Ketoprofen 200 mg Capsule, Extended Release, 100-count
🆔 Identity & classification
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🏷️ RxNorm drug class
This medicine belongs to the Nonsteroidal Anti-inflammatory Drug class.
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🏭 Manufacturer & labeler
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🩺 Clinical
Prescription ketoprofen is used to relieve pain, tenderness, swelling, and stiffness caused by osteoarthritis (arthritis caused by a breakdown of the lining of the joints) and rheumatoid arthritis (arthritis caused by swelling of the lining of the joints). Prescription ketoprofen capsules are also used to relieve pain, including menstrual pain (pain that occurs before or during a menstrual period). Nonprescription ketoprofen is used to relieve minor aches and pain from headaches, menstrual periods, toothaches, the common cold, muscle aches, and backaches, and to reduce fever. Ketoprofen is in...
Read the full MedlinePlus article ↗- The main difference is how quickly they release the drug. Regular capsules dissolve in your stomach and are absorbed quickly — usually within 30 minutes to 2 hours — making them us...
- What's the difference between regular ketoprofen capsules and the extended-release capsules?
- Yes, taking it with food, milk, or an antacid is a good idea if your stomach is sensitive — it can help reduce nausea and upset. Food slows down how quickly the drug is absorbed, b...
- This is a really important question to raise with your doctor. Ketoprofen and blood thinners like warfarin can both cause bleeding on their own, and together they significantly rai...
Patient education
Supplement & herbal interactions
Some supplements/herbs that may interact with Ketoprofen — tap one for details:
Ketoprofen may be associated with lower levels of 1 nutrient — worth a chat with your pharmacist, not a cause for alarm.
Where does this data come from?
Ask a licensed pharmacist directly — free, answered by our team.
🧪 Inactive Ingredients / Excipients
Inactive ingredients, also called excipients, are components of the drug product other than the active ingredient. They may include fillers, dyes, coatings, preservatives, flavors, or other formulation ingredients.
💡 Tap an ingredient (hover on desktop) to see what it is and why it’s used.
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Ammonia is a colorless gas made from nitrogen and hydrogen. It's used in medicines as a pH buffer to maintain the correct acidity level and help keep the product stable.
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D&C Yellow No. 10 Aluminum Lake is a yellow colorant made by combining a dye with aluminum salts. It's used in medicines to add color for product identification and visual appeal.
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A clear, oily liquid derived from sebacic acid and butanol. It works as a plasticizer and solvent in pharmaceutical coatings and films, helping them stay flexible and smooth.
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A plant-based polymer that forms a protective coating on tablets or capsules. It helps control how quickly the medicine dissolves and protects the contents from moisture and air.
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FD&C Blue No. 1 Aluminum Lake is a blue colorant made by combining FD&C Blue No. 1 dye with aluminum salts. It is used to color tablets, capsules, and other medicines for easy identification and appearance.
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A synthetic blue dye combined with aluminum to create a stable colorant. It's used in medicines and supplements to add blue color or create specific shades for product identification and appearance.
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A synthetic red dye used to color medications and make them easier to identify. It serves as a colorant in tablets, capsules, and liquid formulations.
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Ferric oxide yellow is a naturally occurring iron compound used as a colorant in medications. It gives tablets, capsules, and other forms a yellow or golden hue for identification and appearance.
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A dark iron oxide compound that gives medicines their black or dark color. It's used as a colorant in tablets and capsules to help identify the product and make it visually distinctive.
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Gelatin is a protein derived from animal collagen, commonly used in medicines as a gelling agent and capsule material. It helps create soft or hard capsule shells that hold and release medication, and can also thicken liquid formulations.
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Hypromellose 2910 is a plant-derived thickening agent made from cellulose. In medicines, it forms protective coatings on tablets or capsules, controls how fast the drug releases, and thickens liquid formulations.
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Hypromellose 2910 is a plant-derived cellulose compound used as a thickener and film-former in medicines. It helps control how quickly the medication dissolves and creates protective coatings on tablets or capsules.
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Hypromellose 2910 is a plant-based cellulose derivative that acts as a thickener, binder, and film-coating agent. It helps control how quickly the medicine dissolves and protects the tablet or capsule from moisture and light.
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A starch-derived carbohydrate produced by breaking down corn, potato, or tapioca starch. It functions as a filler and binder to give the medicine bulk and texture, and sometimes as a mild sweetener or texture enhancer in powders and tablets.
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A synthetic plastic polymer made from two chemical compounds combined in a specific ratio. It forms a coating on tablets and capsules to control how and where the medication dissolves in the digestive tract.
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Oleic acid is a naturally occurring fatty acid derived from plant or animal oils. It functions as an emulsifier and solvent in medicines, helping blend water and oil-based ingredients together and dissolving other components.
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Propylene glycol is a clear liquid derived from petroleum or vegetable sources. It acts as a solvent, humectant, and preservative in medicines, helping dissolve active ingredients and maintain product stability.
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Shellac is a natural resin secreted by the lac beetle. It's used as a coating on tablets and capsules to control how quickly the medicine dissolves and to improve appearance and stability.
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Silicon dioxide is a naturally occurring mineral used as a glidant and anti-caking agent. It helps powder ingredients flow smoothly and prevents clumping during manufacturing and storage.
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A detergent and foaming agent derived from coconut or palm oil. In medications, it helps break down and mix oil and water-based ingredients, aids in tablet disintegration, and improves how the drug dissolves and spreads in the mouth or digestive system.
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A plant-based carbohydrate derived from corn kernels. It acts as a filler to add bulk, a binder to hold ingredients together, and a disintegrant to help the tablet break apart in your stomach for absorption.
