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Gefitinib

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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-50895
    Gefitinib
    Maximum Cited Publications
    139 Publications Verification

    ZD1839

    		 EGFR Autophagy Apoptosis Cancer
    Gefitinib (ZD1839) is a potent, selective and orally active EGFR tyrosine kinase inhibitor with an IC50 of 33 nM. Gefitinib selectively inhibits EGF-stimulated tumor cell growth (IC50 of 54 nM) and that blocks EGF-stimulated EGFR autophosphorylation in tumor cells. Gefitinib also induces autophagy and cell apoptosis, which can be used for cancer related research, such as Lung cancer and breast cancer .
    Gefitinib
  • HY-100663
    Gefitinib impurity 2

    		EGFR Others Cancer
    Gefitinib impurity 2 is the impurity of Gefitinib. Gefitinib (ZD1839; HY-50895) is a potent, selective and orally active EGFR tyrosine kinase inhibitor with an IC50 of 33 nM. Gefitinib selectively inhibits EGF-stimulated tumor cell growth (IC50 of 54 nM) and that blocks EGF-stimulated EGFR autophosphorylation in tumor cells. Gefitinib also induces autophagy. Gefitinib has antitumour activity .
    Gefitinib impurity 2
  • HY-50895S
    Gefitinib-d8

    ZD1839-d8

    		 EGFR Autophagy Cancer
    Gefitinib-d8 is a deuterium labeled Gefitinib. Gefitinib is an EGFR tyrosine kinase inhibitor, with IC50 of 2-37 nM in NR6wtEGFR cells[1][2].
    Gefitinib-d8
  • HY-50895A
    Gefitinib hydrochloride
    Maximum Cited Publications
    139 Publications Verification

    ZD-1839 hydrochloride

    		 EGFR Cancer
    Gefitinib hydrochloride (ZD1839 hydrochloride) is a potent, selective and orally active EGFR tyrosine kinase inhibitor with an IC50 of 33 nM. Gefitinib hydrochloride selectively inhibits EGF-stimulated tumor cell growth (IC50 of 54 nM) and that blocks EGF-stimulated EGFR autophosphorylation in tumor cells. Gefitinib hydrochloride also induces autophagy. Gefitinib hydrochloride has antitumour activity .
    Gefitinib hydrochloride
  • HY-133779
    Gefitinib impurity 5

    		Drug Metabolite Others Cancer
    Gefitinib impurity 5 is the impurity of Gefitinib. Gefitinib (ZD1839) is a potent, selective and orally active EGFR tyrosine kinase inhibitor with an IC50 of 33 nM. Gefitinib selectively inhibits EGF-stimulated tumor cell growth (IC50 of 54 nM) and that blocks EGF-stimulated EGFR autophosphorylation in tumor cells. Gefitinib also induces autophagy. Gefitinib has antitumour activity .
    Gefitinib impurity 5
  • HY-131257
    Gefitinib impurity 1

    		Drug Metabolite Others Cancer
    Gefitinib impurity 1 is the impurity of Gefitinib. Gefitinib (ZD1839) is a potent, selective and orally active EGFR tyrosine kinase inhibitor with an IC50 of 33 nM. Gefitinib selectively inhibits EGF-stimulated tumor cell growth (IC50 of 54 nM) and that blocks EGF-stimulated EGFR autophosphorylation in tumor cells. Gefitinib also induces autophagy. Gefitinib has antitumour activity .
    Gefitinib impurity 1
  • HY-100636
    Gefitinib N-oxide

    		EGFR Cancer
    Gefitinib N-oxide is the N-oxide derivative of Gefitinib. Gefitinib is an EGFR tyrosine kinase inhibitor, with IC50 of 2-37 nM in NR6wtEGFR cells .
    Gefitinib N-oxide
  • HY-100636A
    Gefitinib N-oxide hydrochloride

    		EGFR Cancer
    Gefitinib N-oxide hydrochloride is the N-oxide derivative of Gefitinib. Gefitinib is an EGFR tyrosine kinase inhibitor, with IC50 of 2-37 nM in NR6wtEGFR cells .
    Gefitinib N-oxide hydrochloride
  • HY-50895S2
    Gefitinib-d3

