British Journal of Cancer (1999) 79, 1672–1678. doi:10.1038/sj.bjc.6690267 www.bjcancer.com
Published online 12 March 1999
In vivo efficacy of XR9051, a potent modulator of P-glycoprotein mediated multidrug resistance
P Mistry1, J Plumb2, S Eccles3, S Watson4, I Dale1, H Ryder1, G Box3, P Charlton1, D Templeton1 and P B Bevan1
- 1Xenova Ltd, 240 Bath Road, Slough, SL1 4EF, UK
- 2CRC Department of Oncology, University of Glasgow, Glasgow, G61 1BD, UK
- 3Institute of Cancer Research, Sutton, SM2 5NG, UK
- 4Cancer Studies Unit, University of Nottingham, Nottingham, NG7 2UH,UK
Received 14 April 1998; Revised 27 July 1998; Accepted 7 August 1998.
Top of pageAbstract
Overexpression of P-glycoprotein (P-gp) is a potential cause of multidrug resistance (MDR) in tumours. We have previously reported that XR9051 (N-(4-(2-(6,7-dimethoxy-1,2,3,4-tetrahydro-2-
isoquinolyl)ethyl)phenyl)-3-((3Z,6Z)-6-benzylidene-1-methyl-2,5-dioxo-3-piperazinylidene)-
methylbenzamide) is a potent and specific inhibitor of P-gp, which reverses drug resistance in several murine and human MDR cell lines. In this study we have evaluated the in vivo efficacy of this novel modulator in a panel of murine and human tumour models and examined its pharmacokinetic profile. Efficacy studies in mice bearing MDR syngeneic tumours (P388/DX Johnson, MC26) or human tumour xenografts (A2780AD, CH1/DOXr, H69/LX) demonstrated that co-administration of XR9051 significantly potentiated the anti-tumour activity of a range of cytotoxic drugs. This modulatory activity was observed following parenteral and oral co-administration of XR9051. In addition, the combination schedules were well-tolerated. Following intravenous administration in mice, XR9051 is rapidly distributed and accumulates in tumours and other tissues. In addition, the compound is well-absorbed after oral administration. These data suggest that XR9051 has the potential for reversing clinical MDR mediated by P-glycoprotien.
Keywords:
multidrug resistance, P-glycoprotein, XR9051, resistance modulators
Top of pageReferences
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