Sunset over Boston Commons

Cancer remains one of the most intractable diseases, with certain types and subtypes continuing to evade effective treatment. While great progress has been made with immunotherapies and molecularly targeted drugs, cancers driven by notorious oncogenes like KRAS, MYC, and p53 remain challenging to drug.

These key transcriptional and signalling proteins play vital roles in normal cell physiology, meaning inhibiting them often causes toxicity. However, the allure of tackling cancers addicted to these oncoproteins keeps researchers striving for more precise, selective ways to target them.

One emerging approach is to inhibit a key transcriptional kinase involved in regulating MYC and other cancer-promoting genes. Several inhibitors of this kinase have been tested clinically, but most were either insufficiently selective or too toxic.

A new compound profiled in the post below shows early signs of being a more optimised inhibitor. It displays high selectivity and a long half-life, enabling sustained target inhibition without excessive toxicity. Early data from a phase 1 trial in solid tumours has demonstrated clinical activity, including exceptional responses in MYC-driven sarcomas.

These promising results highlight the potential of this new wave of inhibitors to tackle MYC-dependent cancers, including aggressive lymphomas. Other companies are advancing selective inhibitors of this kinase into clinical trials for hematologic malignancies.

Overall, these precision inhibitors represent an exciting targeted strategy against transcriptional addictions in cancer. The initial clinical success offers hope for making meaningful advances against once intractable oncogenes…

To continue reading our latest highlights on oncology new product development including commentary and analysis BSB subscribers can log-in or you can click to access the content.

This content is restricted to subscribers

Posted by