    		Isotope-Labeled Compounds EGFR Autophagy Cancer
    Gefitinib-d3 (ZD1839-d3) is the deuterium labeled Gefitinib. Gefitinib (ZD1839) is a potent, selective and orally active EGFR tyrosine kinase inhibitor with an IC50 of 33 nM. Gefitinib selectively inhibits EGF-stimulated tumor cell growth (IC50 of 54 nM) and that blocks EGF-stimulated EGFR autophosphorylation in tumor cells. Gefitinib also induces autophagy. Gefitinib has antitumour activity[1][2].
    Gefitinib-d3
  • HY-133779R
    Gefitinib impurity 5 (Standard)

    		Drug Metabolite Others Cancer
    Gefitinib impurity 5 (Standard) is the analytical standard of Gefitinib impurity 5. This product is intended for research and analytical applications. Gefitinib impurity 5 is the impurity of Gefitinib. Gefitinib (ZD1839) is a potent, selective and orally active EGFR tyrosine kinase inhibitor with an IC50 of 33 nM. Gefitinib selectively inhibits EGF-stimulated tumor cell growth (IC50 of 54 nM) and that blocks EGF-stimulated EGFR autophosphorylation in tumor cells. Gefitinib also induces autophagy. Gefitinib has antitumour activity .
    Gefitinib impurity 5 (Standard)
  • HY-50895R
    Gefitinib (Standard)

    ZD1839 (Standard)

    		 EGFR Autophagy Apoptosis Cancer
    Gefitinib (Standard) is the analytical standard of Gefitinib. This product is intended for research and analytical applications. Gefitinib (ZD1839) is a potent, selective and orally active EGFR tyrosine kinase inhibitor with an IC50 of 33 nM. Gefitinib selectively inhibits EGF-stimulated tumor cell growth (IC50 of 54 nM) and that blocks EGF-stimulated EGFR autophosphorylation in tumor cells. Gefitinib also induces autophagy and cell apoptosis, which can be used for cancer related research, such as Lung cancer and breast cancer .
    Gefitinib (Standard)
  • HY-50895G
    Gefitinib

    ZD1839

    		 EGFR Autophagy Apoptosis Cancer
    Gefitinib (ZD1839) (GMP) is Gefitinib (HY-50895) produced by using GMP guidelines. GMP small molecules work appropriately as an auxiliary reagent for cell therapy manufacture. Gefitinib is a potent, selective and orally active EGFR tyrosine kinase inhibitor .
    Gefitinib
  • HY-50895S1
    Gefitinib-d6

    ZD1839-d6

    		 EGFR Autophagy Cancer
    Gefitinib-d6 is the deuterium labeled Gefitinib. Gefitinib (ZD1839) is a potent, selective and orally active EGFR tyrosine kinase inhibitor with an IC50 of 33 nM. Gefitinib selectively inhibits EGF-stimulated tumor cell growth (IC50 of 54 nM) and that blocks EGF-stimulated EGFR autophosphorylation in tumor cells. Gefitinib also induces autophagy. Gefitinib has antitumour activity[1][2].
    Gefitinib-d6
  • HY-50895B
    Gefitinib dihydrochloride

    ZD 1839 dihydrochloride

    		 EGFR Autophagy Apoptosis Cancer
    Gefitinib (ZD 1839) dihydrochloride is a potent, selective and orally active EGFR tyrosine kinase inhibitor with an IC50 of 33 nM. Gefitinib dihydrochloride selectively inhibits EGF-stimulated tumor cell growth (IC50 of 54 nM) and blocks EGF-stimulated EGFR autophosphorylation in tumor cells. Gefitinib dihydrochloride also induces autophagy and cell apoptosis, which can be used for cancer related research, such as Lung cancer and breast cancer .
    Gefitinib dihydrochloride
  • HY-123921
    Gefitinib-based PROTAC 3
    3 Publications Verification

    		 PROTACs EGFR Cancer
    Gefitinib-based PROTAC 3, conjugating an EGFR binding element to a von Hippel-Lindau ligand via a linker, induces EGFR degradation with DC50s of 11.7 nM and 22.3 nM in HCC827(exon 19 del) and H3255 (L858R mutantion) cells, respectively .
    Gefitinib-based PROTAC 3
  • HY-131257R
    Gefitinib impurity 1 (Standard)

    		Drug Metabolite Others Cancer
    Hydroxymetronidazole (Standard) is the analytical standard of Hydroxymetronidazole. This product is intended for research and analytical applications. Hydroxymetronidazole (Metronidazole-OH) is a metabolite of Metronidazole belonging to the class of nitroimidazoles. Hydroxymetronidazole can be used for the research of certain bacterial and protozoal diseases in poultry, swine dysentery and genital trichomoniasis in cattle .
    Gefitinib impurity 1 (Standard)
  • HY-100064
    O-Desmethyl gefitinib

