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    Valdecoxib (SC65872)
    Valdecoxib (SC65872)

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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 #: V1071
    CAS #: 181695-72-7Purity ≥98%

    Description: Valdecoxib (SC-65872; SC65872; SC 65872; Bextra), a nonsteroidal anti-inflammatory drug (NSAID), is a potent and selective inhibitor of COX-2 enzyme with potential anti-inflammatory activity. It inhibits COX-2 with an IC50 of 5 nM. Valdecoxib has been approved for the treatment of pain and inflammation. Valdecoxib and its intravenous prodrug parecoxib exert significant opioid-sparing effects after dental, gynecologic, orthopedic and other noncardiac surgical procedures. In the cellular assay, valdecoxib shows inhibitory activity on human recombinant COX-2 with IC50 value of 5nM. It shows no significant effect on COX-1 with IC50 value of 140μM. In the ex vivo assay using human whole blood, valdecoxib prevents PGE2 production with IC50 value of 0.89μM. 

    References: J Med Chem. 2000 Mar 9;43(5):775-7; J Pharmacol Exp Ther. 2005 Mar;312(3):1206-12. 

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    Molecular Weight (MW)314.36 
    CAS No.181695-72-7 
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 63 mg/mL (200.4 mM)
    Water: <1 mg/mL
    Ethanol: 18 mg/mL (57.2 mM) 
    Solubility (In vivo)0.5% methylcellulose+0.2% Tween 80: 19 mg/mL 
    SynonymsSC-65872; SC 65872; Bextra; SC65872; 

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    In Vitro

    In vitro activity: Valdecoxib inhibits LPS-induced PGE2 production in plasma with IC50 of 0.89 μM for assessment of the extent of COX-2 inhibition.  Valdecoxib inhibits TxB2 production in plasma with IC50 of 25.4 μM for assessment of the extent of COX-1 inhibition. Valdecoxib binds to COX-2 with Ka of 1.1×105 M/s. The overall saturation binding affinity for COX-2 of Valdecoxib is 2.6 nM. Valdecoxib shows similar activity in the human whole-blood COX assay (COX-2 IC50 = 0.24 μM; COX-1 IC50 = 21.9 μM). The affinity of [3H]Valdecoxib for COX-2 with KD of 3.2 nM. The binding of Valdecoxib to COX-2 seems to be both rapid and slowly reversible with association rates of 4.5 × 106/M/min and dissociation rates of 7.0 × 10-3/min (t1/2 of 98 min). The percent of dissolved Valdecoxib at 15 min (DP15) is 10.5% for Valdecoxib and 50%, 91% and 93% for its hydrophilic derivatives (VALD-βCd, VALD-HPβCd and VALD-SBE7βCd complexes), respectively.

    Cell Assasy: HMEC-1 cells proliferation is measured using the MTT conversion method. Cells are seeded (50.000 cells/well) into 96-well plates. The cells are incubated for 24 h with LPS 100 µg/mL, CoCl2 200 µM, Valdecoxib 10 or 100 µM, LPS and Valdecoxib or CoCl2 and Valdecoxib or without tested chemicals (control group). All the substances are added at the same time. After incubation, 50 µL MTT (1 mg/mL) is added and the plates are incubated at 37°C for 4 h. At the end of the experiment, cells are exposed to 100 µL DMSO, which enables the release of the blue reaction product-formazan. The absorbance at 570 nm is read on a microplate reader and results are expressed as a percentage of the absorbance measured in control cells

    In Vivo
    Valdecoxib administrated orally inhibits rat carrageenan foot pad edema with ED50 of 10.2 mg/kg. Valdecoxib administrated orally shows chronic antiinflammatory activity with ED50 of 0.032 mg/kg/day in rat adjuvant arthritis model. Valdecoxib administrated orally shows blockade of prostaglandin production at the inflammatory site with ED50 of 0.02 mg/kg in the rat carrageenan air pouch model. Valdecoxib demonstrates marked potency in acute and chronic models of inflammation (air pouch ED50 = 0.06 mg/kg; paw edema ED50 = 5.9 mg/kg; adjuvant arthritis ED50 = 0.03 mg/kg) in rats. Valdecoxib alone shows slow in vivo absorption giving maximum % inhibition of edema (16%) after a period of 3 hour. In contrast, VALD-βCd and VALD-SBE7βCd complexes shows high absorption rate in vivo achieving more than 50% inhibition of edema in the 1 hour and maximum percentage of inhibition of edema (66%) after a period of 3 hours. Valdecoxib (5 mg/kg, po) results in AUC in plasma of 3.58 μg*h/mL and 2.08 μg*h/mL in males and female mice, respectively. Valdecoxib (5 mg/kg, po) results in AUC red blood cells of 12.1 μg*h/mL and 6.42 μg*h/mL in males and female mice, respectively. 
    Animal modelMale Sprague-Dawley rats 
    Formulation & DosageFormulated in  0.5% methyl cellulose and 0.025% Tween-20; 10.2 mg/kg; Oral gavage

    J Med Chem. 2000 Mar 9;43(5):775-7; J Pharmacol Exp Ther. 2005 Mar;312(3):1206-12.  

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


    Human whole-blood assay. Compounds were evaluated for their ability to inhibit either COX-1 from platelets or COX-2 from LPS-simulated whole blood as described under Materials and Methods. J Pharmacol Exp Ther. 2005 Mar;312(3):1206-12.


    Rat air pouch model of inflammation and gastrointestinal PGE2 production. J Pharmacol Exp Ther. 2005 Mar;312(3):1206-12.


    Carrageenan-induced inflammation and the measurement of hyperalgesia (withdrawal latency) and edema (paw volume).


    Rat adjuvant arthritis model of chronic inflammation. J Pharmacol Exp Ther. 2005 Mar;312(3):1206-12.


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