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• W2154518689 abstract "The insulin-like growth factor-1 receptor (IGF-1 receptor) is a receptor tyrosine kinase, highly homologous to the insulin receptor. In contrast to the insulin receptor, which is mostly involved in metabolic pathways, the IGF-1 system plays a pivotal role in normal and neoplastic cell growth through anti-apoptotic, proliferative and metastatic pathways. Furthermore, IGF-1 receptor over-activation is found to correlate with a variety of tumors, such as breast cancer, prostate cancer, hematological malignancies, colorectal cancer and other proliferative diseases, such as psoriasis and papilloma. In addition, accumulating evidence implies that blockade of IGF-1 receptor activity causes reversal of tumor progression in cell lines as well as in animal tumor models. Because of the central role the IGF-1 receptor plays in oncogenic maintenance and metastatic processes, it is a highly appropriate target for anti-cancer agents. Here we report on a novel substrate-mimic family of IGF-1 receptor inhibitors. These compounds are tertiary aromatic amines, non-competitive with ATP and possess high affinity towards the IGF-1 receptor. The most potent compound, SBL02 inhibited the IGF-1 receptor with an IC(50) of 170 nM in a cell-free kinase assay and was found to inhibit IGF-1 receptor auto-phosphorylation and substrate phosphorylation at the low micromolar range in cellular assays. SBL02 also blocks the formation of colonies in soft agar by cancer cells and inhibits the growth of keratinocytes and of HPV16 immortalized keratinocytes. This new family of non-ATP competitive, IGF-1 receptor inhibitors can serve as a lead for the development of anti-cancer, anti-psoriatic and anti-papilloma agents." @default.
• W2154518689 created "2016-06-24" @default.
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• W2154518689 date "2007-05-01" @default.
• W2154518689 modified "2023-10-16" @default.
• W2154518689 title "ATP non-competitive IGF-1 receptor kinase inhibitors as lead anti-neoplastic and anti-papilloma agents" @default.
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• W2154518689 doi "https://doi.org/10.1016/j.ejphar.2007.01.052" @default.
• W2154518689 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17376430" @default.
• W2154518689 hasPublicationYear "2007" @default.
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