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NST-628

CAS No. : 3002056-30-3

MCE 國際站：NST-628

產(chǎn)品活性：NST-628 是具有血腦屏障滲透性的 MAPK 通路分子膠，能夠抑制 RAF 磷酸化和 MEK 激活。NST-628 還結(jié)合 RAF，并阻止 BRAF-CRAF 和 BRAF-ARAF 異二聚體的形成，有效抑制 RAS-MAPK 通路。NST-628 可抑制 RAS 和 RAF 驅(qū)動的癌癥，并在突變KRAS、NRAS、BRAF II/III 類和 NF1 突變腫瘤中表現(xiàn)出有效抑制。

研究領(lǐng)域：PROTAC  |  MAPK/ERK Pathway

作用靶點：Molecular Glues  |  Raf  |  MEK

In Vitro: NST-628 (100 nM; 2 h) has higher antiproliferative activity in BRAF class II/III mutant cell models compared to other RAF and MEK inhibitors, and it does not promote the formation of BRAF and CRAF heterodimers.
NST-628 (4-100 nM; 48 h) increases the levels of early and late apoptotic cells and reduces the number of live cells in a dose-dependent manner in NRAS mutant IPC-298 and SK-MEL-2, NF1 mutant MeWo, and KRAS mutant HCT116 cell lines.

In Vivo: qd: once daily ; b.i.d: twice daily
NST-628 (p.o.; 3 mg/kg; qd, 5 mg/kg; qd, or 1.5 mg/kg; b.i.d) can significantly slow tumor growth in mouse models with KRAS and NRAS mutations. NST-628 also leads to tumor regressions in the SK-MEL-2-luc model.
NST-628 (i.g.; 0.3-3 mg/kg; qd; 18-20 days) inhibites the RAS-MAPK pathway in mice in a dose-dependent manner. NST-628 also exhibites strong antitumor activity in the MeWo-luc model.
NST-628 (i.g.; 2 mg/kg; qd; 26 days) slows tumor growth and effectively inhibits the RASMAPK pathway in NCI-H23 KRASG12C-mutant lung adenocarcinoma model.

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