egfrl858r/t790m/c797s

EGFR-IN-11 is a selective inhibitor of EGFR-tyrosine kinase and induces cell apoptosis. EGFR-IN-11 inhibits triple mutant EGFRL858R/T790M/C797S with an IC50 of 18 nM and arrests cell cycle at G0/G1.

EGFR-IN-5 is a selective inhibitor of EGFR. The IC50s for EGFR, EGFR(L858R), EGFR(L858R/T790M), and EGFR(L858R/T790M/C797S) are 10.4, 1.1, 34, 7.2 nM, respectively.

EGFR mutant- in-1, A 5-methylpyrimidopyridone derivative are effective selective EGFRL858R/T790M/C797S mutant inhibitors with IC50 of 27.5 nM, which significantly weakened EGFRWT effect.

JBJ-04-125-02 can inhibit cancer cell proliferation and EGFRL858R/T790M/C797S signaling. JBJ-04-125-02 has anti-tumor activities. JBJ-04-125-02 is a potent, mutant-selective, allosteric and orally active EGFR inhibitor with an IC50 of 0.26 nM for EGFRL858

JND3229 is a reversible EGFRC797S inhibitor with IC50 values of 5.8, 6.8 and 30.5 nM for EGFRL858R/T790M/C797S, EGFRWT and EGFRL858R/T790M, respectively. JND3229 has good anti-proliferative activity and can effectively inhibit tumour growth in vivo. JND3229 can be used in cancer research, especially in non-small cell carcinoma.

EGFR-IN-126 (compound 9d) is an effective inhibitor of EGFR L858R/T790M/C797S, displaying an IC50 value of 0.005 μM. It exhibits antitumor activity both in vivo and in vitro.

EGFR-IN-140 (Compound 31) is an inhibitor of EGFR, effectively targeting both wild-type EGFR and the EGFRL858R/T790M/C797S mutant, with Ki values of 0.95 nM and 2.1 nM, respectively. Additionally, it inhibits EGFRdel19/T790M/C797S in Ba/F3 cells with an IC50 of 56.9 nM and demonstrates antitumor activity in mouse models.

LSD1/EGFR-IN-1 (compound L-1) is an effective inhibitor of LSD1, EGFRT790M/L858R, and EGFRL858R/T790M/C797S, with IC50 values of 6.24, 2.06, and 5.01 μM, respectively. This compound plays a significant role in cancer research.

EGFR-IN-160 is an EGFR inhibitor with IC50 values of 1.62, 0.49, and 0.98 μM for EGFRWT, EGFRT790M, and EGFRL858R/T790M/C797S, respectively. It can induce cell cycle arrest at the G2/M and S phases and apoptosis (Apoptosis) in NCI-H522 cells, demonstrating anticancer properties. Additionally, EGFR-IN-160 exhibits antioxidant activity against DPPH (IC50: 12.11 µM) and H2O2 (IC50: 8.89 µM).

EGFR kinase inhibitor 2 (compound A-7) is a potent EGFR inhibitor targeting the mutations EGFRL858R/T790M/C797S and EGFRDel19/T790M/C797S. This compound shows potential in addressing acquired resistance in the treatment of non-small cell lung cancer.

PROTACEGFRdegrader 9 (Compound C6) is an orally active, CRBN-based PROTAC EGFR degrader. It has a DC50 of 10.2 nM and a Kd of 240.2 nM against EGFRL858R/T790M/C797S. PROTACEGFRdegrader 9 demonstrates effective degradation activity against various EGFR mutants while not affecting EGFRWT.

ZSH-2117 is a covalent and selective EGFR PROTAC degrader, with a DC50 of 45 nM in Ba/F3-EGFR[L858R/T790M/C797S] cells. It significantly inhibits cell proliferation and reduces AKT and ERK protein levels in downstream EGFR signaling pathways. ZSH-2117 effectively suppresses tumor growth in Ba/F3-EGFR[L858R/T790M/C797S] xenograft mouse models.

EGFR-IN-164 (Compound 4) is a selective covalent allosteric inhibitor of EGFR. It effectively inhibits the activity of EGFR^L858R/T790M/C797S kinase with an IC50 of 48.1 nM and suppresses the proliferation of EGFR-mutant cells. EGFR-IN-164 is applicable in research focused on cancer resistance.

PROTACEGFRdegrader 14 is a potent and selective EGFR PROTAC degrader with a DC50 value of approximately 2.9 nM against EGFRL858R/T790M/C797S and a Dmax of 93.1%. It induces the selective degradation of EGFRC797S via a VHL and proteasome-dependent mechanism, downregulating EGFR-related transcriptomes. PROTACEGFRdegrader 14 exhibits high selectivity for EGFRWT, induces cell cycle arrest and apoptosis, and effectively inhibits tumor growth. It is applicable for research on non-small cell lung cancer (NSCLC).

