Topic
Canertinib
About: Canertinib is a research topic. Over the lifetime, 64 publications have been published within this topic receiving 2052 citations. The topic is also known as: CI 1033 & CI-1033.
Papers published on a yearly basis
Papers
TL;DR: Small molecule inhibitors of tyrosine kinase are an important new class of targeted therapy that interfere with specific cell signaling pathways and thus allow target-specific therapy for selected malignancies.
Abstract: Cancer chemotherapy has been one of the major medical advances in the last few decades. However, the drugs used for this therapy have a narrow therapeutic index, and often the responses produced are only just palliative as well as unpredictable. In contrast, targeted therapy that has been introduced in recent years is directed against cancer-specific molecules and signaling pathways and thus has more limited nonspecific toxicities. Tyrosine kinases are an especially important target because they play an important role in the modulation of growth factor signaling. This review focuses on small molecule inhibitors of tyrosine kinase. They compete with the ATP binding site of the catalytic domain of several oncogenic tyrosine kinases. They are orally active, small molecules that have a favorable safety profile and can be easily combined with other forms of chemotherapy or radiation therapy. Several tyrosine kinase inhibitors (TKIs) have been found to have effective antitumor activity and have been approved or are in clinical trials. The inhibitors discussed in this manuscript are imatinib mesylate (STI571; Gleevec), gefitinib (Iressa), erlotinib (OSI-1774; Tarceva), lapatinib (GW-572016), canertinib (CI-1033), semaxinib (SU5416), vatalanib (PTK787/ZK222584), sorafenib (BAY 43-9006), sutent (SU11248), and leflunomide (SU101). TKIs are thus an important new class of targeted therapy that interfere with specific cell signaling pathways and thus allow target-specific therapy for selected malignancies. The pharmacological properties and anticancer activities of these inhibitors are discussed in this review. Use of these targeted therapies is not without limitations such as the development of resistance and the lack of tumor response in the general population. The availability of newer inhibitors and improved patient selection will help overcome these problems in the future.
1,060 citations
TL;DR: CI-1033 is a highly potent and selective pan-erbB inhibitor that efficiently blocks signal transduction through all four members of the erbB receptor family, and covalently binds to these receptors, irreversibility inhibiting them, and thereby provides for prolonged suppression of erb B receptor-mediated signaling.
106 citations
TL;DR: EGFR has now been validated as a clinically relevant target, and several different types of agents inhibiting this receptor are currently in development, including ZD6474, which has undergone the most extensive clinical testing.
Abstract: The epidermal growth factor receptor (EGFR) inhibitors erlotinib, gefitinib, and cetuximab have undergone extensive clinical testing and have established clinical activity in non-small cell lung cancer and other types of solid tumors. A number of newer inhibitors are currently in clinical development with different spectra of activity or mechanisms of receptor inhibition. These include monoclonal antibodies, such as panitumumab and matuzumab; dual inhibitors of EGFR and vascular endothelial growth factor receptor, such as ZD6474 and AEE788; inhibitors of multiple EGFR family members, such as lapatinib; and irreversible inhibitors, such as canertinib and HKI272. Preclinical studies suggest that several of these agents may have activity in tumors refractory to erlotinib or gefitinib. Among these agents, ZD6474 has undergone the most extensive clinical testing. The antitumor activity of ZD6474 in these two randomized phase II clinical trials in patients with non-small cell lung cancer was felt to be sufficiently promising to warrant phase III clinical testing. Several of the other EGFR inhibitors are also undergoing advanced clinical testing, either alone or in combination with other agents. EGFR has now been validated as a clinically relevant target, and several different types of agents inhibiting this receptor are currently in development. Future research will be needed to elucidate the role of these agents in patients with EGFR inhibitor-naive and EGFR inhibitor-refractory disease, to define the molecular characteristics that predict response, and to determine whether these drugs should be used in combination with other targeted agents or chemotherapy.
104 citations
TL;DR: Interference with FASN and ErbB abrogates their oncogenicity and should be exploited for ovarian cancer treatment, and data indicate that AKT is crucial for ErbbB/FASN interaction, AKT cross-inhibits ERK and feeds loops that boost F ASN and EGFR transcription, and EG FR and ErBB2 must be co-silenced for maximal FASn downregulation.
90 citations
TL;DR: Wang et al. as discussed by the authors used PROTAC to degrade EGFRL858R+T790M resistant proteins in H1975 cells at the concentration of 30-50 nM, and EGFREx19del proteins in PC9 cells.
75 citations
Related Topics (5)
Performance Metrics
| Year | Papers |
|---|---|
| 2021 | 2 |
| 2020 | 1 |
| 2019 | 5 |
| 2018 | 4 |
| 2017 | 7 |
| 2016 | 5 |