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A natural sugar derived from sugar cane or sugar beets. It's used as a sweetener, filler, and binder to improve taste, add bulk, and help hold tablet or capsule ingredients together.
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A powder made from a naturally occurring mineral. In medicines, talc works as a glidant and anti-caking agent, helping tablets and capsules flow smoothly during manufacturing and preventing clumping.
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Titanium dioxide is a bright white mineral powder commonly used as a colorant and opacifying agent. It makes pills and tablets white or lighter in color and helps make coatings non-transparent.
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Triacetin is a clear, oily liquid made from glycerin and acetic acid. It works as a plasticizer and solvent in medicines, helping soften coatings and improve how liquids mix together in formulations.
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UNII 8Z96QXD6UM
Triethyl citrate is a clear liquid derived from citric acid. It acts as a plasticizer and solvent in tablet coatings and film formulations, helping the coating remain flexible and adhere properly to the medicine.
26 inactive ingredients listed in the exact product block matched to this NDC.
Where does this data come from?
ingredient classCode="IACT" elements from the exact product block matched by this NDC. Label-section narrative from DailyMed / the openFDA label index is shown separately when available.Inactive ingredient FAQ
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💲 Pricing
A drug doesn't have one price. Each row is a different public payment system, and none is what you'd pay at the counter — that depends on your insurance. The ⓘ on each row explains what it measures.
| Price system | Per ea | Per package |
|---|---|---|
| Retail pharmacies payNADAC · weekly | $6.462 | $646.18 / 100 capsules |
| Medicaid paysCMS SDUD · 12 mo | $10.08 | $1,007.53 / 100 capsules |
| Medicare drug plans payPart D · Q2 2026 | $6.63 | $662.90 / 100 capsules |
Where does this data come from?
🔁 Therapeutic equivalents
| Product | Labeler | Pack | NADAC/unit | TE | Status | Price vs. this |
|---|---|---|---|---|---|---|
| Ketoprofen 200 mgthis 00378-8200-01 | Mylan | 100 capsules | $6.462 | — | Availability likely | — |
Where does this data come from?
⏳ Availability & generic status
This product is an FDA-approved generic. Other versions of the same drug are listed under Therapeutic equivalents, least expensive first.
Where does this data come from?
🗺️ Medicaid utilization & spend
📊 Medicare Part D spend CMS · PART D · 2026 (Q1)
🔬 Reported adverse events (FAERS)
Top reported reactions
Age at onset
Reporter sex
Serious outcomes
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📦 Packaging — all sizes for this product
| Package NDC | Description | Marketing start | Status |
|---|---|---|---|
| 00378-8200-01 You're viewing this | 100 CAPSULE, EXTENDED RELEASE in 1 BOTTLE (0378-8200-01) | 2003-09-04 | Active |
📄 Full prescribing information FDA SPL
🚨 Boxed Warning ▾
Cardiovascular Thrombotic Events • Nonsteroidal anti-inflammatory drugs (NSAIDs) cause an increased risk of serious cardiovascular thrombotic events, including myocardial infarction and stroke, which can be fatal. This risk may occur early in treatment and may increase with duration of use (see WARNINGS and PRECAUTIONS ). • Ketoprofen extended-release capsules are contraindicated in the setting of coronary artery bypass graft (CABG) surgery (see CONTRAINDICATIONS and WARNINGS ). Gastrointestinal Risk • NSAIDs cause an increased risk of serious gastrointestinal adverse events including bleeding, ulceration, and perforation of the stomach or intestines, which can be fatal.
These events can occur at any time during use and without warning symptoms. Elderly patients are at greater risk for serious gastrointestinal (GI) events (see WARNINGS ).
🎯 Indications and Usage ▾
INDICATIONS AND USAGE Carefully consider the potential benefits and risks of ketoprofen extended-release capsules before deciding to use ketoprofen extended-release capsules. Use the lowest effective dose for the shortest duration consistent with individual patient treatment goals (see WARNINGS ). Ketoprofen extended-release capsules are indicated for the management of the signs and symptoms of rheumatoid arthritis and osteoarthritis.
Ketoprofen extended-release capsules are not recommended for treatment of acute pain because of its extended-release characteristics (see CLINICAL PHARMACOLOGY: Pharmacokinetics ).
⏱️ Dosage and Administration ▾
DOSAGE AND ADMINISTRATION Carefully consider the potential benefits and risks of ketoprofen extended-release capsules and other treatment options before deciding to use ketoprofen extended-release capsules. Use the lowest effective dose for the shortest duration consistent with individual patient treatment goals (see WARNINGS ). After observing the response to initial therapy with ketoprofen extended-release capsules, the dose and frequency should be adjusted to suit an individual patient’s needs.
Concomitant use of ketoprofen extended-release capsules is not recommended. If minor side effects appear, they may disappear at a lower dose which may still have an adequate therapeutic effect. If well tolerated but not optimally effective, the dosage may be increased.
Individual patients may show a better response to 300 mg of ketoprofen capsules daily as compared to 200 mg, although in well-controlled clinical trials patients on 300 mg did not show greater mean effectiveness. They did, however, show an increased frequency of upper- and lower-GI distress and headaches. It is of interest that women also had an increased frequency of these adverse effects compared to men.
When treating patients with 300 mg/day, the physician should observe sufficient increased clinical benefit to offset potential increased risk. In patients with mildly impaired renal function, the maximum recommended total daily dose of ketoprofen extended-release capsules is 150 mg. In patients with a more severe renal impairment (GFR less than 25 mL/min/1.73 m 2 or end-stage renal impairment), the maximum total daily dose of ketoprofen extended-release capsules should not exceed 100 mg.