    		EGFR Cancer
    O-Desmethyl gefitinib is an active metabolite of Gefitinib in human plasma. The formation of O-desmethyl gefitinib is dependent on CYP2D6 activity. O-desmethyl gefitinib inhibits EGFR with an IC50 of 36 nM in subcellular assays .
    O-Desmethyl gefitinib
  • HY-148871
    Mc-Val-Cit-PAB-Gefitinib chloride

    		Drug-Linker Conjugates for ADC Cancer
    Mc-Val-Cit-PAB-Gefitinib chloride is a agent-linker conjugates for ADC. Mc-Val-Cit-PAB-Gefitinib chloride consists of Gefitinib (HY-50895) (an EGFR tyrosine kinase inhibitor) and the ADC linker Mc-Val-Cit-PAB .
    Mc-Val-Cit-PAB-Gefitinib chloride
  • HY-100064S1
    O-Desmethyl gefitinib-d6

    		Isotope-Labeled Compounds EGFR Cancer
    O-Desmethyl gefitinib-d6 is the deuterium labeled O-Desmethyl gefitinib. O-Desmethyl gefitinib is an active metabolite of Gefitinib in human plasma. The formation of O-desmethyl gefitinib is dependent on CYP2D6 activity. O-desmethyl gefitinib inhibits EGFR with an IC50 of 36 nM in subcellular assays[1][2].
    O-Desmethyl gefitinib-d6
  • HY-100064S
    O-Desmethyl gefitinib-d8

    		EGFR Cancer
    O-Desmethyl gefitinib-d8 is a deuterium labeled O-Desmethyl gefitinib. O-Desmethyl gefitinib is an active metabolite of Gefitinib in human plasma. The formation of O-desmethyl gefitinib is dependent on CYP2D6 activity. O-desmethyl gefitinib inhibits EGFR with an IC50 of 36 nM in subcellular assays[1][2].
    O-Desmethyl gefitinib-d8
  • HY-128893
    MC-Sq-Cit-PAB-Gefitinib

    		Drug-Linker Conjugates for ADC Cancer
    MC-Sq-Cit-PAB-Gefitinib is a agent-linker conjugate for ADC with potent antitumor activity by using Gefitinib (an EGFR tyrosine kinase inhibitor), linked via the ADC linker MC-Sq-Cit-PAB.
    MC-Sq-Cit-PAB-Gefitinib
  • HY-79511
    FAAH-IN-2
    1 Publications Verification

    O-Desmorpholinopropyl Gefitinib

    		 FAAH Autophagy Others
    FAAH-IN-2 (O-Desmorpholinopropyl Gefitinib) is a potent FAAH(fatty acid amide hydrolase) inhibitor extracted from Patent WO/2008/100977A2.
    FAAH-IN-2
  • HY-131088
    N3-PEG8-Phe-Lys-PABC-Gefitinib

    		Drug-Linker Conjugates for ADC Cancer
    N3-PEG8-Phe-Lys-PABC-Gefitinib is a agent-linker conjugate for ADC with potent antitumor activity by using the anti-tumor agent, Gefitinib (orally active EGFR tyrosine kinase inhibitor), linked via the cleavable linker N3-PEG8-Phe-Lys-PABC. N3-PEG8-Phe-Lys-PABC-Gefitinib is a click chemistry reagent, it contains an Azide group and can undergo copper-catalyzed azide-alkyne cycloaddition reaction (CuAAc) with molecules containing Alkyne groups. It can also undergo strain-promoted alkyne-azide cycloaddition (SPAAC) reactions with molecules containing DBCO or BCN groups.
    N3-PEG8-Phe-Lys-PABC-Gefitinib
  • HY-164548
    WK88-1

    		HSP Apoptosis Cancer
    WK88-1, a Hsp90 inhibitor, induces overall degradation of multiple oncogenic signaling molecules including EGFR, ErbB2 and ErbB3, leading to subsequent growth arrest and apoptosis in the Gefitinib-resistant H1975 cell line .
    WK88-1
  • HY-108016
    Peruvoside

