EGFR-targeting proteolysis targeting chimeras (PROTACs) offer a potential strategy to overcome drug resistance mediated by various mutants. A number of EGFR-targeting PROTACs designed to degrade EGFR mutant proteins are based on either the first, second, or third generations of EGFR inhibitors, and rare data shows EGFR-targeting PROTACs that
In this study, we used a 2D well plate and a 3D lung chip to test the effects of three kinds of EGFR-targeted drugs, (i.e, the first-generation EGFR-targeted drug gefitinib, the second-generation EGFR-targeted drug afatinib, and the third-generation EGFR-targeted drug osimertinib) with different concentrations on the viability of HCI-H1650 cells.
There are 102 EGFR-targeted drugs that are approved globally and in clinical research in total. Up to now, there are 20 EGFR-targeted drugs approved by the
It is known that all patients with mutant EGFR will ultimately generate resistance to EGFR TKI therapy after first or secondary generation EGFR TKI. Drugs targeting these mutations have been published, such as third-generation EGFR TKIs. Now, four-generation EGFR TKIs targeting three-generation drug resistance drugs are also on the road. Then what?
Significant advances have been made in the novel targeted drugs specifically targeting the EGFR Ex20ins in NSCLC, however, the efficacy data
Additionally, EGFR is responsible for maintaining the functions of CSCs, indicating the potential for combining TMZ with EGFR-targeting drugs for GBM treatment. In Table 1, the clinical trials investigating the combination of TMZ with targeted EGFR drugs are summarized. The combination effects of erlotinib, afatinib, and ABT-414 with TMZ were
Drugs that target EGFR (EGFR inhibitors) can be used to treat some advanced colon or rectal cancers. These include: Cetuximab (Erbitux)
Exon 19 deletions and exon 21 L858R point mutations represent the majority of EGFR mutations sensitive to targeted treatment with EGFR drivers in lung cancers to select targeted drugs. J. Am.
Since the initial identification of the EGFR gene as a driver in the development of NSCLC, there has been a demand for drugs targeting EGFR. Advancements in molecular targeting drugs, known as EGFR-TKIs, have significantly improved the progression-free survival and overall survival of patients with lung cancer harboring EGFR mutations (Hsu et
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