In elderly patients, renal function may be reduced with apparently normal serum creatinine and/or BUN levels. Therefore, it is recommended that the initial dosage of ketoprofen extended-release capsules should be reduced for patients over 75 years of age (see PRECAUTIONS: Geriatric Use ). It is recommended that for patients with impaired liver function and serum albumin concentration less than 3.5 g/dL, the maximum initial total daily dose of ketoprofen extended-release capsules should be 100 mg.
All patients with metabolic impairment, particularly those with both hypoalbuminemia and reduced renal function, may have increased levels of free (biologically active) ketoprofen and should be closely monitored. The dosage may be increased to the range recommended for the general population, if necessary, only after good individual tolerance has been ascertained. Because hypoalbuminemia and reduced renal function both increase the fraction of free drug (biologically active form), patients who have both conditions may be at greater risk of adverse effects.
Therefore, it is recommended that such patients also be started on lower doses of ketoprofen extended-release capsules and closely monitored. Rheumatoid Arthritis and Osteoarthritis The recommended starting dose of ketoprofen in otherwise healthy patients is for ketoprofen extended-release capsules 200 mg administered once a day. Smaller doses of ketoprofen extended-release capsules should be utilized initially in small individuals, or in debilitated or elderly patients.
The recommended maximum daily dose of ketoprofen is 200 mg/day for ketoprofen extended-release capsules. Dosages higher than 200 mg/day of ketoprofen extended-release capsules are not recommended because they have not been studied. Concomitant use of ketoprofen extended-release capsules is not recommended.
Relatively smaller people may need smaller doses. As with other nonsteroidal anti-inflammatory drugs, the predominant adverse effects of ketoprofen are gastrointestinal. To attempt to minimize these effects, physicians may wish to prescribe that ketoprofen extended-release capsules be taken with antacids, food, or milk.
Although food delays the absorption of both formulations (see CLINICAL PHARMACOLOGY ) in most of the clinical trials ketoprofen was taken with food or mi…
⛔ Contraindications ▾
CONTRAINDICATIONS Ketoprofen extended-release capsules are contraindicated in patients who have shown hypersensitivity to ketoprofen. Ketoprofen extended-release capsules should not be given to patients who have experienced asthma, urticaria, or allergic-type reactions after taking aspirin or other NSAIDs. Severe, rarely fatal, anaphylactic reactions to ketoprofen have been reported in such patients (see WARNINGS: Anaphylactoid Reactions and PRECAUTIONS: General: Preexisting Asthma ).
Ketoprofen extended-release capsules are contraindicated in the setting of coronary artery bypass graft (CABG) surgery (see WARNINGS ).
⚠️ Warnings ▾
WARNINGS Cardiovascular Effects Cardiovascular Thrombotic Events Clinical trials of several COX-2 selective and nonselective NSAIDs of up to three years duration have shown an increased risk of serious cardiovascular (CV) thrombotic events, including myocardial infarction (MI) and stroke, which can be fatal. Based on available data, it is unclear that the risk for CV thrombotic events is similar for all NSAIDs. The relative increase in serious CV thrombotic events over baseline conferred by NSAID use appears to be similar in those with and without known CV disease or risk factors for CV disease.
However, patients with known CV disease or risk factors had a higher absolute incidence of excess serious CV thrombotic events, due to their increased baseline rate. Some observational studies found that this increased risk of serious CV thrombotic events began as early as the first weeks of treatment. The increase in CV thrombotic risk has been observed most consistently at higher doses.
To minimize the potential risk for an adverse CV event in NSAID-treated patients, use the lowest effective dose for the shortest duration possible. Physicians and patients should remain alert for the development of such events, throughout the entire treatment course, even in the absence of previous CV symptoms. Patients should be informed about the symptoms of serious CV events and the steps to take if they occur.
There is no consistent evidence that concurrent use of aspirin mitigates the increased risk of serious CV thrombotic events associated with NSAID use. The concurrent use of aspirin and an NSAID, such as ketoprofen, increases the risk of serious gastrointestinal (GI) events (see WARNINGS ). Status Post Coronary Artery Bypass Graft (CABG) Surgery Two large, controlled clinical trials of a COX-2 selective NSAID for the treatment of pain in the first 10–14 days following CABG surgery found an increased incidence of myocardial infarction and stroke.
NSAIDs are contraindicated in the setting of CABG (see CONTRAINDICATIONS ). Post-MI Patients Observational studies conducted in the Danish National Registry have demonstrated that patients treated with NSAIDs in the post-MI period were at increased risk of reinfarction, CV-related death, and all-cause mortality beginning in the first week of treatment. In this same cohort, the incidence of death in the first year post MI was 20 per 100 person years in NSAID-treated patients compared to 12 per 100 person years in non-NSAID exposed patients.
Although the absolute rate of death declined somewhat after the first year post-MI, the increased relative risk of death in NSAID users persisted over at least the next 4 years of follow-up. Avoid the use of ketoprofen extended-release capsules in patients with a recent MI unless the benefits are expected to outweigh the risk of recurrent CV thrombotic events. If ketoprofen extended-release capsules are used in patients with a recent MI, monitor patients for signs of cardiac ischemia.
Hypertension NSAIDs, including ketoprofen extended-release capsules, can lead to onset of new hypertension or worsening of pre-existing hypertension, either of which may contribute to the increased incidence of CV events. Patients taking thiazides or loop diuretics may have impaired response to these therapies when taking NSAIDs. NSAIDs, including ketoprofen extended-release capsules, should be used with caution in patients with hypertension.
