1. Protein Tyrosine Kinase/RTK
    JAK/STAT Signaling
  2. EGFR
  3. Naquotinib

Naquotinib (Synonyms: ASP8273)

Cat. No.: HY-19729
Handling Instructions

Naquotinib (ASP8273) is an orally available, mutant-selective and irreversible EGFR inhibitor; with IC50s of 8-33 nM toward EGFR mutants and 230 nM for EGFR.

For research use only. We do not sell to patients.

Naquotinib Chemical Structure

Naquotinib Chemical Structure

CAS No. : 1448232-80-1

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Naquotinib (ASP8273) is an orally available, mutant-selective and irreversible EGFR inhibitor; with IC50s of 8-33 nM toward EGFR mutants and 230 nM for EGFR.

IC50 & Target[1]


230 nM (IC50)







EGFRExon 19 deletion/T790M


In Vitro

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[1]. 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[2].

In Vivo

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[2].

Clinical Trial
Molecular Weight







O=C(C1=NC(CC)=C(O[[email protected]]2CN(C(C=C)=O)CC2)N=C1NC3=CC=C(N4CCC(N5CCN(C)CC5)CC4)C=C3)N


Room temperature in continental US; may vary elsewhere.


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NaquotinibASP8273ASP 8273ASP-8273EGFREpidermal growth factor receptorErbB-1HER1Inhibitorinhibitorinhibit

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