EGFR Inhibitor

EGFR-IN-12 (EGFR Inhibitor) is a cell permeable and selective inhibitor of EGFR kinase (IC50: 21 nM) and blocks receptor autophosphorylation in cells.

Mutant EGFR inhibitor is a selective and potent Mutated EGFR inhibitor, inhibits L858R activating mutant, the Exonl9 deletion activating mutant and the T790M resistance mutant.

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

EGFR/ErbB-2/ErbB-4 inhibitor-2 (EGFR/ErbB2 Inhibitor) is a cell-permeable compound that inhibits EGFR and c-ErbB2 with IC50 values of 20 nM and 79 nM, respectively.

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.

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).

EGFR kinase inhibitor 6 (Compound 4b) is an orally active epidermal growth factor receptor (EGFR) kinase inhibitor with an IC50 of 24.34 μM. It induces apoptosis and demonstrates anticancer and anti-inflammatory properties, exhibiting low toxicity with an LD50 range of 500-2000 mg/kg.

EGFR kinase inhibitor 1 is a potent inhibitor of EGFR that acts on WT (IC50: 37 nM), l885R/T790M (IC50: 1.7 nM), and L858R/T790M/C797S (IC50>300 nM). It is capable of blocking the cell cycle in G0/G1 phase, inducing apoptosis, and has an inhibitory effect on cell metastasis. Additionally, EGFR kinase inhibitor 1 exhibits anti-proliferative and anti-tumor effects.

EGFR kinase inhibitor 3 (compound 2) serves as a dual-action inhibitor targeting both ATP and allosteric sites of the EGFR kinase, exhibiting potent IC50 values of less than 10 nM for wild-type EGFR, 1.5 nM for the L858R mutation, 0.059 nM for the L858R T790M mutation, and 0.064 nM for the L858R T790M C797S mutation. It is classified as a C-linked inhibitor [1].

EGFR Kinase Inhibitor 4 (Compound 4) acts as a bivalent ATP-allosteric inhibitor targeting EGFR, with a potent inhibitory effect (IC 50: 1.8 nM) on mutant EGFR (LRTMCS). It is primarily utilized in the study of non-small cell lung cancer (NSCLC) [1].

EGFRkinase inhibitor 7 (compound 18i) is an EGFR inhibitor with an IC50 of 42.3 nM, exhibiting anticancer properties. This compound demonstrates significant in vitro cytotoxicity and capacity to induce apoptosis. Furthermore, EGFRkinase inhibitor 7 displays anti-proliferative activity against human colon cancer cell line HCT116 and human non-small cell lung cancer cell line A549, with IC50 values of 4.82 µM and 1.43 µM, respectively.

Gefitinib (ZD1839) is an EGFR first-generation inhibitor with oral activity that inhibits the EGFR 19 Del and L858R mutations. Gefitinib has antitumor activity and is used for the treatment of EGFR-mutated non-small-cell lung cancers. Gefitinib administration RESULTS in the development of the EGFR C797S resistance mutation.

Trastuzumab is a humanized monoclonal antibody for patients with invasive breast cancers that overexpress HER2. Trastuzumab has been clinically used to treat HER2 Positive Metastatic Breast Cancer and HER2 Positive Gastric Cancer.

Leptomycin B (LMB) is a potent inhibitor of the nuclear export of proteins and is a potent antifungal antibiotic blocking the eukaryotic cell cycle. Leptomycin B inactivates CRM1/exportin 1 by covalent modification at a cysteine residue.

Semaxinib (SU5416) is a potent and selective VEGFR2 inhibitor (IC50: 1.23 μM), exhibiting a 20-fold greater selectivity for VEGFR2 over PDGFRβ, with no activity against InsR, EGFR, and FGFR. Semaxinib reversibly inhibits ATP binding to the tyrosine kinase domain of VEGFR2, potentially inhibiting VEGF-stimulated endothelial cell migration and proliferation, thereby reducing tumor microvasculature.

Osimertinib (AZD-9291) is an EGFR third-generation inhibitor that inhibits the T790M resistance mutation produced by second-generation EGFR inhibitors with irreversible and oral activity. Osimertinib has antitumor activity for the treatment of EGFR-mutated non-small-cell lung cancer.

Saracatinib (AZD0530) (AZD0530) is an effective Src inhibitor (IC50: 2.7 nM), and effective to Lck, Fyn, Lyn, Blk, Fgr and c-Yes.

NSC 228155 is an activator of EGFR, binding to the sEGFR dimerization domain II and modulating EGFR tyrosine phosphorylation.

Cetuximab (C225) is a monoclonal antibody that is an inhibitor of human epidermal growth factor receptor (EGFR) (Kd=0.201 nM). Cetuximab has antitumor activity, inhibiting tumor cell proliferation and inducing apoptosis.

Panitumumab is a fully human IgG2 monoclonal antibody targeting the epidermal growth factor receptor EGFR).

BI-4020 is a fourth-generation, orally active, and non-covalent inhibitor of EGFR tyrosine kinase. It exhibits activity against the triple mutant EGFR del19 T790M C797S variant (IC50=0.2 nM in BaF3 cell lines), the double mutant EGFR del19 T790M and primary mutant EGFR del19 (IC50=1 nM), and EGFR wt (IC50=190 nM). BI-4020 also shows high kinome selectivity and good DMPK properties.

CGP52411 is an orally active, and ATP-competitive inhibitor of EGFR (IC50: 0.3 μM). CGP52411 blocks the toxic influx of Ca2+ ions into neuronal cells and dramatically inhibits and reverses the formation of β-amyloid Aβ42 fibril aggregates. CGP52411 can be used in studies about Alzheimer's diseases.

CHMFL-EGFR-202 is a potent, irreversible inhibitor of EGFR mutant kinase with IC50 values of 5.3 nM for drug-resistant mutant EGFR T790M and 8.3 nM for WT EGFR kinases.

CP-547632 is an orally available and potent, ATP-competitive dual inhibitor of VEGFR-2 and FGF kinase F with IC50s of 11 nM and 9 nM, respectively. CP-547632 is selective, with higher selectivity for VEGFR2 and bFGF than for EGFR, PDGFRβ and related tyrosine kinases (TKs). PDGFRβ and related tyrosine kinases (TKs) CP-547632 has antitumour activity.