Blood pressure (BP) should be monitored closely during the initiation of NSAID treatment and throughout the course of therapy. Heart Failure and Edema The Coxib and traditional NSAID Trialists’ Collaboration meta-analysis of randomized controlled trials demonstrated an approximately two-fold increase in hospitalizations for heart failure in COX-2 selective-treated patients and nonselective NSAID-treated patients compared to placebo-treated patients. In a Danish National Registry study of patients with heart failure, NSAID use increased the risk of…
🤒 Adverse Reactions ▾
ADVERSE REACTIONS The incidence of common adverse reactions (above 1%) was obtained from a population of 835 ketoprofen capsules-treated patients in double-blind trials lasting from 4 to 54 weeks and in 622 ketoprofen extended-release capsules treated (200 mg/day) patients in trials lasting from 4 to 16 weeks. Minor gastrointestinal side effects predominated; upper gastrointestinal symptoms were more common than lower gastrointestinal symptoms. In crossover trials in 321 patients with rheumatoid arthritis or osteoarthritis, there was no difference in either upper or lower gastrointestinal symptoms between patients treated with 200 mg of ketoprofen extended-release capsules once a day or 75 mg of ketoprofen capsules TID (225 mg/day).
Peptic ulcer or GI bleeding 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 incidence of peptic ulceration in patients on NSAIDs is dependent on many risk factors including age, sex, smoking, alcohol use, diet, stress, concomitant drugs such as aspirin and corticosteroids, as well as the dose and duration of treatment with NSAIDs (see WARNINGS ). Gastrointestinal reactions were followed in frequency by central nervous system side effects, such as headache, dizziness, or drowsiness.
The incidence of some adverse reactions appears to be dose-related (see DOSAGE AND ADMINISTRATION ). Rare adverse reactions (incidence less than 1%) were collected from one or more of the following sources: foreign reports to manufacturers and regulatory agencies, publications, U.S. clinical trials, and/or U.S. postmarketing spontaneous reports. Reactions are listed below under body system, then by incidence or number of cases in decreasing incidence.
Incidence Greater Than 1% (Probable Causal Relationship) Digestive: Dyspepsia (11%), nausea*, abdominal pain*, diarrhea*, constipation*, flatulence*, anorexia, vomiting, stomatitis. Nervous System: Headache*, dizziness, CNS inhibition (i.e., pooled reports of somnolence, malaise, depression, etc.) or excitation (i.e., insomnia, nervousness, dreams, etc.)*. Special Senses: Tinnitus, visual disturbance.
Skin and Appendages: Rash. Urogenital: Impairment of renal function (edema, increased BUN)*, signs or symptoms of urinary-tract irritation. *Adverse events occurring in 3 to 9% of patients. Incidence Less than 1% (Probable Causal Relationship) Body as a Whole: Chills, facial edema, infection, pain, allergic reaction, anaphylaxis.
Cardiovascular: Hypertension, palpitation, tachycardia, congestive heart failure, peripheral vascular disease, vasodilation. Digestive: Appetite increased, dry mouth, eructation, gastritis, rectal hemorrhage, melena, fecal occult blood, salivation, peptic ulcer, gastrointestinal perforation, hematemesis, intestinal ulceration, hepatic dysfunction, hepatitis, cholestatic hepatitis, jaundice. Hemic: Hypocoagulability, agranulocytosis, anemia, hemolysis, purpura, thrombocytopenia.
Metabolic and Nutritional: Thirst, weight gain, weight loss, hyponatremia. Musculoskeletal: Myalgia. Nervous System: Amnesia, confusion, impotence, migraine, paresthesia, vertigo.
Respiratory: Dyspnea, hemoptysis, epistaxis, pharyngitis, rhinitis, bronchospasm, laryngeal edema. Skin and Appendages: Alopecia, eczema, pruritus, purpuric rash, sweating, urticaria, bullous rash, exfoliative dermatitis, photosensitivity, skin discoloration, onycholysis, toxic epidermal necrolysis, erythema multiforme, Stevens‑Johnson syndrome, and fixed drug eruption (FDE). Special Senses: Conjunctivitis, conjunctivitis sicca, eye pain, hearing impairment, retinal hemorrhage and pigmentation change, taste perversion.
Urogenital: Menometrorrhagia, hematuria, renal failure, interstitial nephritis, nephrotic syndrome. Incidence Less Than 1% (Causal Relationship Unknown) The following rare adverse reactions, whose causal relationship to ketoprofen is uncertain, are being listed to se…
🔄 Drug Interactions ▾
Drug Interactions The following drug interactions were studied with ketoprofen doses of 200 mg/day. The possibility of increased interaction should be kept in mind when ketoprofen immediate-release doses greater than 50 mg as a single dose or 200 mg of ketoprofen per day are used concomitantly with highly bound drugs. ACE Inhibitors Reports suggest that NSAIDs may diminish the antihypertensive effect of ACE-inhibitors.
This interaction should be given consideration in patients taking NSAIDs concomitantly with ACE-inhibitors. Antacids Concomitant administration of magnesium hydroxide and aluminum hydroxide does not interfere with the rate or extent of the absorption of ketoprofen administered as the immediate-release capsules. Aspirin Ketoprofen does not alter aspirin absorption; however, in a study of 12 normal subjects, concurrent administration of aspirin decreased ketoprofen protein binding and increased ketoprofen plasma clearance from
0.07 L/kg/h without aspirin to
0.11L/kg/h with aspirin. The clinical significance of these changes is not known; however, as with other NSAIDs, concomitant administration of ketoprofen and aspirin is not generally recommended because of the potential of increased adverse effects. Diuretics NSAIDs can reduce the natriuetic effect of furosemide and thiazides in some patients.
Hydrochlorothiazide, given concomitantly with ketoprofen, produces a reduction in urinary potassium and chloride excretion compared to hydrochlorothiazide alone. Patients taking diuretics are at a greater risk of developing renal failure secondary to a decrease in renal blood flow caused by prostaglandin inhibition (see PRECAUTIONS ). During concomitant therapy with NSAIDs, the patient should be observed closely for signs of renal failure (see WARNINGS: Renal Effects ), as well as to assure diuretic efficacy.
