mutated egfr-in-2

Mutated EGFR-IN-2 is an inhibitor of mutant-selective EGFR.

EGFR/ErbB-2 inhibitor-1 is a selective ErbB2/HER2 inhibitor that effectively blocks ErbB2 and HER2 signaling.

Mutated EGFR-IN-3 is a ATP-competitive and highly selective allosteric dibenzodiazepinone EGFR(L858R/T790M) and EGFR(L858R/T790M/C797S) inhibitor(IC50 of 12 nM and 13 nM, respectively. )

EGFR/HER2/DHFR-IN-2 (Compound 4b) serves as an inhibitor for EGFR, HER2, and DHFR, with IC50 values of 0.248, 0.156, and 0.138 μM, respectively. It exhibits anticancer activity, displaying IC50 values of 9.14, 7.33, 14.18, 24.87, 20.07, and 6.16 μM in Hep G2, HeLa, HEp-2, HCT 116, PC-3, and MCF7 cancer cell lines, respectively. Additionally, EGFR/HER2/DHFR-IN-2 has been shown to reduce the growth of breast cancer tumors [1].

PROTAC EGFR degrader 2 is a potent compound with exceptional antiproliferative activity, evidenced by its IC50 of 4.0 nM, and exhibits strong EGFR degradation activity with a DC50 of 36.51 nM. It is suitable for synthesizing nitroreductase (NTR)-responsive PROTACs [1].

EGFR/CDK2-IN-2 (compound 6a) serves as a dual inhibitor targeting both EGFR and CDK-2, exhibiting IC50 values of 19.6 nM and 87.9 nM, respectively. It promotes apoptosis in MCF-7 cells and halts cell cycle progression during the S phase. Additionally, this compound demonstrates notable anticancer activity, inhibiting MCF-7 cells with an IC50 of 0.39 μM [1].

E07 Aptamer, targeting the human epidermal growth factor receptor (hEGFR), competes with epidermal growth factor (EGF) for binding to a unique epitope on EGFR. This aptamer not only binds to EGFR-expressing cells but also inhibits receptor autophosphorylation and thwarts tumor cell proliferation in three-dimensional matrices, positioning it as a useful tool for tumor disease research [1].

ALK/EGFR-IN-2 is a potent dual inhibitor targeting ALK and EGFR, promoting apoptosis and G0/G1 cell cycle arrest in cancer cells. It effectively suppresses proliferation in H1975, PC9, and Baf3-EML4-ALK cancer cell lines, demonstrating IC50s of 0.0034, 0.0065, and 0.0018 μM, respectively [1].

EGFR/ErbB-2/ErbB-4 inhibitor-2 (EGFR/ErbB2 Inhibitor) is a cell-permeable inhibitor of EGFR and c-ErbB2 (IC50s = 20 and 79 nM, respectively)

Mutated EGFR-IN-1 (Osimertinib analog) is a useful intermediate for the inhibitors design for mutated EGFR, such as L858R EGFR, Exonl9 deletion activating mutant, and T790M resistance mutant.

EGFR/HER2-IN-2 (Compound ZINC35560729) is a dual EGFR and HER2 inhibitor that acts on both EGFR (IC50: 5.02 μM) and HER2 (IC50: 0.83 μM).

EGFR/HER2/TS-IN-2 is a potent inhibitor of EGFR (IC50: 0.173 μM), HER2 (IC50: 0.125 μM) and TS (IC50: 1.12 μM). EGFR/HER2/TS-IN-2 exhibited cytotoxic effects on MDA-MB-231 cancer cells (IC50: 1.69 μM ).

EGFR-IN-2 is a non-covalent, mutation-selective and irreversible second-generation EGFR inhibitor.

EGFR/HER2/CDK9-IN-2 are potent inhibitors of EGFR/HER2/CDK9, and they exhibited significant antitumor effects with IC50s of 145.35, 129.07 and 117.13 nM, respectively.

EGFRT790M/L858R-IN-2 is a potent, selective inhibitor of EGFRT790M/L858R, exhibiting IC50 values of 3.5 nM for EGFRT790M/L858R and 1290 nM for EGFR WT. This compound effectively decreases the expression of p-EGFR, P-AKT, P-ERK1/2, and induces apoptosis as well as cell cycle arrest in the G1 phase, demonstrating anti-cancer activity [1].

Erlotinib (NSC-718781) is an EGFR inhibitor (IC50: 2 nM). It is used for the treatment of non-small cell lung cancer.

MAPK-IN-2 (compound 3h) is an efficacious MAPK inhibitor with antineoplastic properties that significantly hinders proliferation across various cancer cell lines. It demonstrates robust suppression of the MAPK pathway (EGFR WT IC50 = 281 nM, c-MET IC50 = 205 nM, B-RAF WT IC50 = 112 nM, CDK4/6 IC50 = 95 and 184 nM, respectively) and exhibits pronounced activity against mutated forms of EGFR and B-RAF (EGFR T790M IC50 = 69 nM and B-RAF V600E IC50 = 83 nM) [1].