QuickView for ketoprofen (compound)

Summary
General Info

PubChem

PubChem Compound 10706176

Name:	Ketoprofen
PubChem Compound ID:	10706176
Description:	An IBUPROFEN-type anti-inflammatory analgesic and antipyretic. It is used in the treatment of rheumatoid arthritis and osteoarthritis.
Molecular formula:	C₁₆H₁₄O₃
Molecular weight:	255.273 g/mol

DrugBank

Identification

Name:	Ketoprofen
Name (isomeric):	DB01009
Drug Type:	small molecule
Description:	An IBUPROFEN-type anti-inflammatory analgesic and antipyretic. It is used in the treatment of rheumatoid arthritis and osteoarthritis.
Synonyms:	m-Benzoylhydratropic acid
Brand:	Epatec, Orugesic, Alrheumun, Meprofen, Toprek, Profenid, Fastum, Orudis KT, Capisten, Oscorel, Kefenid, Oruvail, Alrheumat, Ketopron, Lertus, Toprec, Dexal, Actron, Iso-K, Menamin, Orudis
Category:	Analgesics, Non-Narcotic, Antipyretics, Cyclooxygenase Inhibitors, Analgesics, Anti-inflammatory Agents, Nonsteroidal Anti-inflammatory Agents (NSAIAs)
CAS number:	22071-15-4

Pharmacology

Indication:	For symptomatic treatment of acute and chronic rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, primary dysmenorrhea and mild to moderate pain associated with musculotendinous trauma (sprains and strains), postoperative (including dental surgery) or postpartum pain.
Pharmacology:	Ketoprofen is a nonsteroidal anti-inflammatory agent (NSAIA) with analgesic and antipyretic properties. Ketoprofen has pharmacologic actions similar to those of other prototypical NSAIDs, which inhibit prostaglandin synthesis. Ketoprofen is used to treat rheumatoid arthritis, osteoarthritis, dysmenorrhea, and alleviate moderate pain.
Mechanism of Action:	The anti-inflammatory effects of ketoprofen are believed to be due to inhibition cylooxygenase-2 (COX-2), an enzyme involved in prostaglandin synthesis via the arachidonic acid pathway. This results in decreased levels of prostaglandins that mediate pain, fever and inflammation. Ketoprofen is a non-specific cyclooxygenase inhibitor and inhibition o... show more » The anti-inflammatory effects of ketoprofen are believed to be due to inhibition cylooxygenase-2 (COX-2), an enzyme involved in prostaglandin synthesis via the arachidonic acid pathway. This results in decreased levels of prostaglandins that mediate pain, fever and inflammation. Ketoprofen is a non-specific cyclooxygenase inhibitor and inhibition of COX-1 is thought to confer some of its side effects, such as GI upset and ulceration. Ketoprofen is thought to have anti-bradykinin activity, as well as lysosomal membrane-stabilizing action. Antipyretic effects may be due to action on the hypothalamus, resulting in an increased peripheral blood flow, vasodilation, and subsequent heat dissipation. show less «
Absorption:	Ketoprofen is rapidly and well-absorbed orally, with peak plasma levels occurring within 0.5 to 2 hours.
Protein binding:	99% bound, primarily to albumin
Biotransformation:	Rapidly and extensively metabolized in the liver, primarily via conjugation to glucuronic acid. No active metabolites have been identified.
Route of elimination:	In a 24 hour period, approximately 80% of an administered dose of ketoprofen is excreted in the urine, primarily as the glucuronide metabolite.
Half Life:	Conventional capsules: 1.1-4 hours Extended release capsules: 5.4 hours due to delayed absorption (intrinsic clearance is same as conventional capsules)
Clearance:	Oral-dose cl=6.9 +/- 0.8 L/h [Ketoprofen Immediate-release capsules (4 × 50 mg)] Oral-dose cl=6.8 +/- 1.8 L/h [Ketoprofen Extended-release capsules (1 × 200 mg)] 0.08 L/kg/h 0.7 L/kg/h [alcoholic cirrhosis patients]
Toxicity:	LD₅₀=62.4 mg/kg (rat, oral). Symptoms of overdose include drowsiness, vomiting and abdominal pain. Side effects are usually mild and mainly involved the GI tract. Most common adverse GI effect is dyspepsia (11% of patients). May cause nausea, diarrhea, abdominal pain, constipation and flatulence in greater than 3% of patients.
Affected organisms:	Humans and other mammals

Interactions

Food interaction:

Avoid alcohol.

Take with food to reduce gastric irritation.

Food prolongs rate of absorption and decreases peak plasma concentration. Extent of absorption is not affected.

Drug interaction:

Fluvoxamine	Concomitant therapy may result in additive antiplatelet effects and increase the risk of bleeding. Monitor for increased risk of bleeding during concomitant therapy.
Pemetrexed	The NSAID, ketoprofen, may increase increase the serum concentration of pemetrexed by decreasing its renal clearance. Patients with mild to moderate renal insufficiency (CrCl 45-79 ml/min) should avoid use of ketoprofen within 2 days of a pemetrexed dose. Patients with better renal function do not appear to be at risk. Monitor for toxicity in all patients during concomitant therapy.
Treprostinil	The prostacyclin analogue, Treprostinil, may increase the risk of bleeding when combined with the NSAID, Ketoprofen. Monitor for increased bleeding during concomitant thearpy.
Dicumarol	The NSAID, ketoprofen, may increase the anticoagulant effect of dicumarol.
Methotrexate	The NSAID, ketoprofen, may decrease the renal excretion of methotrexate. Increased risk of methotrexate toxicity.

