egfr mutants

EAI045, an allosteric inhibitor, targets towards drug-resistant EGFR mutants but avoids the wild-type receptor.

PF-06459988 is a novel, effective, orally active, irreversible, and selective epidermal growth factor receptor (EGFR) mutant inhibitor. PF-06459988 has high efficiency and high affinity for EGFRs double mutants containing T790M, and has minimal activity against WT EGFR. PF-06459988 makes a candidate drug for the treatment of cancer.

SKLB 1028 (Ruserontinib) is a new type of oral multikinase inhibitor of EGFR, FLT3, and Abl. SKLB 1028 shows excellent activity in FLT3-driven AML models and considerable potency in CML models containing Abl mutants.

Poziotinib hydrochloride irreversibly inhibits EGFR (HER1 or ErbB1), including EGFR mutants, HER2, and HER4, thereby inhibiting the proliferation of tumor cells that overexpress these receptors. It is an orally bioavailable, quinazoline-based pan epidermal growth factor receptor (EGFR or HER) inhibitor with potential antineoplastic activity.

MS 154N is a negative control for MS 154. The compound exhibits high binding-affinity for WT and L858R-mutant EGFR (Kdvalues are 3 and 4.3 nM, respectively), but does not significantly induce degradation of EGFR mutants.

Naquotinib mesylate (ASP8273 (mesylate)) is an orally available, mutant-selective and irreversible inhibitor of EGFR(iC50s of 8-33 nM and 230 nM for toward EGFR mutants and EGFR).

DDC-01-163 is a selective PROTAC degrader targeting EGFR mutants, with an IC50 of 45 nM.

Icotinib Hydrochloride (BPI-2009H) is the hydrochloride salt form of icotinib, an orally available quinazoline-based inhibitor of EGFR, with potential antineoplastic activity. Icotinib selectively inhibits the wild-type and several mutated forms of EGFR tyrosine kinase. This may lead to an inhibition of EGFR-mediated signal transduction and may inhibit cancer cell proliferation. EGFR, a receptor tyrosine kinase, has been upregulated in a variety of cancer cell types.

EMI56, a derivative of EMI1, exhibits enhanced potency against mutant EGFR compared to EMI1. Additionally, EMI56 effectively inhibits EGFR triple mutants[1].

EMI48, a derivative of EMI1, exhibits increased efficacy against mutant EGFR compared to EMI1. It specifically inhibits EGFR triple mutants [1].

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.

ALK EGFR-IN-1 (Compound 8l) is a dual inhibitor targeting both ALK and EGFR, effectively blocking their phosphorylation. It demonstrates potent inhibition of ALK EGFR mutants with IC50 values of 4.3 nM for EGFR L858R T790M in H1975 cells and 3.6 nM for EML4-ALK in BaF3 cells. This compound may be applicable in the research of non-small cell lung cancer (NSCLC) [1].

EGFR mutant-IN-2 (Compound D51) is an inhibitor of EGFR mutants, specifically targeting EGFR L858R T790M C797S and EGFR del19 T790M C797S mutants with IC50 values of 14 nM and 62 nM, respectively. This compound exhibits favorable pharmacokinetic (PK) parameters, safety properties, in vivo stability, and demonstrates antitumor activity [1].

Tuxobertinib (BDTX-189) is a potent and selective inhibitor of allosteric EGFR and HER2 oncogenic mutations, with KDs of 0.2, 0.76, 13, and 1.2 nM for EGFR, HER2, BLK, and RIPK2, respectively, and exhibits anticancer activity.

Naquotinib (ASP8273) (ASP8273) is an orally available, mutant-selective and irreversible EGFR inhibitor; (IC50s: 8-33 nM and 230 nM toward EGFR mutants and EGFR.