| Identification | Back Directory | [Name]
(E)-3-(3-bromo-4,5-dihydroxyphenyl)-N-(3,4,5-trihydroxybenzyl)prop-2-enethioamide | [CAS]
1384426-12-3 | [Synonyms]
NT-157
CS-5531
CS-2283
AK174915
NT157;NT 157
AKOS025404921
Tyrphostin NT157
NT-157; NT 157; NT157.
NT-157;NT 157;TYRPHOSTIN NT157
NT 157 (This product is only available in Japan.)
(E)-3-(3-bromo-4,5-dihydroxyphenyl)-N-(3,4,5-trihydroxybenzyl)prop-2-enethioamide
(2E)-3-(3-Bromo-4,5-dihydroxyphenyl)-N-[(3,4,5-trihydroxyphenyl)methyl]-2-propenethioamide
2-Propenethioamide, 3-(3-bromo-4,5-dihydroxyphenyl)-N-[(3,4,5-trihydroxyphenyl)methyl]-, (2E)- | [Molecular Formula]
C16H14BrNO5S | [MDL Number]
MFCD28127272 | [MOL File]
1384426-12-3.mol | [Molecular Weight]
412.26 |
| Chemical Properties | Back Directory | [Boiling point ]
660.3±65.0 °C(Predicted) | [density ]
1.794±0.06 g/cm3(Predicted) | [storage temp. ]
Store at -20°C | [solubility ]
insoluble in H2O; ≥21.5 mg/mL in EtOH; ≥50 mg/mL in DMSO | [form ]
solid | [pka]
8.06±0.36(Predicted) | [color ]
Light yellow to yellow |
| Hazard Information | Back Directory | [Uses]
NT157 (Tyrphostin NT157) is a selective IRS-1/2 inhibitor that induces Ser-phosphorylation and consequently the degradation of IRS-1/2. NT157 (Tyrphostin NT157) is a first-in-class anti-cancer agent that also targets Stat3 signaling pathway[1][2]. | [Biological Activity]
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]. | [IC 50]
0.3 to 0.8 μm | [References]
[1] ibuki n et al. the tyrphostin nt157 suppresses insulin receptor substrates and augments therapeutic response of prostate cancer. mol cancer ther. 2014 dec;13(12):2827-39. |
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