egfr in 5

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/VEGFR2-IN-5 (Compound 14) is an orally active dual inhibitor of EGFR and VEGFR2, exhibiting an IC50 value of 1.15 µM for VEGFR2 and 0.28 µM for EGFRT790M. This compound demonstrates significant anticancer activity.

EGFR-TK-IN-5 (Compound NCE 2) is a thiazolyl pyrazoline derivative with significant inhibitory activity and stability against EGFR. It is applicable in tumor research.

EGFR/BRAFV600E-IN-5 (Compound 7I) is a dual inhibitor targeting both BRAFV600E and EGFR, with IC50 values of 0.048 μM and 0.037 μM, respectively. It exhibits potent anti-melanoma activity, showing IC50 values of 3.16 μM for MALME-3M cells and 2.50 μM for LOX-IMVI cells. The compound exerts its antitumor effects by inducing G1 phase arrest, inhibiting DNA synthesis, and activating the mitochondrial apoptosis pathway. EGFR/BRAFV600E-IN-5 is useful for melanoma research, especially in studies focusing on the combined inhibition of the BRAFV600E mutation and EGFR signaling pathways.

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.

EGFR/HER2-IN-5 is an irreversible, orally active dual inhibitor of EGFR activity (IC50: 0.6 nM). EGFR/HER2-IN-4 shows potent EGFR kinase inhibitory activity against L858R and T790M mutations. EGFR/HER2-IN-4 exhibits significant anti-tumour effects in vivo and can be used to study lung cancer.

PROTAC EGFR Degrader 5 (Compound 10), a potent degrader of EGFR Del19 in HCC827 cells, achieves this with a DC50 of 34.8 nM. This compound effectively induces apoptosis in HCC827 cells and causes cell cycle arrest in the G1 phase [1].

EGFR T790M/L858R-IN-5 (example 52) functions as a potent EGFR T790M/L858R inhibitor, demonstrating a 92.9% inhibition rate at a concentration of 0.05 μM [1].

PRMT5/EGFR-IN-1 (Compound 10p) is an orally active dual inhibitor targeting PRMT5 and EGFR, with IC50 values of 15.47 μM and 19.31 μM, respectively. It demonstrates antiproliferative activity against the A549, MCF7, HeLa, and MDA-MB-231 cell lines. This compound also exhibits favorable pharmacokinetic (PK) and pharmacodynamic (PD) properties in vivo and significantly inhibits the growth of MCF7 orthotopic xenograft tumors.

EGFRkinase inhibitor 5 (Compound 4c) is an orally active epidermal growth factor receptor (EGFR) kinase inhibitor with an IC50 of 18.35 μM. It induces apoptosis and exhibits anticancer and anti-inflammatory properties while maintaining low toxicity (LD50 range of 500-2000 mg/kg).

[pTyr5] EGFR (988-993) TFA, derived from the Tyr992 autophosphorylation site of the epidermal growth factor receptor (EGFR 988-993), often complexes with catalytically inactive protein-tyrosine phosphate 1B (PTP1B) [1].

[pTyr5] EGFR (988-993) is a compound derived from the auto-phosphorylation site Tyr992 in the epidermal growth factor receptor (EGFR 988-993), and it is often associated with the catalytically inactive protein-tyrosine phosphatase 1B (PTP1B).

EGFR-IN-542 is a novel EGFR inhibitor. EGFR-IN-542 significantly reduces myocardial inflammation, fibrosis, apoptosis and dysfunction. It shows promise for use in the treatment of obesity-induced cardiac complications.

EGFR-IN-53 (Compound 7) is a potent EGFR inhibitor (IC50 = 8.264 μM) with cytotoxic activity against cancer cell lines [1].

EGFR-IN-51 (Compound 6) is a highly potent EGFR inhibitor with IC50 values of 0.493, 102.60, and 461.63 μM against EGFR, EGFR L858R-TK, and EGFR T790M-TK targets, respectively. Additionally, EGFR-IN-51 exhibits cytotoxicity against cancer cell lines, effectively inducing apoptosis [1].

EGFR-IN-52 (Compound 4) is a highly effective inhibitor of the epidermal growth factor receptor (EGFR) with IC50 values of 0.358, 86.02, and 432.67 μM against EGFR, EGFR L858R-TK, and EGFR T790M-TK, respectively. Additionally, it demonstrates potent cytotoxic effects on cancer cell lines and triggers apoptosis [1].

EGFR-IN-57 (Compound 25a) is a potent, orally active EGFR tyrosine kinase (EGFR-TK) inhibitor with an IC50 of 0.054 μM. It also inhibits VEGFR-2, CK2α, topoisomerase IIβ, and tubulin polymerization with IC50 values of 0.087, 0.171, 0.13, and 3.61 μM, respectively. The compound promotes cell cycle arrest at the G2/M and pre-G1 phases and induces apoptosis in cancer cells [1].

EGFR-IN-54 (Compound 3c) is a potent EGFR inhibitor (IC50: 1.623 μM) with cytotoxicity against cancer cells.

EGFR-IN-56 (Compound 13a) is a potent inhibitor of EGFR, targeting EGFRT790M (IC50: 541.7 nM) and EGFRT790M/L858R (IC50: 132.1 nM), blocking the G2/M phase of the cancer cell cycle and inducing apoptosis.

EGFR-IN-59 is a potent and selective EGFR inhibitor. It downregulates PI3K/AKT/mTOR signaling by blocking receptor autophosphorylation, exhibiting significant anti-proliferative activity in A431 and NSCLC cells.

EGFR-IN-55 is a potent inhibitor of EGFR, acting on EGFRWT (IC50: 70 nM) and EGFRL858R/T790M (IC50: 3.9 nM). EGFR-IN-55 was able to block the cell cycle of NCI-H1975 cells in G0/G1 phase, exhibiting anticancer effects.

EGFR-IN-58 is a potent, selective, ATP-competitive inhibitor of EGFR. EGFR-IN-58 exhibits significant cytotoxicity against melanoma, colon and blood cancers.

EGFR-IN-50 is a potent EGFR inhibitor targeting L858R resistance mutations, acting on TEL-EGFR-L858R-BaF3 and TEL-EGFR-T790M-L858R-BaF3 with GI50 values of 8 nM and 6.03 μM, respectively. EGFR-IN-50 exhibits anti-proliferative effects on cancer cells. .

Diethanolamine Fusidate is a bacteriostatic antibiotic with similar activity and better absorption after oral administration (in animals) than the sodium salt of Fusidic Acid. This product inhibits protein synthesis in prokaryotes by inhibiting the ribosome-dependent activity of G factor and translocation of peptidyl-tRNA.