egfr-in-9

EGFR-IN-9 is a potent EGFR kinase inhibitor with IC50s of 7 nM, 28 nM for the wild type EGFR kinase and double mutant EGFR kinase (L858R/T790M). EGFR-IN-9 has antitumor activity.

EGFR-IN-91 (compound 9) is an orally active EGFR inhibitor capable of crossing the blood-brain barrier. It effectively inhibits EGFRL858R/C797S and EGFRexon 19del/C797S, leading to tumor regression in patient-derived xenograft (PDX) mouse models. EGFR-IN-91 shows potential for inhibiting locally advanced and metastatic non-small cell lung cancer (NSCLC) driven by EGFR mutations.

EGFR-IN-95 is a derivative of 2,4-diaminonicotinamide. It effectively inhibits the activity of EGFRdel19/T790M/C797S and L858R/T790M/C797S.

EGFR-IN-94 (compound 5a) is an EGFR inhibitor with an IC50 of 0.086 μM. It exhibits IC50 values of 0.107 μM for VEGFR-2 and 2.52 μM for Topo II. In HepG-2 cells, EGFR-IN-94 induces apoptosis and causes cell cycle arrest at the S phase.

EGFR-IN-92 (compound 15) is an allosteric inhibitor targeting both T790M and L858R double-mutated EGFR. It exhibits antiproliferative activity against H1975 non-small cell lung cancer (NSCLC) cells expressing these double mutations.

EGFR-IN-93 (compound 18) is an allosteric inhibitor of the T790M/L858R double mutant EGFR. It is applicable for research in non-small cell lung cancer (NSCLC).

EGFR-IN-96 (compound 7a) is a thiophene[2,3-d]pyrimidine EGFR inhibitor that can induce apoptosis. It causes HepG2 cells to arrest in the S and G2/M phases and inhibits the growth of cancer cells with wild-type EGFR and EGFRT790M.

EGFR-IN-98 (Compound 4c) is an EGFR inhibitor, exhibiting IC50 values of 0.277 μM for L858R/T790M/C797S and 0.089 μM for Del19/T790M/C797S enzymes. It is applicable in tumor research.

EGFR-IN-99 (JBJ-03-142-02) is an EGFR and HER2 Exon 20 insertion mutation inhibitor with antiproliferative activity for the study of non-small cell lung cancer (NSCLC).

EGFR-IN-90 (compound 34), an orally active EGFR inhibitor, demonstrates potent activity against EGFRL858R/T790M/C797S with an IC50 of 5.1 nM and effectively inhibits the proliferation of the H1975-TM cell line carrying EGFRL858R/T790M/C797S mutations with an IC50 of 0.05 μM. Additionally, EGFR-IN-90 suppresses tumor growth in the H1975-TM xenograft tumor model [1].

EGFR-IN-97 (compound 6q), an EGFR inhibitor, demonstrates effectiveness in inhibiting Ba/F3-EGFR L858R/T790M/C797S and Ba/F3-EGFR Del19/T790M/C797S cells, exhibiting IC 50 values of 0.42 μM and 0.41 μM, respectively. Additionally, at a concentration of 0.8 μM, EGFR-IN-97 is capable of inducing apoptosis in NCI-H1975-EGFR L858R/T790M/C797S cells [1].

EGFR/VEGFR2-IN-3 (compound 9) is an effective inhibitor of EGFR and VEGFR-2, demonstrating IC50 values of 0.129 µM for EGFR, 0.142 µM for VEGFR-2, and 3.428 µM for COX-2. This compound exhibits cytotoxic properties and induces cell apoptosis (apoptosis) as well as cell cycle arrest at the G2/M phase.

EGFR-IN-134 (compound 3f) is a triazolo[3,4-a]quinoline derivative and functions as a potent EGFR inhibitor with an IC50 of 0.023 µM. It induces apoptosis and necrosis in cells, and causes cell cycle arrest in the G2/M and pre-G1 phases. EGFR-IN-134 modulates the expression of apoptosis-regulating proteins by downregulating anti-apoptotic protein Bcl2 and upregulating pro-apoptotic proteins p53, Bax, and caspases 3, 8, and 9, demonstrating significant antiproliferative and anticancer activities.

