Ketoprofen

254.28100

254.28

244-759-8

758144

DTXSID6020771

M02AA10|M - Musculo-skeletal system

2916392000

54.37000

3.1

White crystalline powder

1.198 g/cm3

94 °C

431.3ºC at 760 mmHg

147ºC

1.592

209mg/L(room temperature)

0-6ºC

0mmHg at 25°C

LD50 orally in rats: 101 mg/kg (Ueno)

4.45

157.5 Ų [M+H]+ [CCS Type: TW, Method: calibrated with polyalanine and drug standards]|155.4 Ų [M+H]+ [CCS Type: TW]|158.08 Ų [M+H]+

III

6.1(b)

UN 2811 6.1/PG 3

3

R25; R36/37/38

26-45-36/37/39

UE7570000

T

Stable at normal temperatures and pressures.

P261-P301 + P310-P305 + P351 + P338

H301-H315-H319-H335

|Danger|H301 (99.84%): Toxic if swallowed [Danger Acute toxicity, oral]|P261, P264, P270, P271, P280, P301+P310, P302+P352, P304+P340, P305+P351+P338, P312, P321, P330, P332+P313, P337+P313, P362, P403+P233, P405, and P501|Aggregated GHS information provided by 637 companies from 21 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

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.

Prospective studies show that 1% to 2% of patients taking ketoprofen experience at least transient serum aminotransferase elevations. These may resolve even with drug continuation. Marked aminotransferase elevations (>3 fold elevated) occur in

99% bound, primarily to albumin

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.|FDA Label|Treatment of musculoskeletal and connective tissue pain|Treatment of pain

Ketoprofen is a nonsteroidal antiinflammatory drug (NSAID) used in treatment of acute pain and chronic arthritis. Ketoprofen has been linked to a low rate of serum enzyme elevations during therapy and to rare instances of clinically apparent acute liver injury.

Antiinflammatory Agents, Nonsteroidal

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.

Anti-inflammatory agents that are non-steroidal in nature. In addition to anti-inflammatory actions, they have analgesic, antipyretic, and platelet-inhibitory actions.They act by blocking the synthesis of prostaglandins by inhibiting cyclooxygenase, which converts arachidonic acid to cyclic endoperoxides, precursors of prostaglandins. Inhibition of prostaglandin synthesis accounts for their analgesic, antipyretic, and platelet-inhibitory actions; other mechanisms may contribute to their anti-inflammatory effects. (See all compounds classified as Anti-Inflammatory Agents, Non-Steroidal.)|Compounds or agents that combine with cyclooxygenase (PROSTAGLANDIN-ENDOPEROXIDE SYNTHASES) and thereby prevent its substrate-enzyme combination with arachidonic acid and the formation of eicosanoids, prostaglandins, and thromboxanes. (See all compounds classified as Cyclooxygenase Inhibitors.)

Ketoprofen is rapidly and well-absorbed orally, with peak plasma levels occurring within 0.5 to 2 hours.|In a 24 hour period, approximately 80% of an administered dose of ketoprofen is excreted in the urine, primarily as the glucuronide metabolite.|Oral-dose cl=6.9 +/- 0.8 L/h [Ketoprofen Immediate-release capsules (4 × 50 mg)]

Rapidly and extensively metabolized in the liver, primarily via conjugation to glucuronic acid. No active metabolites have been identified.|Ketoprofen has known human metabolites that include Ketoprofen glucuronide.

Conventional capsules: 1.1-4 hours

Extended release capsules: 5.4 hours due to delayed absorption (intrinsic clearance is same as conventional capsules)

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.

19,583 RP

Benzeneacetic acid, 3-benzoyl-.alpha.-methyl-: INACTIVE

Human Drugs -> EU pediatric investigation plans|Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients|Animal Drugs -> FDA Approved Animal Drug Products (Green Book) -> Active Ingredients|Pharmaceuticals -> Animal Drugs -> Approved in Taiwan