ALK and c-Met

Class

ALK/c-Met inhibitor

Pathway

ALK- and c-Met-mediated signaling

ALK (anaplastic lymphoma kinase) and c-Met (also called hepatocyte growth factor receptor) are both receptor tyrosine kinases—proteins embedded in the cell membrane that, once activated, trigger internal signaling cascades controlling cell growth, survival, and movement. In certain cancers, ALK becomes permanently switched on through chromosomal rearrangements that fuse it to another gene, producing a constant growth signal independent of normal regulatory control. c-Met, meanwhile, is a receptor for hepatocyte growth factor and can drive tumor growth when amplified or overexpressed; notably, increased c-Met signaling is a recognized route by which tumors escape drugs that target ALK alone. A single agent designed to inhibit both kinases addresses the primary oncogenic driver (mutant ALK) while simultaneously blunting a common escape pathway, an approach relevant chiefly in lung cancers and other tumors defined by ALK gene rearrangements. This dual-inhibition strategy reflects a broader principle in oncology drug design: targeting a driver mutation together with a frequently co-occurring resistance mechanism can produce more durable disease control than targeting the driver in isolation. Because both targets belong to the same broad kinase family, a single small molecule can often be engineered to bind both ATP pockets, though this comes with trade-offs in selectivity that must be balanced against efficacy.