Ketoprofen

DEA NFLIS-Drug Category -> Analgesics

Pharmaceuticals -> NSAIDs

Pharmaceutical

Pharmaceuticals

3.2

3.12

Breast Feeding; Lactation; Milk, Human; Analgesic Agents; Anti-inflammatory Agents, Nonsteroidal

FDA approved drugs -> Active ingredient

FDA approved drugs -> Active ingredient

Active Ingredients (Ketoprofen) -> FDA Greenbook

Pharmaceuticals -> Animal Drugs -> Approved in Taiwan

Pharmaceuticals -> UK Veterinary Medicines Directorate List

3.98

4

3.8

4.45

155.4 Ų [M+H]+ [CCS Type: TW]

157.5 Ų [M+H]+ [CCS Type: TW; Method: calibrated with polyalanine and drug standards]

148.63 Ų [M+H-H2O]+ [CCS Type: TW; Method: calibrated with polyalanine and drug standards]

165.87 Ų [M+Na]+

This chemical does not meet GHS hazard criteria for 0.1% (1 of 672) of reports.

Danger

H301 (99.7%): Toxic if swallowed [Danger Acute toxicity, oral]

P261, P264, P264+P265, P270, P271, P280, P301+P316, P302+P352, P304+P340, P305+P351+P338, P319, P321, P330, P332+P317, P337+P317, P362+P364, P403+P233, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 672 reports by companies from 29 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Status: Active Update: 30-06-2020 https://echa.europa.eu/registration-dossier/-/registered-dossier/24605

Ketoprofen: Does not have an individual approval but may be used under an appropriate group standard

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

Drug Induced Liver Injury Rank (DILIrank 2.0)

Ketoprofen

vLess-DILI-concern

3

Warnings & precautions

DOI:10.1016/j.drudis.2016.02.015

M02AA10

M - Musculo-skeletal system

M - Musculo-skeletal system

QM - Musculo-skeletal system

QM - Musculo-skeletal system

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.

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.

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.

90Y4QC304K

KETOPROFEN

Mechanisms of Action [MoA] - Cyclooxygenase Inhibitors

Chemical Structure [CS] - Anti-Inflammatory Agents, Non-Steroidal

Established Pharmacologic Class [EPC] - Nonsteroidal Anti-inflammatory Drug

Ketoprofen is a Nonsteroidal Anti-inflammatory Drug. The mechanism of action of ketoprofen is as a Cyclooxygenase Inhibitor.

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.

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.

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)]

Animal Drugs -> FDA Approved Animal Drug Products (Green Book) -> Active Ingredients

Pharmaceuticals -> Animal Drugs -> Approved in Taiwan