In LPS-stimulated monocytes isolated from human blood, ketoprofen inhibits COX with IC50 values of 2 nM (COX-1) and 26 nM (COX-2)[1]. In LPS-stimulated bovine mammary epithelial cells, ketoprofen (2.5 mg/mL, 3–24 hours) reduces the mRNA level of immune factors (TNFα, IL-8, SAA, and COX-2) and PTGES[3].

In HFD-induced obese C57BL/6 mice, ketoprofen (oral treatment, 10 mg/kg, three times a week for 10 weeks) reduces relative body weight (15.41%), iWAT mass (about 41%), and the levels of leptin (58.68%) and resistin (12.88%)[2]. In dairy cows exposed with lipopolysaccharide (LPS), ketoprofen (50 mg/kg) reduces the rise in somatic cell count (SCC), serum albumin (SA), immunoglobulin G (IgG), and lactate dehydrogenase (LDH) activity in milk[3].

RT-PCR[3]
Cell Types: LPS (0.2 μg/mL)-stimulated bovine mammary epithelial cells
Tested Concentrations: 2.5 mg /mL
Incubation Duration: 3, 6, 24 h
Experimental Results: diminished the mRNA level of TNFα, IL-8, SAA, COX-2 and PTGES.

Animal/Disease Models: HFD-induced obese C57BL/6 mice[2]
Doses: 10 mg/kg
Route of Administration: Oral administration, three times a week for 10 weeks
Experimental Results: diminished in relative body weight, the iWAT mass, and the level of leptin and resistin.

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Animal/Disease Models: LPS (0.2 μg/mL)-treated dairy cows [3]
Doses: 50 mg/kg
Route of Administration: Injection (Milk samples were taken every 30 min until 6 and 9 h )
Experimental Results: Lowered the increase of somatic cell count (SCC), serum albumin (SA), IgG and lactate dehydrogenase (LDH) activity in milk.

Absorption, Distribution and Excretion
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)]
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]

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Metabolism / Metabolites
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.

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Biological 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)

Hepatotoxicity
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
Likelihood score: C (probable rare cause of clinically apparent liver injury).

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Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Although ketoprofen has low levels in breastmilk, one center reported that they had received reports of adverse renal and gastrointestinal side effects in breastfed infants whose mothers were taking ketoprofen. Other agents are preferred, especially while nursing a newborn or preterm infant.
◉ Effects in Breastfed Infants
All adverse reactions in breastfed infants reported in France between January 1985 and June 2011 were compiled by a French pharmacovigilance center. Of 174 reports, ketoprofen was reported to cause adverse reactions in 8 infants and to be one of the drugs most often suspected in serious adverse reactions, such as esophageal ulceration, erosive gastritis, meningeal hemorrhage, and renal insufficiency.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.

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Protein Binding
99% bound, primarily to albumin

[1]. Structure-based design of cyclooxygenase-2 selectivity into ketoprofen. Bioorg Med Chem Lett. 2002 Feb 25;12(4):533-7.

[2]. NamHyeon Kang Ketoprofen alleviates diet-induced obesity and promotes white fat browning in mice via the activation of COX-2 through mTORC1-p38 signaling pathway. Pflugers Arch. 2020 May;472(5):583-596.

[3]. Ketoprofen affects the mammary immune response in dairy cows in vivo and in vitro. J Dairy Sci. 2018 Dec;101(12):11321-11329.

Ketoprofen is an oxo monocarboxylic acid that consists of propionic acid substituted by a 3-benzoylphenyl group at position 2. It has a role as a non-steroidal anti-inflammatory drug, an antipyretic, an EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor, an environmental contaminant, a xenobiotic and a drug allergen. It is a member of benzophenones and an oxo monocarboxylic acid. It is functionally related to a propionic acid.
Ketoprofen, a propionic acid derivative, is a nonsteroidal anti-inflammatory agent (NSAIA) with analgesic and antipyretic properties.
Ketoprofen is a Nonsteroidal Anti-inflammatory Drug. The mechanism of action of ketoprofen is as a Cyclooxygenase Inhibitor.
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.
Ketoprofen has been reported in Homo sapiens with data available.
Ketoprofen is a propionic acid derivate and nonsteroidal anti-inflammatory drug (NSAID) with anti-inflammatory, analgesic and antipyretic effects. Ketoprofen inhibits the activity of the enzymes cyclo-oxygenase I and II, resulting in a decreased formation of precursors of prostaglandins and thromboxanes. The resulting decrease in prostaglandin synthesis, by prostaglandin synthase, is responsible for the therapeutic effects of ibuprofen. Ketoprofen also causes a decrease in the formation of thromboxane A2 synthesis, by thromboxane synthase, thereby inhibiting platelet aggregation.
An IBUPROFEN-type anti-inflammatory analgesic and antipyretic. It is used in the treatment of rheumatoid arthritis and osteoarthritis.
See also: Ketoprofen lysine (is active moiety of); Ketoprofen sodium (is active moiety of); Ketoprofen; Tulathromycin (component of) ... View More ...

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Drug 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.
FDA Label
Treatment of musculoskeletal and connective tissue pain

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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.

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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.

C16H14O3

254.28

254.094

22071-15-4

Ketoprofen-d3;159490-55-8;Ketoprofen-d4;1219805-29-4;S-(+)-Ketoprofen;22161-81-5;Ketoprofen (lysinate);57469-78-0;Ketoprofen-13C,d3;1189508-77-7;Dexketoprofen (trometamol);156604-79-4

3825

White to off-white solid powder

1.2±0.1 g/cm3

431.3±28.0 °C at 760 mmHg

93-96°C

228.8±20.5 °C

0.0±1.1 mmHg at 25°C

1.592

2.81

1

3

4

19

331

0

DKYWVDODHFEZIM-UHFFFAOYSA-N

InChI=1S/C16H14O3/c1-11(16(18)19)13-8-5-9-14(10-13)15(17)12-6-3-2-4-7-12/h2-11H,1H3,(H,18,19)

2-(3-benzoylphenyl)propanoic acid

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

Solubility in Formulation 1: ≥ 2.5 mg/mL (9.83 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (9.83 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (9.83 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)