Surprisingly, cytoplasmic factors which regulate EGFR activation have been identified by the inventors. Inhibition of these so-called cytohesins decreased EGFR signalling whereas cytohesin overexpression stimulated receptor activation.
With cytohesins thus being an interesting target for compounds treating cancer, the inventors have evaluated small molecules which exhibit a high selectivity for cytohesins as well as a low toxicity. They were able to demonstrate that the inhibition of cytohesins resulted in a reduced proliferation of EGFR-dependent lung cancer cells in vitro and in vivo. Furthermore, it was found that the substances exhibit a strong inhibition of glioblastoma cell proliferation.
Additional data give reason to expect synergistic effects of a simultaneous treatment of cytohesin inhibitors and state of the art tyrosine kinase inhibitors.
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