药品详细
Ketoprofen (酮基布洛芬 )
化学结构式图
中文名
酮基布洛芬
英文名
Ketoprofen
分子式
Not Available
化学名
2-(3-benzoylphenyl)propanoic acid
分子量
Average: 254.2806
Monoisotopic: 254.094294314
Monoisotopic: 254.094294314
CAS号
22071-15-4
ATC分类
M01A 未知;M01A 未知;M02A 未知
药物类型
small molecule
阶段
商品名
Actron;Alrheumat;Alrheumun;Capisten;Dexal;Epatec;Fastum;Iso-K;Kefenid;Ketopron;Lertus;Menamin;Meprofen;Orudis;Orudis KT;Orugesic;Oruvail (Wyeth);Oscorel;Profenid;Toprec;Toprek;
同义名
m-Benzoylhydratropic acid;
基本介绍
Ketoprofen, a propionic acid derivative, is a nonsteroidal anti-inflammatory agent (NSAIA) with analgesic and antipyretic properties.
生产厂家
- Bayer healthcare llc
- Elan pharmaceutical research corp
- Heritage pharmaceuticals inc
- L perrigo co
- Mylan pharmaceuticals inc
- Novartis consumer health inc
- Sandoz inc
- Teva pharmaceuticals usa inc
- Watson laboratories inc florida
- Wyeth ayerst laboratories
- Wyeth consumer healthcare
- Wyeth pharmaceuticals inc
封装厂家
参考
Synthesis Reference | Not Available |
General Reference |
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剂型
Form | Route | Strength |
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Capsule | Oral | 100 mg |
Capsule | Oral | 50 mg |
Capsule | Oral | 75 mg |
Capsule, extended release | Oral | 200 mg |
规格
Unit description | Cost | Unit |
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Ketoprofen powder | 43.74 USD | g |
Ketoprofen micronized powder | 3.84 USD | g |
Ketoprofen CR 200 mg 24 Hour Capsule | 2.8 USD | capsule |
Orudis 75 mg capsule | 1.58 USD | capsule |
Apo-Keto Sr 200 mg Sustained-Release Tablet | 1.46 USD | tablet |
Ketoprofen 75 mg capsule | 1.12 USD | capsule |
Pms-Ketoprofen 100 mg Suppository | 1.1 USD | suppository |
Ketoprofen 50 mg capsule | 1.0 USD | capsule |
Apo-Keto-E 100 mg Enteric-Coated Tablet | 0.71 USD | tablet |
Apo-Keto 50 mg Capsule | 0.35 USD | capsule |
Apo-Keto-E 50 mg Enteric-Coated Tablet | 0.35 USD | tablet |
Orudis kt 12.5 mg tablet | 0.3 USD | tablet |
化合物类型
Type | small molecule |
Classes |
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Substructures |
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适应症
ANTIINFLAMMATORY AND ANTIRHEUMATIC 消炎抗风湿;
药理
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. | ||||||
Pharmacodynamics | 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 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. | ||||||
Absorption | Ketoprofen is rapidly and well-absorbed orally, with peak plasma levels occurring within 0.5 to 2 hours. | ||||||
Volume of distribution | Not Available | ||||||
Protein binding | 99% bound, primarily to albumin | ||||||
Metabolism |
Rapidly and extensively metabolized in the liver, primarily via conjugation to glucuronic acid. No active metabolites have been identified. |
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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) |
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Clearance |
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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. |
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Affected organisms |
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Pathways |
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理化性质
Properties | |||||||||||||||||||||||||||||||||||||
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State | solid | ||||||||||||||||||||||||||||||||||||
Melting point | 94 oC | ||||||||||||||||||||||||||||||||||||
Experimental Properties |
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Predicted Properties |
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药物相互作用
Drug | Interaction |
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Acenocoumarol | The NSAID, ketoprofen, may increase the anticoagulant effect of acenocoumarol. |
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. |
Anisindione | The NSAID, ketoprofen, may increase the anticoagulant effect of anisindione. |
Citalopram | 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. |
Dicumarol | The NSAID, ketoprofen, may increase the anticoagulant effect of dicumarol. |
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. |
Escitalopram | Concomitant therapy may result in additive antiplatelet effects and increase the risk of bleeding. Monitor for increased risk of bleeding during concomitant therapy. |
Fluoxetine | Concomitant therapy may result in additive antiplatelet effects and increase the risk of bleeding. Monitor for increased risk of bleeding during concomitant therapy. |
Fluvoxamine | Concomitant therapy may result in additive antiplatelet effects and increase the risk of bleeding. Monitor for increased risk 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. |
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. |
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. |
Methotrexate | The NSAID, ketoprofen, may decrease the renal excretion of methotrexate. Increased risk of methotrexate toxicity. |
Paroxetine | 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. |
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. |
Sertraline | Concomitant therapy may result in additive antiplatelet effects and increase the risk of bleeding. Monitor for increased risk of bleeding during concomitant therapy. |
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. |
Timolol | The NSAID, Ketoprofen, may antagonize the antihypertensive effect of Timolol. |
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. |
Treprostinil | The prostacyclin analogue, Treprostinil, may increase the risk of bleeding when combined with the NSAID, Ketoprofen. Monitor for increased bleeding during concomitant thearpy. |
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. |
食物相互作用
- Avoid alcohol.
- Food prolongs rate of absorption and decreases peak plasma concentration. Extent of absorption is not affected.
- Take with food to reduce gastric irritation.