A hyper-active thymidine kinase mutant locally administered into the solid tumor via viral transfection drives tumour cells into cell cycle arrest and subsequent cell death. The effect requires very low to physiological substrate concentrations, which is expected to keep side effects at bay due to very low to no systemic exposure.
A super active human thymidine kinase 1 enzyme (superTK1), engineered by recombinant technology based on theoretical protein calculations, allows to dramatically reduce the growth inhibitory substrate levels of deoxythymidine to almost physiological substrate concentrations. The engineered enzyme is locally administered to tumor cells by AAV (adeno associated virus). Cytostatic as well as cytotoxic effects on tumor cells can be induced and maintained by very low deoxythymidine serum levels (< 0,1 mM). This avoids systemic exposure of high inhibitor concentrations to healthy cells and thus hardly entails any side effects. Combination treatment with cytostatics (e.g. 5-FU, AraC) is possible and expected to reduce concentrations of chemotherapeutics in a similar manner. Therefore lower side effects without diminishing treatment efficacy can be expected.
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