EGFR-IN-175 is an orally active and selective EGFRL858R/T790M/C797S inhibitor, with an IC50 value of 18.94 nM. It induces apoptosis and causes G1 phase arrest. Additionally, EGFR-IN-175 downregulates the expression of p-EGFR, p-AKT, and p-ERK. It is applicable in cancer research, including studies on lung cancer.

EGFR-IN-176 is an orally active and ATP-competitive inhibitor specifically targeting mutated forms of EGFR, particularly the C797S-mediated EGFR triple mutant. It effectively inhibits the activation of the AKT signaling pathway and induces apoptosis in Ba/F3 and PC-9 cells, which express EGFR19del/T790M/C797S or EGFRL858R/T790M/C797S mutations, respectively. EGFR-IN-176 selectively blocks EGFR signaling in cell lines with the EGFR triple mutation, without affecting wild-type EGFR expressed in A431 cells. Additionally, EGFR-IN-176 effectively inhibits ALK enzyme activity with an IC50 of less than 0.5 nM and is useful in the study of non-small cell lung cancer.

EGFR-IN-179 (Compound 8d) is an EGFR inhibitor with an IC50 of 0.068 μM for EGFRL858R/T790M/C797S and 2.56 μM for EGFR-WT-TK. It exhibits anticancer activity against non-small cell lung cancer.

EGFR-IN-152 (compound D4) is a potent inhibitor of the EGFR tyrosine kinase and exhibits significant inhibitory activity against the EGFRL858R/T790M/C797S mutations (IC50= 40 nM). It induces cell cycle arrest at the G0/G1 phase and apoptosis, thereby hindering the clonogenic growth and proliferation of non-small cell lung cancer (NSCLC) cells. EGFR-IN-152 is applicable for NSCLC research.

EGFR-IN-47 (compound 14aj) is a potent, fourth-generation, and orally active EGFR inhibitor. It specifically targets the EGFR L858R/T790M/C797S triple mutation with an IC50 of 0.01 uM. In NSCLC research, EGFR-IN-47 effectively overcomes C797S-mediated resistance to Osimertinib by inhibiting the phosphorylation of EGFR and its downstream mediators, subsequently inducing cell cycle arrest and apoptosis.

JBJ-09-063 is a mutant-selective allosteric inhibitor of the epidermal growth factor receptor (EGFR), with potent inhibitory activity demonstrated by half-maximal inhibitory concentrations (IC50s) of 0.147 nM for EGFR L858R, 0.063 nM for EGFR L858R/T790M, 0.083 nM for EGFR L858R/T790M/C797S, and 0.396 nM for EGFR L747S. This compound effectively decreases phosphorylation of EGFR, Akt, and ERK1/2, showing efficacy in both EGFR tyrosine kinase inhibitor (TKI)-sensitive and resistant models. JBJ-09-063 holds potential for research into EGFR-mutant lung cancer.

JBJ-09-063 hydrochloride is an EGFR inhibitor selective for mutants, demonstrating IC50 values of 0.147 nM, 0.063 nM, 0.083 nM, and 0.396 nM against EGFR L858R, EGFR L858R/T790M, EGFR L858R/T790M/C797S, and EGFR L747S, respectively. It effectively inhibits EGFR, Akt, and ERK1/2 phosphorylation, showing efficacy in both EGFR tyrosine kinase inhibitor (TKI)-sensitive and -resistant models. This compound holds potential for research on EGFR-mutant lung cancer.

EGFR-IN-69 is a potent inhibitor of the EGFR enzyme, demonstrating IC50 values of 4.3 nM for EGFR L858R/T790M/C797S, 6.6 nM for EGFR L858R/T790M, and 25.6 nM for EGFR 19del/T790M/C797S. This compound is utilized in the research of non-small-cell lung cancer (NSCLC).

EGFR-IN-22 is a highly effective inhibitor targeting wild type EGFR and its mutant form, EGFR L858R/T790M/C797S, displaying IC50 values of 4.91 nM and 0.54 nM, respectively.

JBJ-09-063 TFA is a mutant-selective allosteric EGFR inhibitor with IC50 values of 0.147 nM for EGFR L858R, 0.063 nM for EGFR L858R/T790M, 0.083 nM for EGFR L858R/T790M/C797S, and 0.396 nM for EGFR L747S mutations. It effectively reduces phosphorylation of EGFR, Akt, and ERK1/2, demonstrating efficacy in models both sensitive and resistant to EGFR tyrosine kinase inhibitors (TKI). JBJ-09-063 TFA holds potential for research in EGFR-mutant lung cancer [1].