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Overview
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Please contact us at for specific academic pricing.
Background
IC50: 0.3 to 0.8 μM
NT157 is an IRS-1/2 inhibitor.
Insulin receptor substrates 1 and 2 (IRS1/2) mediate antiapoptotic and mitogenic signaling from insulin receptor (IR), insulin-like growth factor 1 receptor (IGF-IR), and other oncoproteins. IRS1 plays a critical role in cancer cell proliferation, and its expression is increased in many human malignancies.
In vitro: NT157 treatment was fonund to be able to lead to dose-dependent suppression of IRS protein expression, inhibition of IGF1R activation, inhibition of IGF1-induced AKT activation, but increased ERK activation in NT157-treated cells. These effects were associated with decreased proliferation, increased apoptosis of LNCaP cells and increased G2-M arrest in PC3 cells. Moreover, NT157 could significantly affect the cell migratory ability, as demonstrated by a wound-healing assay. In addition, the NT157 treatment was able to induce cell cycle arrest and inhibit IGF system signaling [1].
In vivo: In previous animal study, NT157 was found to suppress androgen-responsive growth, delay CRPC progression of LNCaP xenografts, and suppress PC3 tumor growth alone or in combination with docetaxel. This study reported the first preclinical proof-of-principle data that NT157 suppressed IRS1/2 expression, delayed CRPC progression, and suppressed growth of CRPC tumors in vivo [1].
Clinical trial: Up to now, NT157 is still in the preclinical development stage.
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