Despite progress in recent years, with several new drugs gaining regulatory approval for the treatment of AML, it is unclear whether single drugs targeting a specific genomic alteration will be sufficient to eradicate disease.
Our novel approach to target synergistically both FLT3-kinase and TAF1-bromodomain may potentially eliminate drug-resistant leukemic cells more efficiently.
Compounds show high affinity for TAF1 and FLT3 and selectivity among bromodomain and protein kinase families.
Compared to other bromodomain-inhibitors, our initial results show an improved toxicity profile of the lead compounds while maintaining potency against haematological cancers.
The compounds are patentable and could be further developed into a novel drug candidate.