Preferred Label : Axl/Mer/CSF1R Inhibitor Q702;
NCIt synonyms : RTK Inhibitor Q702; Axl/Mer Inhibitor INCB081776; Axl/Mer/CSF1R Selective Tyrosine Kinase Inhibitor Q702;
NCIt definition : An orally bioavailable inhibitor of the receptor tyrosine kinases (RTKs) Axl (UFO),
Mer, and colony stimulating factor-1 receptor (CSF1R; CSF-1R; CD115; M-CSFR), with
potential immunomodulatory, chemo-sensitizing and antineoplastic activities. Upon
oral administration, Axl/Mer/CSF1R inhibitor Q702 targets, binds to and blocks the
activity of Axl, Mer and CSF1R, thereby blocking Axl-, Mer- and CSF1R-mediated signaling
pathways. This inhibits proliferation of Axl- and Mer-expressing tumor cells. In addition,
blocking Axl- and Mer-mediated signaling may re-activate the innate immune system
against cancer cells. Blocking CSF1R-mediated signaling inhibits the activities of
tumor-associated macrophages (TAMs), regulatory T cells (Tregs) and recruitment of
myeloid-derived suppressor cells (MDSCs). Altogether, this abrogates immune suppression
in the tumor microenvironment (TME), enhances antitumor T-cell immune responses and
inhibits the proliferation of tumor cells. CSF1R, also known as macrophage colony-stimulating
factor receptor (M-CSFR) and CD115 (cluster of differentiation 115), is a cell-surface
receptor that plays major roles in tumor cell proliferation, metastasis, and cancer-associated
immune suppression. Axl and Mer, both members of the TAM (Tyro3, Axl and Mer) family
of RTKs, are overexpressed by many tumor cell types. They play key roles in tumor
cell proliferation, survival, invasion, angiogenesis and metastasis, and the inactivation
of innate immunity in cancer. Their expression is associated with drug resistance
and poor prognosis.;
Molecule name : Q-702; Q 702;
NCI Metathesaurus CUI : CL1643184;
Origin ID : C177458;
UMLS CUI : C5447779;
Semantic type(s)
- chemical_or_drug_has_physiologic_effect
- concept_is_in_subset
- has_target
