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    Ketoprofen (RP-19583)
    Ketoprofen (RP-19583)

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V1053
    CAS #: 22071-15-4Purity ≥98%

    Description: Ketoprofen (formerly RP 19583; RP-19583; Ketoprofen, Profenid, Orudis, Alrheumun, Capisten) is a potent nonsteroidal anti-inflammatory drugs (NSAID), acting as a dual COX1/2 inhibitor with potential anti-inflammatory activity. It was approved as a nonsteroidal anti-inflammatory drug to treat arthritis-related inflammatory pains. Ketoprofen combined with UVB irradiation induces the cytotoxicity and suppresses DNA synthesis in HaCaT cells in a concentration-dependent manner. Ketoprofen combined with UVB irradiation inhibits the cell growth and induces G2/M cell cycle arrest by modulating the levels of cdc2, cyclin B1, Chk1, Tyr15-phosphorylated cdc2 and p21. 

    References: Biochem Biophys Res Commun. 2007 Dec 21;364(3):650-5; J Periodontal Res. 1996 Nov;31(8):525-32.

    Related CAS#: 76690-94-3 [(±)-Ketoprofen glucuronide]

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    Molecular Weight (MW)254.28 
    FormulaC16H14O3 
    CAS No.22071-15-4 
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 51 mg/mL (200.6 mM) 
    Water: <1 mg/mL
    Ethanol: 51 mg/mL (200.6 mM) 
    Solubility (In vivo)
    SynonymsRP-19583; Ketoprofen, Profenid, RP 19583; Alrheumun, RP19583; Orudis, Capisten


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    In Vitro

    In vitro activity: Ketoprofen combined with UVB irradiation induces the cytotoxicity and suppresses DNA synthesis in HaCaT cells in a concentration-dependent manner. Ketoprofen combined with UVB irradiation inhibits the cell growth and induces G2/M cell cycle arrest by modulating the levels of cdc2, cyclin B1, Chk1, Tyr15-phosphorylated cdc2 and p21. Ketoprofen combined with UVB irradiation also provokes a striking accumulation of cyclin B1-cdc2-p21 complexes, concomitantly with an increase in the levels of Tyr15-phosphorylated cdc2 and p21 protein. Ketoprofen combined with UVB irradiation accentuates the apoptotic response to UVB radiation in HaCaT cells as evidenced by DAPI staining.


    Kinase Assay: Ketoprofen (RP-19583) is a non-steroidal antiinflammatory agent, acting as a potent inhibitor of COX, with IC50s of 2 nM and 26 nM for COX-1 and COX-2 in human blood monocytes, respectively.

    In VivoKetoprofen at 1% level in suitable topical vehicles can effectively inhibit GCF-LTB4 and GCF-PGE2 and positively alter alveolar bone activity in the ligature-induced model of periodontitis in the monkey. Ketoprofen (3.63 mg/kg bwt) reduces hoof pain andlameness to a greater extent than the 2.2 mg/kg dose and phenylbutazone. Ketoprofen is more effective than local anesthesia (LA), or caudal epidural anesthesia (EPI) in decreasing cortisol and partially reverses the reduction in average daily gain (ADG) following castration. Ketoprofen (40 and 80 mg/kg diet) reduces the incidence of transitional cell carcinoma of the urinary bladder by >70% from that seen in dietary mice. 
    Animal modelMice
    Formulation & DosageKetoprofen (RP-19583) (0.1-1.0 mg/kg) and morphine (0.1-1.0 mg/kg) are evaluated for their effectiveness to block U69,593-induced depression of nesting. For these studies, Ketoprofen (RP-19583) or morphine is administered 30 min before nesting, 1.0 mg/kg U69,593 is administered 15 min before nesting, and each set of conditions is tested in a group of six mice.
    References

    Biochem Biophys Res Commun. 2007 Dec 21;364(3):650-5; J Periodontal Res. 1996 Nov;31(8):525-32. 


    These protocols are for reference only. InvivoChem does not independently validate these methods.

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