Drug compounds have included stable heavy isotopes of carbon, hydrogen, and other elements, mostly as quantitative tracers while the drugs were being developed. Due to its potential effects on medication pharmacokinetics and metabolic properties, deuteration has drawn interest [1][2].

Absorption, Distribution and Excretion
Ketoprofen is rapidly and well absorbed orally, with peak plasma concentrations reached within 0.5 to 2 hours. Approximately 80% of the administered dose is excreted in the urine within 24 hours, primarily as a glucuronide metabolite. Oral dose clearance = 6.9 ± 0.8 L/h [Ketoprofen immediate-release capsules (4 × 50 mg)] Oral dose clearance = 6.8 ± 1.8 L/h [Ketoprofen extended-release capsules (1 × 200 mg)] 0.08 L/kg/h 0.7 L/kg/h [Patients with alcoholic cirrhosis] Metabolism/Metabolites Metabolism is rapid and extensive in the liver; ketoprofen is primarily metabolized by conjugation with glucuronic acid. No active metabolites have been identified. Known metabolites of ketoprofen include ketoprofen glucuronide.

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Biological Half-Life
Regular Capsules: 1.1-4 hours

Sustained-Release Capsules: 5.4 hours, due to delayed absorption (inherent clearance rate is the same as regular capsules)

Hepatotoxicity
Prospective studies have shown that 1% to 2% of patients taking ketoprofen experience at least transient increases in serum transaminases. These increases may resolve spontaneously with continued use. Significant increases in transaminases (more than 3-fold) are seen in a probability score of C (likely a rare cause of clinically significant liver injury). Pregnancy and Lactation Effects
◉ Overview of Use During Lactation
Although ketoprofen concentrations in breast milk are low, one center has reported receiving reports of renal and gastrointestinal adverse reactions in breastfed infants born to mothers taking ketoprofen. It is recommended to prioritize other medications, especially for breastfed newborns or premature infants.
◉ Effects on Breastfed Infants
The French National Center for Drug Vigilance compiled all adverse reactions reported in breastfed infants in France between January 1985 and June 2011. Of the 174 reports, ketoprofen was reported to cause adverse reactions in 8 infants and is one of the most common suspected drugs causing serious adverse reactions such as esophageal ulcers, erosive gastritis, meningeal hemorrhage, and renal insufficiency.
◉ Effects on lactation and breast milk
As of the revision date, no relevant published information was found.

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Protein binding
99% bound to proteins, primarily albumin.

[1]. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-223.

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

Ketoprofen is an oxomonocarboxylic acid formed by replacing propionic acid with 3-benzoylphenyl at the 2-position. It is a nonsteroidal anti-inflammatory drug (NSAID), antipyretic, EC 1.14.99.1 (prostaglandin intraperoxidase) inhibitor, environmental pollutant, exogenous substance, and drug allergen. It belongs to the benzophenone class of compounds and is an oxomonocarboxylic acid functionally related to propionic acid. Ketoprofen is a propionic acid derivative and a nonsteroidal anti-inflammatory drug (NSAID) with analgesic and antipyretic effects. The mechanism of action of ketoprofen is as a cyclooxygenase inhibitor. Ketoprofen is an NSAID used to treat acute pain and chronic arthritis. Ketoprofen is associated with a low incidence of elevated serum enzymes during treatment and rare cases of clinically significant acute liver injury. There are reports and data regarding the use of ketoprofen in Homo sapiens. Ketoprofen is a propionic acid derivative, belonging to the nonsteroidal anti-inflammatory drug (NSAID) class, and possesses anti-inflammatory, analgesic, and antipyretic effects. Ketoprofen inhibits the activity of cyclooxygenase I and II, thereby reducing the production of prostaglandins and thromboxane precursors. The reduced prostaglandin synthesis mediated by prostaglandin synthase is the reason for ketoprofen's therapeutic effect. Ketoprofen also reduces the production of thromboxane A2 mediated by thromboxane synthase, thereby inhibiting platelet aggregation. It is also an ibuprofen-like anti-inflammatory, analgesic, and antipyretic drug. It is used to treat rheumatoid arthritis and osteoarthritis. See also: Ketoprofen lysine (its active fraction); Ketoprofen sodium (its active fraction); Ketoprofen; Tulamycin (ingredient)... See more...

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Drug Indications
For the treatment of acute and chronic rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, primary dysmenorrhea, and mild to moderate pain associated with muscle and tendon injuries (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 effect of ketoprofen is believed to be achieved by inhibiting cyclooxygenase-2 (COX-2), an enzyme involved in prostaglandin synthesis via the arachidonic acid pathway. This leads to a decrease in prostaglandin levels that mediate pain, fever, and inflammation. Ketoprofen is a nonspecific cyclooxygenase inhibitor, and inhibition of COX-1 is considered to be the source of some of its side effects, such as gastrointestinal discomfort and ulcers. Ketoprofen is believed to have anti-bradykinin activity and lysosomal membrane stabilizing effects. Its antipyretic effect may stem from its action on the hypothalamus, thereby increasing peripheral blood flow, vasodilation, and ultimately heat dissipation.

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Pharmacodynamics
Ketoprofen is a nonsteroidal anti-inflammatory drug (NSAID) with analgesic and antipyretic effects. The pharmacological action of ketoprofen is similar to other typical NSAIDs, all of which inhibit prostaglandin synthesis. Ketoprofen is used to treat rheumatoid arthritis, osteoarthritis, dysmenorrhea, and to relieve moderate pain.

C16H14O3

258.291704654694

258.116

1189508-77-7

Ketoprofen;22071-15-4

3825

Typically exists as solid at room temperature

3.105

1

3

4

19

331

0

CC(C1=CC(=CC=C1)C(=O)C2=CC=CC=C2)C(=O)O

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)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*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.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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