Digoxin In a study in 12 patients with congestive heart failure where ketoprofen and digoxin were concomitantly administered, ketoprofen did not alter the serum levels of digoxin. Lithium NSAIDs have produced an elevation of plasma lithium levels and a reduction in renal lithium clearance. The mean minimum lithium concentration increased 15% and the renal clearance was decreased by approximately 20%.
These effects have been attributed to inhibition of renal prostaglandin synthesis by the NSAID. Thus, when NSAIDs and lithium are administered concurrently, subjects should be observed carefully for signs of lithium toxicity. Methotrexate Ketoprofen, like other NSAIDs, may cause changes in the elimination of methotrexate leading to elevated serum levels of the drug and increased toxicity.
NSAIDs have been reported to competitively inhibit methotrexate accumulation in rabbit kidney slices. This may indicate that they could enhance the toxicity of methotrexate. Caution should be used when NSAIDs are administered concomitantly with methotrexate.
Probenecid Probenecid increases both free and bound ketoprofen by reducing the plasma clearance of ketoprofen to about one-third, as well as decreasing its protein binding. Therefore, the combination of ketoprofen and probenecid is not recommended. Warfarin The effects of warfarin and NSAIDs on GI bleeding are synergistic, such that users of both drugs together have a risk of serious GI bleeding higher than users of either drug alone.
In a short-term controlled study in 14 normal volunteers, ketoprofen did not significantly interfere with the effect of warfarin on prothrombin time. Bleeding from a number of sites may be a complication of warfarin treatment and GI bleeding a complication of ketoprofen treatment. Because prostaglandins play an important role in hemostasis and ketoprofen has an effect on platelet function as well (see PRECAUTIONS: Drug/Laboratory Test Interactions: Effect on Blood Coagulation ), concurrent therapy with ketoprofen and warfarin requires close monitoring of patients on both drugs.
🔄 Drug / Laboratory Test Interactions ▾
Drug/Laboratory Test Interactions Effect on Blood Coagulation 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.
🤰 Pregnancy ▾
Pregnancy Risk Summary Use of NSAIDs, including ketoprofen extended-release capsules, can cause premature closure of the fetal ductus arteriosus and fetal renal dysfunction leading to oligohydramnios and, in some cases, neonatal renal impairment. Because of these risks, limit dose and duration of ketoprofen extended-release capsules use between about 20 and 30 weeks of gestation, and avoid ketoprofen extended-release capsules use at about 30 weeks of gestation and later in pregnancy (see WARNINGS: Fetal Toxicity ). Premature Closure of Fetal Ductus Arteriosus Use of NSAIDs, including ketoprofen extended-release capsules, at about 30 weeks gestation or later in pregnancy increases the risk of premature closure of the fetal ductus arteriosus.
Oligohydramnios/Neonatal Renal Impairment Use of NSAIDs at about 20 weeks gestation or later in pregnancy has been associated with cases of fetal renal dysfunction leading to oligohydramnios, and in some cases, neonatal renal impairment. Data from observational studies regarding other potential embryofetal risks of NSAID use in women in the first or second trimesters of pregnancy are inconclusive. In animal reproduction studies, ketoprofen administered to mice at doses up to 12 mg/kg/day (36 mg/m 2 /day) and rats at doses up to 9 mg/kg/day (54 mg/m 2 /day), the approximate equivalent of 0.2 times the maximum recommended therapeutic dose of 185 mg/m 2 /day, showed no teratogenic or embryotoxic effects.
In separate studies in rabbits, maternally toxic doses were associated with embryotoxicity but not teratogenicity. However, animal reproduction studies are not always predictive of human response. Based on animal data, prostaglandins have been shown to have an important role in endometrial vascular permeability, blastocyst implantation, and decidualization.
In animal studies, administration of prostaglandin synthesis inhibitors such as ketoprofen, resulted in increased pre- and post-implantation loss. Prostaglandins also have been shown to have an important role in fetal kidney development. In published animal studies, prostaglandin synthesis inhibitors have been reported to impair kidney development when administered at clinically relevant doses.
The estimated background risk of major birth defects and miscarriage for the indicated population(s) is unknown. All pregnancies have a background risk of birth defect, loss, or other adverse outcomes. In the U.S. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2-4% and 15-20%, respectively.
Clinical Considerations Fetal/Neonatal Adverse Reactions Premature Closure of Fetal Ductus Arteriosus Avoid use of NSAIDs in women at about 30 weeks gestation and later in pregnancy, because NSAIDs, including ketoprofen extended-release capsules, can cause premature closure of the fetal ductus arteriosus (see WARNINGS: Fetal Toxicity ). Oligohydramnios/Neonatal Renal Impairment If an NSAID is necessary at about 20 weeks gestation or later in pregnancy, limit the use to the lowest effective dose and shortest duration possible.
If ketoprofen extended-release capsules treatment extends beyond 48 hours, consider monitoring with ultrasound for oligohydramnios. If oligohydramnios occurs, discontinue ketoprofen extended-release capsules and follow up according to clinical practice (see WARNINGS: Fetal Toxicity ). Data Human Data Premature Closure of Fetal Ductus Arteriosus Published literature reports that the use of NSAIDs at about 30 weeks of gestation and later in pregnancy may cause premature closure of the fetal ductus arteriosus.
