Naquotinib (ASP8273) 是有口服活性，不可逆的 EGFR 突变体抑制剂；对EGFR突变体和EGFR的 IC₅₀ 值分别为8-33和230 nM。

Naquotinib (ASP8273) is an orally available, mutant-selective and irreversible EGFR inhibitor; with IC 50 s of 8-33 nM toward EGFR mutants and 230 nM for EGFR.

EGFR 230 nM (IC50) EGFR

In assays using endogenously EGFR-dependent cells, Naquotinib inhibits the growth of PC-9(del ex19), HCC827(del ex19), NCI-H1975(del ex19/T790M) and PC-9ER(del ex19/T790M) with IC50s of 8-33 nM. Naquotinib selectively inhibits phosphorylation of EGFR and its down-stream signal pathway, ERK and Akt from 10nM in HCC827 and NCI-H1975 while inhibitory effects are only detected at 1000nM in A431.In NCI-H1650 (del ex19), Naquotinib inhibits cell growth with an IC50 value of 70nM while other EGFR-TKIs are only partially effective. has not independently confirmed the accuracy of these methods. They are for reference only.

Oral Naquotinib treatment dose dependently induces tumor regression in NCI-H1975 (L858R/T790M), HCC827 (del ex19) and PC-9 (del ex19) xenograft models. Dosing schedules does not affect the efficacy of Naquotinib. In an NCI-H1975 xenograft model, complete regression of tumor is achieved after 14-days of Naquotinib treatment. Complete regression is maintained in 50% of mice more than 85 days after cessation of Naquotinib treatment. has not independently confirmed the accuracy of these methods. They are for reference only.

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[1]. Sakagami H, et al. ASP8273, a novel mutant-selective irreversible EGFR inhibitor, inhibits growth of non-small cell lung cancer (NSCLC) cells with EGFR activating and T790M resistance mutations. [abstract]. In: Proceedings of the 105th Annual Meeting of t
[2]. Konagai S, et al. ASP8273 selectively inhibits mutant EGFR signal pathway and induces tumor shrinkage in EGFR mutated tumor models. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Ph