reduced by 1/2 to 1/3 in patients with impaired renal function and the elderly.
Children: Not indicated in children under 12 years of age because clinical experience in this group of patients is insufficient.
Availability And Storage: Orudis: Capsules: Each ivory and dark green capsule, marked with the logo on one side and identified ORUDIS 50 on the other, contains: ketoprofen 50 mg. Nonmedicinal ingredients: D&C Yellow No 10, FD&C Green No 3, FD&C Yellow No 6, gelatin, lactose, magnesium stearate and titanium dioxide. Tartrazine-free. Bottles of 100 and 500.
Suppositories: Each white to off-white suppository contains: ketoprofen 50 or 100 mg. Nonmedicinal ingredients: colloidal silicon dioxide and hydrogenated vegetable glycerides. Tartrazine-free. Boxes of 30. Store below 30°C.
Orudis E: Each yellow, round, biconvex enteric-coated tablet, marked with on one side and identified 50 or 100 on the other, contains: ketoprofen 50 or 100 mg. Nonmedicinal ingredients: carnauba wax, cornstarch, D&C Yellow No 10 aluminum lake, dextrin, FD&C Yellow No 6 aluminum lake, lactose, magnesium stearate, polyvinyl acetate phthalate, polacrilin potassium, stearic acid, sucrose, talc, titanium dioxide and triethyl citrate. Tartrazine-free. Bottles of 100 and 500.
Orudis SR: Each white, round, biconvex, enteric-coated sustained release tablet, marked with on one side and identified ORUDIS SR 200 on the other, contains: ketoprofen 200 mg. Nonmedicinal ingredients: calcium phosphate dibasic, carnauba wax, cellulose acetate phthalate, diethyl phthalate, ethyl acetate, hydroxyethyl cellulose and magnesium stearate. Tartrazine-free. Bottles of 100 and 500. (Shown in Product Recognition Section)
ORUDIS® ORUDIS® E ORUDIS® SR Rhône-Poulenc Rorer Ketoprofen Anti-inflammatory – Analgesic
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