Catalog Number: 4042
Alternate Names: Valspodar
Chemical Name: 6-[(2S,4R,6E)-4-methyl-2-(methylamino)-3-oxo-6-octenoic acid]-7-L-valine-cyclosporin A
Biological Activity
P-glycoprotein (P-gp) modulator; inhibits P-gp-mediated multidrug-resistance (MDR). Reverses resistance to several cytotoxic drugs including mitoxantrone and doxorubicin (resistance factors are 2.0 and 6.5 respectively) in human MDR cancer cell lines. Non-immunosuppressive analog of cyclosporin A (Cat. No. 1101).
Technical Data
  • M.Wt:
    1214.62
  • Formula:
    C63H111N11O12
  • Solubility:
    Soluble to 4 mM in DMSO
  • Purity:
    >98%
  • Storage:
    Store at -20°C
  • CAS No:
    121584-18-7
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis. All Tocris products are intended for laboratory research use only.
Background References
  1. Modulation of the tumor disposition of vinca alkaloids by PSC 833 in vitro and in vivo.
    Song et al.
    J.Pharmacol.Exp.Ther., 1998;287:963
  2. Complete inhibition of P-glycoprotein by simulataneous treatment with a distinct class of modulators and the UIC2 monoclonal antibody.
    Goda et al.
    J.Pharmacol.Exp.Ther., 2007;320:81
  3. Quantitation of doxorubicine uptake, efflux, and modulation of multidrug resistance (MDR) in MDR human cancer cells.
    Shen et al.
    J.Pharmacol.Exp.Ther., 2008;324:95
  4. Dynamic assessment of mitoxantrone resistance and modulation of multidrug resistance by Valspodar (PSC833) in multidrug resistance human cancer cells.
    Shen et al.
    J.Pharmacol.Exp.Ther., 2009;330:423
Citations:

The citations listed below are publications that use Tocris products. Selected citations for PSC 833 include:

2 Citations: Showing 1 - 2
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  1. Sex-specific response of rat costochondral cartilage growth plate chondrocytes to 17β-estradiol involves differential regulation of plasma membrane associated estrogen receptors.
    Authors: Elbaradie Et al.
    Sci Rep 2013;1833:1165
  2. Intracellular retention of ABL kinase inhibitors determines commitment to apoptosis in CML cells.
    Authors: Lipka Et al.
    PLoS One 2012;7:e40853

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