Currently, there have been no effective treatment options against NSCLC patients with the secondary T790M resistance mutation, which occurs in 50% of patients with acquired resistance to EGFR - TKIs . Here we identified two novel HLA-A2-restricted T cell epitopes derived from the T790M resistance ...
[2] Hao Y, et al.Design, Synthesis, and Biological Evaluation of Pyrimido[4,5- d]pyrimidine-2,4(1 H,3 H)-diones as Potent and SelectiveEpidermal Growth Factor Receptor (EGFR) Inhibitors against L858R/T790M Resistance Mutation. JMed Chem.2018 ...
[2] Hao Y, et al.Design, Synthesis, and Biological Evaluation of Pyrimido[4,5- d]pyrimidine-2,4(1 H,3 H)-diones as Potent and SelectiveEpidermal Growth Factor Receptor (EGFR) Inhibitors against L858R/T790M Resistance Mutation. JMed Chem. 2018 相关产品 AZD-9291(Osimertinib;Mereletinib) A...
[2]Hao Y, et al.Design, Synthesis, and Biological Evaluation of Pyrimido[4,5- d]pyrimidine-2,4(1 H,3 H)-diones as Potent and SelectiveEpidermal Growth Factor Receptor (EGFR) Inhibitors against L858R/T790M Resistance Mutation. JMed Chem. 2018 相关产品 AZD-9291(Osimertinib;Mereletinib) AZD...
[2] Hao Y, et al.Design, Synthesis, and Biological Evaluation of Pyrimido[4,5- d]pyrimidine-2,4(1 H,3 H)-diones as Potent and SelectiveEpidermal Growth Factor Receptor (EGFR) Inhibitors against L858R/T790M Resistance Mutation. JMed Chem. 2018 ...
4.Shang-Gin Wu et al. An Observational Study of Acquired EGFR T790M-Dependent Resistance to EGFR-TKI Treatment in Lung Adenocarcinoma Patients in Taiwan. Front. Oncol., 04 September 2020 https://doi.org/10.3389/fonc.2020.01481 ___ 往期文...
[2]Hao Y, et al.Design, Synthesis, and Biological Evaluation of Pyrimido[4,5- d]pyrimidine-2,4(1 H,3 H)-diones as Potent and SelectiveEpidermal Growth Factor Receptor (EGFR) Inhibitors against L858R/T790M Resistance Mutation.JMed Chem.2018 ...
Acquisition of drug resistance is linked to a specific secondary somatic mutation, EGFR T790M. Here we describe a family with multiple cases of non-small cell lung cancer associated with germline transmission of this mutation. Four of six tumors analyzed showed a secondary somatic activatingmutation,...
most frequently owing to the secondary T790M mutation within the ATP site of the receptor3,4. Recently developed mutant-selective irreversible inhibitors are highly active against the T790M mutant5,6, but their efficacy can be compromised by acquired mutation of C797, the cysteine residue with whic...
tions. The T790M resistance mutation closes this window, in part by increasing the affinity of the mutant receptor for ATP, which in turn diminishes the potency of these ATP-competitive inhibitors 14 . Mutant- selective irreversible inhibitors, including the tool compound WZ4002 ...