CSF1R/c-Kit-IN-1

CSF1R/c-Kit-IN-1 (12l) (40 min) potently inhibits human recombinant CSF-1R kinase with an IC₅₀ of 5.88 nM^[1].
CSF1R/c-Kit-IN-1 (20 min pre-incubation; 2 h reaction incubation) potently inhibits c-Kit kinase with an IC₅₀ of 1.47 nM^[1].
CSF1R/c-Kit-IN-1 (1.0 μM; 20 min pre-incubation; 2 h reaction incubation) exhibits a cleaner kinome selectivity profile relative to CSF-1R/c-Kit, with weaker off-target activity against FYN, ABL1, and CSK compared to its primary targets^[1].
CSF1R/c-Kit-IN-1 (1-10 μM; 30 min pre-incubation; 20 min CSF-1 stimulation) potently and concentration-dependently suppresses CSF-1-induced ERK phosphorylation in SIM-A9 mouse microglial cells, leaving only 18.7% residual pERK signal at 10 μM^[1].
CSF1R/c-Kit-IN-1 (10 μM; 6 h) does not reduce SIM-A9 mouse microglial cell viability at a concentration of 10 μM^[1].
CSF1R/c-Kit-IN-1 exhibits high human liver microsomal stability, with 86.8% remaining after 30 min of incubation^[1].
CSF1R/c-Kit-IN-1 exhibits favorable blood-brain barrier permeability, with an effective permeability coefficient (P_e) of 26.27 × 10^-6 cm/s^[1].
CSF1R/c-Kit-IN-1 (up to 60 min at room temperature) exhibits excellent human plasma stability, with >100% remaining after 60 min of incubation at room temperature^[1].
CSF1R/c-Kit-IN-1 adopts a binding mode that maintains essential hinge interactions in both CSF-1R and c-Kit, with enhanced hydrophobic complementarity in c-Kit contributing to its stronger c-Kit potency^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.