Oligohydramnios/Neonatal Renal Impairment Published studies and postmarketing reports describe maternal NSAID use at about 20 weeks gestation or later in pregnancy associated with fetal renal dysfunction leading to oligohydramnios, and in some cases, neonatal renal impairment. These adverse outcomes are seen, on average, after days to weeks of treatment, alth…
🧒 Pediatric Use ▾
Pediatric Use Safety and effectiveness in pediatric patients below the age of 18 have not been established.
🧓 Geriatric Use ▾
Geriatric Use As with any NSAIDs, caution should be exercised in treating the elderly (65 years and older). In pharmacokinetic studies, ketoprofen clearance was reduced in older patients receiving ketoprofen extended-release capsules, compared with younger patients. Peak ketoprofen concentrations and free drug AUC were increased in older patients (see PHARMACOKINETICS: Special Populations ).
The glucuronide conjugate of ketoprofen, which can serve as a potential reservoir for the parent drug, is known to be substantially excreted by the kidney. Because elderly patients are more likely to have decreased renal function, care should be taken in dose selection. It is recommended that the initial dosage of ketoprofen extended-release capsules should be reduced for patients over 75 years of age and it may be useful to monitor renal function (see DOSAGE AND ADMINISTRATION ).
In addition, the risk of toxic reactions to this drug may be greater in patients with impaired renal function. Elderly patients may be more sensitive to the antiprostaglandin effects of NSAIDs (on the gastrointestinal tract and kidneys) than younger patients (see WARNINGS and PRECAUTIONS ). In particular, elderly or debilitated patients who receive NSAID therapy seem to tolerate gastrointestinal ulceration or bleeding less well than other individuals, and most spontaneous reports of fatal GI events are in this population.
Therefore, caution should be exercised in treating the elderly, and when individualizing their dosage, extra care should be taken when increasing the dose (see DOSAGE AND ADMINISTRATION ). In ketoprofen capsules clinical studies involving a total of 1540 osteoarthritis or rheumatoid arthritis patients, 369 (24%) were ≥ 65 years of age, and 92 (6%) were ≥ 75 years of age. For ketoprofen capsules acute pain studies, 23 (5%) of 484 patients were ≥ 60 years of age.
In ketoprofen extended-release capsules clinical studies, 356 (42%) of 840 osteoarthritis or rheumatoid arthritis patients were ≥ 65 years of age, and less than 100 of these were ≥ 75 years of age. No overall differences in effectiveness were observed between these patients and younger patients.
🆘 Overdosage ▾
OVERDOSAGE Signs and symptoms following acute NSAID overdose are usually limited to lethargy, drowsiness, nausea, vomiting, and epigastric pain, which are generally reversible with supportive care. Respiratory depression, coma, or convulsions have occurred following large ketoprofen overdoses. Gastrointestinal bleeding, hypotension, hypertension, or acute renal failure may occur, but are rare.
Patients should be managed by symptomatic and supportive care following an NSAID overdose. There are no specific antidotes. Gut decontamination may be indicated in patients with symptoms seen within 4 hours (longer for sustained‑release products) or following a large overdose (5 to 10 times the usual dose).
This should be accomplished via emesis and/or activated charcoal (60 g to 100 g in adults, 1 to 2 g/kg in children) with a saline cathartic or sorbitol added to the first dose. Forced diuresis, alkalinization of the urine, hemodialysis or hemoperfusion would probably not be useful due to ketoprofen’s high protein binding. Case reports include twenty-six overdoses: 6 were in children, 16 in adolescents, and 4 in adults.
Five of these patients had minor symptoms (vomiting in 4, drowsiness in 1 child). A 12-year-old girl had tonic‑clonic convulsions 1-2 hours after ingesting an unknown quantity of ketoprofen and 1 or 2 tablets of acetaminophen with hydrocodone. Her ketoprofen level was 1128 mg/L (56 times the upper therapeutic level of 20 mg/L) 3-4 hours post ingestion.
Full recovery ensued 18 hours after ingestion following management with intubation, diazepam, and activated charcoal. A 45-year-old woman ingested twelve 200 mg extended-release ketoprofen capsules and 375 mL vodka, was treated with emesis and supportive measures 2 hours after ingestion, and recovered completely with her only complaint being mild epigastric pain.
🧬 Clinical Pharmacology ▾
CLINICAL PHARMACOLOGY Ketoprofen is a nonsteroidal anti-inflammatory drug with analgesic and antipyretic properties. The anti-inflammatory, analgesic, and antipyretic properties of ketoprofen have been demonstrated in classical animal and in vitro test systems. In anti-inflammatory models ketoprofen has been shown to have inhibitory effects on prostaglandin and leukotriene synthesis, to have antibradykinin activity, as well as to have lysosomal membrane-stabilizing action.
However, its mode of action, like that of other nonsteroidal anti-inflammatory drugs, is not fully understood. Pharmacodynamics Ketoprofen is a racemate with only the S enantiomer possessing pharmacological activity. The enantiomers have similar concentration time curves and do not appear to interact with one another.
An analgesic effect‑concentration relationship for ketoprofen was established in an oral surgery pain study with ketoprofen capsules. The effect-site rate constant (K e0 ) was estimated to be 0.9 hour -1 (95% confidence limits: 0 to 2.1), and the concentration (Ce 50 ) of ketoprofen that produced one‑half the maximum PID (pain intensity difference) was 0.3 mcg/mL (95% confidence limits: 0.1 to 0.5). Thirty-three (33) to 68% of patients had an onset of action (as measured by reporting some pain relief) within 30 minutes following a single oral dose in postoperative pain and dysmenorrhea studies.
Pain relief (as measured by remedication) persisted for up to 6 hours in 26 to 72% of patients in these studies. Pharmacokinetics General Ketoprofen extended-release capsules contain ketoprofen. They differ only in their release characteristics.
