Designed to be Different.
MET is a receptor tyrosine kinase that binds with high affinity to hepatocyte growth factor (HGF). MET alterations, including point mutations, amplifications, fusions, exon 14 skipping, and the generation of HGF-MET autocrine loops have been reported in approximately 3-5% of patients with NSCLC or gastric cancer. MET amplification has been detected in 15-20% of NSCLC patients with EGFR mutations who acquired resistance to Iressa (gefitinib), Tarceva (erlotinib) or Tagrisso (osimertinib) treatment.
SRC is a kinase involved in the MET signaling pathway. Inhibition of SRC has the potential to reduce or abolish the upregulation of HGF.
Targeting CSF1R leads to the modulation of tumor-associated macrophages (TAMs), a type of immune cell that suppresses the T-cell mediated anti-tumor immune response. Inhibition of CSF1R with TPX-0022 may be a promising therapeutic strategy as a single agent or in combination with standard of care chemotherapy and immunotherapy in various solid tumors.
We believe the simultaneous inhibition of MET, SRC and CSF1R kinases is a promising strategy for the treatment of MET-driven solid tumors.