Hepatocyte growth factor receptor, Aurora kinase A, Aurora kinase B, Tropomyosin receptor kinase A, Tropomyosin receptor kinase B, and Macrophage-stimulating protein receptor (MET/AURKA/AURKB/NTRK1/NTRK2/MST1R)

The target profile c-Met, Aurora A/B, TrkA/B, Ron represents a specific cluster of kinases often co-targeted by multi-kinase inhibitors in oncology. This group includes receptor tyrosine kinases such as Hepatocyte growth factor receptor (c-Met) and Macrophage-stimulating protein receptor (Ron), which are critical for invasive growth and epithelial-mesenchymal transition (EMT) in solid tumors [1, 2]. It also includes Aurora kinases A and B, which are serine/threonine kinases essential for regulating mitosis, spindle assembly, and chromosomal segregation [3]. Furthermore, Tropomyosin receptor kinases A and B (TrkA/B) are included, which play roles in cell survival and are frequently involved in oncogenic fusions [4]. Drugs like BMS-777607 are designed to inhibit this entire spectrum of kinases to achieve a synergistic anti-tumor effect by disrupting both growth factor signaling and the cell cycle machinery [5]. This multi-target approach is intended to overcome resistance mechanisms that typically arise from the activation of alternative signaling pathways during single-target therapy [6].

Other names

c-MetMETAurora AAURKAAurora BAURKBTrkANTRK1TrkBNTRK2RonMST1RHGFRSTK1TRKMSP receptor

ATP-competitive inhibition of the intracellular kinase domains of MET, AURKA, AURKB, NTRK1, NTRK2, and MST1R, preventing downstream phosphorylation and signaling cascades.