EGFRT790M/L858R-IN-9 (Compound 8) is an inhibitor targeting the EGFR-L858R/T790M mutations. It effectively inhibits the phosphorylation of the EGFR-L858R/T790M mutant kinase, demonstrating an IC50 value of 0.0064 µM. Additionally, EGFRT790M/L858R-IN-9 can suppress the proliferation of non-small cell lung cancer (NSCLC) cells, making it useful for cancer research.

SOS1/EGFR-IN-1 (compound SE-9) is a dual-target inhibitor for prostate cancer, effectively suppressing downstream effector molecules through the inhibition of SOS1 and EGFR. It induces apoptosis and G1 phase cell cycle arrest, reducing angiogenesis and migration. In prostate cancer cells PC-3, it demonstrates significant antitumor activity with an IC50 of 0.45±0.03 μM.

Lenalidomide-C6-Br is a conjugate of an E3 ligase ligand and a linker. It is utilized in the synthesis of PROTAC EGFR degrader 9.

7-Bromoheptanoyl chloride is the link (ligand) in the formation of PROTACEGFR degrader 9.

EGFR/VEGFR2-IN-9 (Compound 9b) is an inhibitor of VEGFR-2 (IC50 = 1.325 μM) and EGFR (IC50 = 1.891 μM). It significantly suppresses the proliferation of various cancer cell lines, particularly leukemia cells. EGFR/VEGFR2-IN-9 increases the expression levels of Bax, caspase-3, and p53, while decreasing Bcl-2 expression. This compound induces apoptosis and causes cell cycle arrest at the G1 phase. It is suitable for research on anti-tumor angiogenesis and multidrug-resistant cancers.

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-182 (Compound 4) is an EGFR inhibitor with an IC50 value of 199 nM. It additionally inhibits HSP90 and PI3K, with IC50 values of 5.007 μM and 13.596 μM, respectively. EGFR-IN-182 demonstrates potent antiproliferative activity against MCF-7 and MDA-MB-231 cells. It downregulates Cyclin D1, induces cell cycle arrest, enhances caspase-9 activity, and triggers apoptosis. EGFR-IN-182 also decreases the expression of ERK and AKT and is applicable for breast cancer research.

EGFR/BRAFV600E-IN-6 (Compound 7c) is a dual inhibitor of EGFR and BRAFV600E, with IC50 values of 0.12 μM and 0.05 μM, respectively. It exhibits antiproliferative activity against HT-29, MCF-7, A549, and Panc-1 cells, with IC50 values of 8, 4, 6, and 7 μM. EGFR/BRAFV600E-IN-6 activates caspase-3/8/9, upregulates Bax expression, and downregulates Bcl-2 levels, inducing apoptosis and exhibiting antioxidant properties. It is applicable in cancer research, such as studies on colon cancer.

EGFR/VEGFR2-IN-10 is a selective inhibitor of EGFR, VEGFR2, and COX2 with IC50 values of 8.5, 68, and 158 nM, respectively. This compound can induce G1 phase cell cycle arrest in MCF-7 cells. EGFR/VEGFR2-IN-10 increases the Bax/Bcl-2 ratio, upregulates caspase-8 expression, and elevates caspase-9 protein levels, thereby activating the intrinsic apoptotic pathway. It demonstrates favorable selectivity by inhibiting tumor proliferation, angiogenesis, and inflammation pathways. EGFR/VEGFR2-IN-10 serves as a tool for the study of cervical cancer, liver cancer, colon cancer, and breast cancer.

EGFR/CDK2-IN-5 is a potent dual inhibitor of EGFR and CDK2, with IC50 values of 17.30 nM and 212.10 nM, respectively. It can also inhibit EGFRT790M with an IC50 of 123.8 nM and demonstrates significant anticancer activity. This compound induces cell cycle arrest in the G1 and S phases and promotes apoptosis (apoptosis), characterized by increased levels of caspase-3/9 and Bax and decreased levels of Bcl-2. EGFR/CDK2-IN-5 is applicable in research related to lung cancer, breast cancer, and leukemia.

BI-8128 is a potent EGFR inhibitor with IC50 values of 12, 6.7, 22, 10, and 3 nM for wild-type EGFR and the T790M, C797S, T790M/C797S, and L858R/T790M/C797S mutant forms, respectively. It significantly inhibits the proliferation of Ba/F3 and PC-9 cells with resistant mutations. BI-8128 is applicable for research in non-small cell lung cancer.