EGFR-IN-173 

EGFR-IN-173 is an orally active, pan-mutant EGFR tyrosine kinase inhibitor that targets EGFR 19del, L858R/T790M and C797S triple-mutations, potently inhibiting EGFR^{19del/T790M/C797S} with an IC₅₀ of 1.19 nM while showing over 100-fold selectivity for mutant over wild-type EGFR (IC₅₀ = 19.362 μM against WT). EGFR-IN-173 significantly inhibits cell migration, induces apoptosis in non-small cell lung cancer (NSCLC) cells. EGFR-IN-173 inhibits EGFR phosphorylation and suppresses the downstream pathways (MAPK/ERK, AKT, STAT3). EGFR-IN-173 exhibits antitumor efficacy in NSCLC and Ba/F3 xenograft models. EGFR-IN-173 can be used for NSCLC research^[1].

EGFR-IN-173 (compound D10) (0.001-0 μM, 72 h) displays broad and robust antiproliferative activity various EGFR mutants, with IC₅₀ values of 0.69 nM in HCC827 cells (EGFR^19del), 0.242 μM in H1975 cells (EGFR^L858R/T790M), 0.192 μM in Ba/F3-EGFR_{19del/T790M/C797S} cells, and 1.303 μM in Ba/F3-EGFR^{L858R/T790M/C797S}, and shows more than 100-fold selectivity for mutant over WT EGFR (IC₅₀ = 19.362 μM against WT) ^[1].
EGFR-IN-173 occupies the active site of EGFR and forms important hydrogen bonds with Lys728 and Ser797^[1].
EGFR-IN-173 (10-100 nM, 14 days) dose-dependently inhibits colony formation in the NSCLC HCC827 cells, suppressing their long-term proliferative capacity^[1].
EGFR-IN-173 (10-100 nM, 0-48 h) effectively suppresses the migration of NSCLC H1975 cells in a concentration-dependent manner^[1].
EGFR-IN-173 (20-200 nM, 48 h) induces G0/G1 phase arrest in a dose-dependent manner in HCC827 cells^[1].
EGFR-IN-173 (1-2000 nM, 48 h) induces both early and late-stage apoptosis in a concentration-dependent manner by triggering hallmark morphological events, including chromatin condensation, nuclear fragmentation, and the formation of apoptotic bodies^[1].
EGFR-IN-173 (0.01-1 μM, 48 h) inhibits EGFR phosphorylation and suppresses the downstream pathways (MAPK/ERK, AKT, STAT3) in a dose-dependent manner, ultimately triggering apoptosis and the degradation of signaling proteins like ERK1/2^[1].

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

EGFR-IN-173 (25 and 50 mg/kg, P.O., daily for 12 days) demonstrates significant tumor growth inhibition in HCC827 xenograft mouse model^[1].
EGFR-IN-173 (50 mg/kg, P.O., daily for 17 days) exhibits a certain inhibitory effect on the EGFR^{19del/T790M/C797S} triple mutation in Ba/F3-EGFR^{19del/T790M/C797S} xenograft mouse model^[1].

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

583.06

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• [1]. Wang L, et al. Pan-EGFR inhibitor targeting EGFR 19del, L858R/T790M and C797S triple-mutations: Design, synthesis, and pharmacological evaluation. Bioorg Chem. 2025 Sep;164:108878.  [Content Brief]