Ketoprofen capsules release drug in stomach whereas ketoprofen extended-release capsules are designed to resist dissolution in the low pH of gastric fluid but release drug at a controlled rate in the higher pH environment of the small intestine (see DESCRIPTION ). Irrespective of the pattern of release, the systemic availability (F s ) when either oral formulation is compared with IV administration is approximately 90% in humans. For 75 to 200 mg single doses, the area under the curve has been shown to be dose proportional.
The figure depicts the plasma time curves associated with both products. Ketoprofen is > 99% bound to plasma proteins, mainly to albumin. Separate sections follow which delineate differences between ketoprofen capsules and ketoprofen extended-release capsules.
Absorption Ketoprofen capsules are rapidly and well-absorbed, with peak plasma levels occurring within 0.5 to 2 hours. Ketoprofen extended-release capsules are also well-absorbed from this dosage form, although an observable increase in plasma levels does not occur until approximately 2 to 3 hours after taking the formulation. Peak plasma levels are usually reached 6 to 7 hours after dosing.
(See Figure and Table, below). When ketoprofen is administered with food, its total bioavailability (AUC) is not altered; however, the rate of absorption from either dosage form is slowed. Ketoprofen capsules – Food intake reduces C max by approximately one-half and increases the mean time to peak concentration (t max ) from 1.2 hours for fasting subjects (range, 0.5 to 3 hours) to 2.0 hours for fed subjects (range, 0.75 to 3 hours).
The fluctuation of plasma peaks may also be influenced by circadian changes in the absorption process. Concomitant administration of magnesium hydroxide and aluminum hydroxide does not interfere with absorption of ketoprofen capsules. Ketoprofen extended-release capsules – Administration of ketoprofen extended-release capsules with a high-fat meal causes a delay of about 2 hours in reaching the C max ; neither the total bioavailability (AUC) nor the C max is affected.
Circadian changes in the absorption process have not been studied. The administration of antacids or other drugs which may raise stomach pH would not be expected to change the rate or extent of absorption of ketoprofen extended-release capsules. Multiple Do…
📦 How Supplied / Storage and Handling ▾
HOW SUPPLIED Ketoprofen Extended-Release Capsules, USP are available containing 200 mg of ketoprofen, USP. The 200 mg capsules are hard-shell gelatin capsules with a blue green opaque cap and an iron gray opaque body filled with white to off-white beads. The capsules are axially printed with MYLAN over 8200 in black ink on both the cap and body.
They are available as follows: NDC 0378-8200-01 bottles of 100 capsules Store at 20° to 25°C (68° to 77°F). [See USP Controlled Room Temperature.] Protect from direct light and excessive heat and humidity. Dispense in a tight, light-resistant container as defined in the USP using a child-resistant closure. PHARMACIST : Dispense a Medication Guide with each prescription.
📋 Description ▾
DESCRIPTION Ketoprofen is a nonsteroidal anti-inflammatory drug. The chemical name for ketoprofen is (±)- m -Benzoylhydratropic acid with the following structural formula: Its molecular formula is C 16 H 14 O 3 , with a molecular weight of 254.29. It has a pKa of 5.94 in methanol:water (3:1) and an n-octanol:water partition coefficient of 0.97 (buffer pH 7.4).
Ketoprofen, USP is a white or off-white, odorless, nonhygroscopic, fine to granular powder, melting at about 95°C. It is freely soluble in ethanol, chloroform, acetone, ether and soluble in benzene and strong alkali, but practically insoluble in water at 20°C. Each ketoprofen extended-release capsule, USP for oral administration contains 200 mg of ketoprofen, USP.
In addition, each capsule contains the following inactive ingredients: ammonium hydroxide, black iron oxide, colloidal anhydrous silica, dibutyl sebacate, ethylcellulose, FD&C Blue No. 2, gelatin, hypromellose, maltodextrin, methacrylic acid copolymer type B, oleic acid, polyacrylate dispersion, silicon dioxide, sodium lauryl sulfate, sugar spheres, talc, titanium dioxide, triacetin, triethyl citrate and yellow iron oxide. In addition, the black imprinting ink contains the following: black iron oxide, D&C Yellow No.
10 Aluminum Lake, FD&C Blue No. 1 Aluminum Lake, FD&C Blue No. 2 Aluminum Lake, FD&C Red No.
40 Aluminum Lake, propylene glycol and shellac glaze. Ketoprofen Structural Formula
💬 Information for Patients ▾
Information for Patients Patients should be informed of the following information before initiating therapy with an NSAID and periodically during the course of ongoing therapy. Patients should also be encouraged to read the NSAID Medication Guide that accompanies each prescription dispensed. 1.
Cardiovascular Thrombotic Events: Advise patients to be alert for the symptoms of cardiovascular thrombotic events, including chest pain, shortness of breath, weakness, or slurring of speech, and to report any of these symptoms to their healthcare provider immediately (see WARNINGS ). 2. Ketoprofen extended-release capsules, like other NSAIDs, can cause GI discomfort and, rarely, serious GI side effects, such as ulcers and bleeding, which may result in hospitalization and even death.
Although serious GI tract ulcerations and bleeding can occur without warning symptoms, patients should be alert for the signs and symptoms of ulcerations and bleeding, and should ask for medical advice when observing any indicative sign or symptoms including epigastric pain, dyspepsia, melena, and hematemesis. Patients should be apprised of the importance of this follow-up (see WARNINGS: Gastrointestinal Effects: Risk of Ulceration, Bleeding, and Perforation ). 3.
Serious Skin Reactions, including DRESS: Advise patients to stop taking ketoprofen extended-release capsules immediately if they develop any type of rash or fever and to contact their healthcare provider as soon as possible (see WARNINGS ). 4. Heart Failure and Edema: Advise patients to be alert for the symptoms of congestive heart failure including shortness of breath, unexplained weight gain, or edema and to contact their healthcare provider if such symptoms occur (see WARNINGS ).