Fluvoxamine	Concomitant therapy may result in additive antiplatelet effects and increase the risk of bleeding. Monitor for increased risk of bleeding during concomitant therapy.
Pemetrexed	The NSAID, ketoprofen, may increase increase the serum concentration of pemetrexed by decreasing its renal clearance. Patients with mild to moderate renal insufficiency (CrCl 45-79 ml/min) should avoid use of ketoprofen within 2 days of a pemetrexed dose. Patients with better renal function do not appear to be at risk. Monitor for toxicity in all patients during concomitant therapy.
Treprostinil	The prostacyclin analogue, Treprostinil, may increase the risk of bleeding when combined with the NSAID, Ketoprofen. Monitor for increased bleeding during concomitant thearpy.
Dicumarol	The NSAID, ketoprofen, may increase the anticoagulant effect of dicumarol.
Methotrexate	The NSAID, ketoprofen, may decrease the renal excretion of methotrexate. Increased risk of methotrexate toxicity.
Colesevelam	Bile acid sequestrants may decrease the absorption of Nonsteroidal Anti-Inflammatory Agents. Monitor for decreased serum concentrations/therapeutic effects of nonsteroidal anti-inflammatory agents (NSAID) if coadministered with bile acid sequestrants. Separating the administration of doses by 2 or more hours may reduce (but not eliminate) the risk of interaction. The manufacturer of colesevelam recommends that drugs should be administered at least 1 hour before or 4 hours after colesevelam.
S-Adenosylmethionine	Increased risk of bleeding due to additive antiplatelet properties of the two agents. Concomitant therapy should be avoided or monitored carefully for bleeding, bruising and altered mental status, which may be caused by CNS bleeds.
Warfarin	The antiplatelet effects of ketoprofen may increase the bleed risk associated with warfarin. Consider alternate therapy or monitor for signs and symptoms of bleeding during concomitant therapy.
Ketorolac	Concomitant use of ketoprofen and ketorolac, two NSAIDs, is contraindicated due to the risk of additive or synergistic NSAID toxicities (e.g. GI bleeding, ulceration, renal dysfunction, etc).
Lithium	The NSAID, ketoprofen, may increase the serum concentration of lithium by decreasing its renal clearance. Consider a dose reduction in lithium upon initiation of ketoprofen therapy. Monitor for changes in the therapeutic and adverse effects of lithium if ketoprofen is initiated, discontinued or does changed.
Fluoxetine	Concomitant therapy may result in additive antiplatelet effects and increase the risk of bleeding. Monitor for increased risk of bleeding during concomitant therapy.
Sertraline	Concomitant therapy may result in additive antiplatelet effects and increase the risk of bleeding. Monitor for increased risk of bleeding during concomitant therapy.
Paroxetine	Concomitant therapy may result in additive antiplatelet effects and increase the risk of bleeding. Monitor for increased risk of bleeding during concomitant therapy.
Cyclosporine	The NSAID, ketoprofen, may increase the serum concentration of cyclosporine. Ketoprofen may also increase the nephrotoxicity of cyclosporine.
Trandolapril	The NSAID, Ketoprofen, may reduce the antihypertensive effect of Trandolapril. Consider alternate therapy or monitor for changes in Trandolapril efficacy if Ketoprofen is initiated, discontinued or dose changed.
Drotrecogin alfa	The antiplatelet effect of ketoprofen may increase the bleed risk associated with drotrecogin alfa. Consider spacing use of the two agents by at least 7 days. Increase monitoring for signs and symptoms of bleeding during concomitant therapy.
Ginkgo biloba	Increased risk of bleeding due to additive antiplatelet properties of the two agents. Concomitant therapy should be avoided or monitored carefully for bleeding, bruising and altered mental status, which may be caused by CNS bleeds.
Escitalopram	Concomitant therapy may result in additive antiplatelet effects and increase the risk of bleeding. Monitor for increased risk of bleeding during concomitant therapy.
Acenocoumarol	The NSAID, ketoprofen, may increase the anticoagulant effect of acenocoumarol.
Anisindione	The NSAID, ketoprofen, may increase the anticoagulant effect of anisindione.
Telmisartan	Concomitant use of Telmisartan and Ketoprofen may increase the risk of acute renal failure and hyperkalemia. Monitor renal function at the beginning and during treatment.
Acetylsalicylic acid	Concomitant therapy of the NSAID, ketoprofen, and acetylsalicylic acid may result in additive adverse/toxic effects (e.g. GI bleeding). The NSAID may also limit the cardioprotective effect of acetylsalicylic acid. Occasional concomitant use may not cause clinically significant problems, but regular, frequent concomitant therapy is not recommended.
Timolol	The NSAID, Ketoprofen, may antagonize the antihypertensive effect of Timolol.
Ginseng	Increased risk of bleeding due to additive anticoagulant properties of the two agents. Concomitant therapy should be avoided or monitored carefully for bleeding, bruising and altered mental status, which may be caused by CNS bleeds.
Citalopram	Concomitant therapy may result in additive antiplatelet effects and increase the risk of bleeding. Monitor for increased risk of bleeding during concomitant therapy.

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Targets

Prostaglandin G/H synthase 1

Prostaglandin G/H synthase 2

High affinity interleukin-8 receptor A

Enzymes

Cytochrome P450 2C9

Cytochrome P450 2C8

Transporters

Multidrug resistance-associated protein 4

Solute carrier organic anion transporter family member 1A2

Solute carrier family 22 member 6

Solute carrier family 22 member 8

Solute carrier family 22 member 11

Solute carrier family 22 member 7

Carriers

Serum albumin