Abstract
Multidrug-resistance (MDR) occurs in many bacterial species and tumour cells. MDR functions by membrane proteins which export drugs from cells, resulting in a low ineffective concentration of the drug. We have shown by molecular modelling that inhibitors of MDR have affinity for substrates of MDR transporters. This affinity may facilitate drug entry into cells and a large inhibitor–drug complex may be a poorer substrate for the MDR mechanism. This complex would effectively ‘cloak’ the drug rendering it unavailable for efflux.
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