5. Patients should be informed of the warning signs and symptoms of hepatotoxicity (e.g., nausea, fatigue, lethargy, pruritus, jaundice, right upper quadrant tenderness, and “flu-like” symptoms). If these occur, patients should be instructed to stop therapy and seek immediate medical therapy.
6. Patients should be informed of the signs of an anaphylactoid reaction (e.g., difficulty breathing, swelling of the face or throat). If these occur, patients should be instructed to seek immediate emergency help (see WARNINGS ).
7. Fetal Toxicity: Inform pregnant women to avoid use of ketoprofen extended-release capsules and other NSAIDs starting at 30 weeks gestation because of the risk of the premature closing of the fetal ductus arteriosus. If treatment with ketoprofen extended-release capsules is needed for a pregnant woman between about 20 to 30 weeks gestation, advise her that she may need to be monitored for oligohydramnios, if treatment continues for longer than 48 hours (see WARNINGS: Fetal Toxicity , PRECAUTIONS: Pregnancy ).
NSAIDs are often essential agents in the management of arthritis and have a major role in the treatment of pain, but they also may be commonly employed for conditions which are less serious. Physicians may wish to discuss with their patients the potential risks (see WARNINGS , PRECAUTIONS: General and ADVERSE REACTIONS ) and likely benefits of NSAID treatment, particularly when the drugs are used for less serious conditions where treatment without NSAIDs may represent an acceptable alternative to both the patient and physician.
Because aspirin causes an increase in the level of unbound ketoprofen, patients should be advised not to take aspirin while taking ketoprofen (see PRECAUTIONS: Drug Interactions ). Ketoprofen extended-release capsules have not been studied with antacids. Because food and milk do affect the rate but not the extent of absorption (see CLINICAL PHARMACOLOGY ), physicians may want to make specific recommendations to patients about when they should take ketoprofen in relation to food and/or what patients should do if they experience minor GI symptoms associated with ketoprofen therapy.
💬 Medication Guide ▾
Medication Guide for Nonsteroidal Anti-inflammatory Drugs (NSAIDs) What is the most important information I should know about medicines called Nonsteroidal Anti-inflammatory Drugs (NSAIDs)? NSAIDs can cause serious side effects, including: • Increased risk of a heart attack or stroke that can lead to death. This risk may happen early in treatment and may increase: o with increasing doses of NSAIDs o with longer use of NSAIDs Do not take NSAIDs right before or after a heart surgery called a “coronary artery bypass graft (CABG).” Avoid taking NSAIDs after a recent heart attack, unless your healthcare provider tells you to.
You may have an increased risk of another heart attack if you take NSAIDs after a recent heart attack. • Increased risk of bleeding, ulcers, and tears (perforation) of the esophagus (tube leading from the mouth to the stomach), stomach and intestines: o anytime during use o without warning symptoms o that may cause death The risk of getting an ulcer or bleeding increases with: o past history of stomach ulcers, or stomach or intestinal bleeding with use of NSAIDs o taking medicines called “corticosteroids”, “anticoagulants”, “SSRIs”, or “SNRIs” o increasing doses of NSAIDs o longer use of NSAIDs o smoking o drinking alcohol o older age o poor health o advanced liver disease o bleeding problems NSAIDs should only be used: o exactly as prescribed o at the lowest dose possible for your treatment o for the shortest time needed What are NSAIDs?
NSAIDs are used to treat pain and redness, swelling, and heat (inflammation) from medical conditions such as different types of arthritis, menstrual cramps, and other types of short-term pain. Who should not take NSAIDs? Do not take NSAIDs: • if you have had an asthma attack, hives, or other allergic reaction with aspirin or any other NSAIDs. • right before or after heart bypass surgery.
Before taking NSAIDs, tell your healthcare provider about all of your medical conditions, including if you: • have liver or kidney problems • have high blood pressure • have asthma • are pregnant or plan to become pregnant. Taking NSAIDs at about 20 weeks of pregnancy or later may harm your unborn baby. If you need to take NSAIDs for more than 2 days when you are between 20 and 30 weeks of pregnancy, your healthcare provider may need to monitor the amount of fluid in your womb around your baby.
You should not take NSAIDs after about 30 weeks of pregnancy. • are breastfeeding or plan to breast feed. Tell your healthcare provider about all of the medicines you take, including prescription or over-the-counter medicines, vitamins or herbal supplements. NSAIDs and some other medicines can interact with each other and cause serious side effects.
Do not start taking any new medicine without talking to your healthcare provider first. What are the possible side effects of NSAIDs? NSAIDs can cause serious side effects, including: See “What is the most important information I should know about medicines called Nonsteroidal Anti-inflammatory Drugs (NSAIDs)?” • new or worse high blood pressure • heart failure • liver problems including liver failure • kidney problems including kidney failure • low red blood cells (anemia) • life-threatening skin reactions • life threatening allergic reactions • Other side effects of NSAIDs include: stomach pain, constipation, diarrhea, gas, heartburn, nausea, vomiting, and dizziness.
Get emergency help right away if you get any of the following symptoms: • shortness of breath or trouble breathing • chest pain • weakness in one part or side of your body • slurred speech • swelling of the face or throat Stop taking your NSAID and call your healthcare provider right away if you get any of the following symptoms: • nausea • more tired or weaker than usual • diarrhea • itching • your skin or eyes look yellow • indigestion or stomach pain • flu-like symptoms • vomit blood • there is blood in your bowel movement or it is black and sticky like tar • unusual weight gain • skin ras…