- |||||||||| canertinib (CI-1033) / Pfizer
Journal: Oncogenic fusion of BCAR4 activates EGFR signaling and is sensitive to dual inhibition of EGFR/HER2. (Pubmed Central) - Sep 13, 2022 In addition, canertinib treatment restored E-cadherin expression and reduced the expression of epithelial-mesenchymal transition regulatory factors such as Slug and Snail. Taken together, these results suggest that EGFR/HER2 inhibitors are potential therapeutic options for BCAR4 fusion-harboring lung cancer patients, even in the absence of EGFR mutations.
- |||||||||| canertinib (CI-1033) / Pfizer
Journal: M1 Macrophages Enhance Survival and Invasion of Oral Squamous Cell Carcinoma by Inducing GDF15-Mediated ErbB2 Phosphorylation. (Pubmed Central) - Apr 14, 2022 The ErbB2 phosphorylation inhibitor (CI-1033) and GDF15 knockout cell lines were used to appraise the role of ErbB2 and GDF15 in mediating the effects of M1-CM...Our results demonstrate that M1 macrophages induce the proliferation, migration, invasion, and xenograft development of OSCC cells. Mechanistically, this protumor effect of M1 macrophages is partly associated with inducing GDF15-mediated ErbB2 phosphorylation.
- |||||||||| nazartinib (EGF816) / Novartis, canertinib (CI-1033) / Pfizer, Vizimpro (dacomitinib) / Pfizer
Journal: New C2- and N3-Modified Thieno[2,3-d]Pyrimidine Conjugates with Cytotoxicity in the Nanomolar Range. (Pubmed Central) - Apr 13, 2022 Based on the analysis of the structure-activity relationship, the observed trends in the cytotoxicity could be related to the lipophilicity and the topological polar surface area of the tested compounds. The docking study on the potential of the new thieno[2,3-d]pyrimidine-4-ones to interact with mutant B-Raf showed that the compounds might be able to stabilize the enzyme in its inactive form.
- |||||||||| canertinib (CI-1033) / Pfizer, Gilotrif (afatinib) / Boehringer Ingelheim, Vizimpro (dacomitinib) / Pfizer
Clinical, Journal: Potential applications of clickable probes in EGFR activity visualization and prediction of EGFR-TKI therapy response for NSCLC patients. (Pubmed Central) - Feb 16, 2022 Moreover, 13 was applied to visualize EGFR mutant activity in tumour tissues from non-small-cell lung cancer (NSCLC) xenograft mouse models, and patients with NSCLC for the prediction of EGFR-TKI sensitivity. These results demonstrate that strategically designed EGFR-TKI-based probes allow discriminating EGFR mutations in human tissues and hold promise as useful diagnostic tools in predicting EGFR-TKI therapy response.
- |||||||||| Selective vulnerability of GBM PDX to a panel of EGFR tyrosine kinase inhibitors (Virtual Meeting II: E-Posters) - May 16, 2020 - Abstract #AACRII2020AACR-II_2319;
GBM76 had IC50 values of 1-8uM with all seven EGFR inhibitors including AZD3759...The drug response mechanism and its correlation with the mutation status of CDKN2A, EGFR, and PTEN will be further investigated cross a broad array of GBM PDX models. Supported by NIH NCI R01 CA204136
- |||||||||| canertinib (CI-1033) / Pfizer
Journal: Parathyroid hormone-like hormone plays a dual role in neuroblastoma depending on PTH1R expression. (Pubmed Central) - May 1, 2020 Accordingly, irreversible EGFR inhibition with canertinib abolished PTHLH expression...This study provides the first evidence of the dual role of PTHLH in the behavior of neuroblastomas. Moreover, identification of the molecule responsible for PTHLH production, EGFR, in neuroblastoma provides novel therapeutic opportunities, since decreased of PTHLH production can be achieved specifically in primary tumors with an irreversible inhibitor of EGFR, leading to a milder neuroblastoma phenotype, without damaging normal tissues.
- |||||||||| canertinib (CI-1033) / Pfizer
Targeting constitutive activation of the EGFR-STAT1 axis decreases proliferation of meningioma tumour cells (Ballroom Lawn) - Oct 29, 2019 - Abstract #SNO2019SNO_396; It caused a significant reduction in meningioma cells proliferation and a reduction of overall levels of Cyclin D1, phospho- AKT and phospho-ERK 1/2. Hence, STAT1 constitutive phosphorylation, initiated by EGFR activation, is responsible for inducing a positive feedback loop causing its own overexpression and consequently an increased proliferation of the tumour cells. These findings underline a pivotal role of the EGFR and STAT1 axis in meningioma and provides the rationale for further studies aiming to identify novel and effective therapeutic options.
- |||||||||| canertinib (CI-1033) / Pfizer
Preclinical, Journal: Insulin-like growth factor binding protein-4 inhibits epithelial growth and proliferation in the rodent intestine. (Pubmed Central) - Jul 4, 2019 ...To investigate whether this occurs through the actions of its intermediaries, IGF-1 and EGF, inducible intestinal epithelial-IGF-1R knockout and control mice were treated for 10 days with and without the pan-ErbB inhibitor, CI-1033...Consistently, IEC-6 cells treated with IGF-1 and/or EGF displayed no alteration in IGFBP-4 mRNA or in cellular and secreted IGFBP-4 protein (p>0.05). Overall, this study establishes that endogenous IGFBP-4 plays an important role in inhibiting IGF-1-induced intestinal epithelial proliferation, and that mucosal IGFBP-4 expression is independent of IGF-1 and EGF.
- |||||||||| Xegafri (rociletinib) / Clovis, canertinib (CI-1033) / Pfizer
Biomarker, Clinical, Review, Journal: Safety and Tolerability of Epidermal Growth Factor Receptor (EGFR) Tyrosine Kinase Inhibitors in Oncology. (Pubmed Central) - Jun 30, 2019 However, available data reviewed herein indicate that not only are these newer agents associated with the aforementioned adverse effects typical of earlier agents, but they are also susceptible to resistance due to tertiary mutations, most frequently C797S. At least three later-generation EGFR-TKIs, canertinib, naquotinib and rociletinib, have been discontinued from further development in NSCLC following concerns about their safety and risk/benefit.
- |||||||||| Erbitux (cetuximab) / Eli Lilly, EMD Serono
Journal: BRAF inhibition upregulates a variety of receptor tyrosine kinases and their downstream effector Gab2 in colorectal cancer cell lines. (Pubmed Central) - Mar 27, 2019 ...This unresponsiveness was mechanistically attributed to the loss of negative feedbacks on the epidermal growth factor receptor (EGFR) and initiated clinical trials that combine BRAF (and MEK) inhibitors, either singly or in combination, with the anti-EGFR antibodies cetuximab or panitumumab...Importantly, combination of the BRAF inhibitors (BRAFi) vemurafenib (PLX4032), dabrafenib, or encorafenib with inhibitors dually targeting the EGFR and HER2 (such as lapatinib, canertinib, and afatinib) significantly reduced the metabolic activity and proliferative potential of CRC cells...Furthermore, Gab2 and Gab2-mediated Shp2 signaling were shown to be functionally important in BRAFi resistance. These findings highlight potential new escape mechanisms to these targeted therapies and indicate that a broad suppression of RTK signaling might be beneficial and should be taken into account in future research addressing targeted therapy in BRAF-mutant CRC.
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