    Encordin

    		 Src PI3K JNK STAT EGFR Apoptosis Autophagy Cancer
    Peruvoside is a potent inhibitor of Src, PI3K, JNK, STAT, and EGFR. Peruvoside induces apoptosis and autophagy and possesses a broad spectrum of anticancer activity in breast, lung, liver cancers and leukemia. Peruvoside is a broad-spectrum and potent antiviral activity against positive-sense RNA viruses. Peruvoside sensitizes Gefitinib (HY-50895)-resistant tumour cells (A549, PC9/gef and H1975) to Gefitinib .
    Peruvoside
  • HY-145823
    EGFR-IN-42

    		EGFR Cancer
    EGFR-IN-42 (Compound 17b) is a potent inhibitor of EGFR with single-digit nanomolar activity. EGFR-IN-42 connects tamoxifen or endoxifen with the EGFR-inhibitor gefitinib via a covalent linkage. EGFR-IN-42 retains both ER antagonist activity and EGFR inhibition. EGFR-IN-42 has superior anti-cancer activity .
    EGFR-IN-42
  • HY-145824
    EGFR-IN-43

    		EGFR Cancer
    EGFR-IN-43 (Compound 17c) is a potent inhibitor of EGFR with single-digit nanomolar activity. EGFR-IN-43 connects tamoxifen or endoxifen with the EGFR-inhibitor gefitinib via a covalent linkage. EGFR-IN-43 retains both ER antagonist activity and EGFR inhibition. EGFR-IN-43 has superior anti-cancer activity .
    EGFR-IN-43
  • HY-162481
    Anticancer agent 210

    		Apoptosis Cancer
    Anticancer agent 210 (Compound 7a) is a Gefitinib (HY-50895) derivative. Anticancer agent 210 inhibits proliferation, migration and colony formation of cancer cells. Anticancer agent 210 induces apoptosis in cells H1299 .
    Anticancer agent 210
  • HY-168492
    TrxR/EGFR-IN-1

    		Ferroptosis EGFR TrxR Apoptosis Cancer
    TrxR/EGFR-IN-1 (Compound L1Au2) is a TrxR/EGFR inhibitor. TrxR/EGFR-IN-1 is active against both Gefitinib (HY-50895)-sensitive and resistant lung cancers, effectively inhibiting tumor proliferation and promoting apoptosis. TrxR/EGFR-IN-1 promotes the degradation of GPX4 protein through autophagolysosomal and proteasomal pathways, leading to ferroptosis. In addition, TrxR/EGFR-IN-1 can induce endoplasmic reticulum stress and trigger immunogenic cell death. TrxR/EGFR-IN-1 can be used for the research of Gefitinib (HY-50895)-resistant lung cancer .
    TrxR/EGFR-IN-1
  • HY-162890
    EGFR-IN-122

    		EGFR Cancer
    EGFR-IN-122 (compound Yfq07) is a potent EGFR inhibitor. EGFR-IN-122 suppresses the proliferation of PC-9GR and HCC827GR cells .
    EGFR-IN-122
  • HY-116504
    WB-308

    		EGFR Akt ERK Apoptosis Cancer
    WB-308 is a novel small molecule that was identified as an inhibitor of EGFR by an in vitro EGFR kinase activity system. WB-308 was able to reduce the proliferation and clonogenicity of NSCLC cells, causing G2/M phase arrest and apoptosis. In addition, WB-308 inhibited tumor growth in two in vivo animal models (lung orthotopic transplantation model and patient-derived clonal mouse model). WB-308 impaired the phosphorylation of EGFR, AKT, and ERK1/2 proteins. Compared with Gefitinib, WB-308 had lower cytotoxicity. This study showed that WB-308 is a new EGFR-TKI that may be considered as an alternative to Gefitinib in the clinical treatment of NSCLC.
    WB-308
  • HY-19617A
    EGFR-IN-1 hydrochloride

    		EGFR Cancer
    EGFR-IN-1 hydrochloride is an orally active and irreversible L858R/T790M mutant selective EGFR inhibitor. EGFR-IN-1 hydrochloride potently inhibits Gefitinib-resistant EGFR L858R, T790M with 100-fold selectivity over wild-type EGFR. EGFR-IN-1 hydrochloride displays strong antiproliferative activity against the H1975 cells and the first line mutant HCC827 cells. Antitumor activity .
    EGFR-IN-1 hydrochloride
  • HY-19617B
    EGFR-IN-1 TFA

    		EGFR Cancer
    EGFR-IN-1 TFA is an orally active and irreversible L858R/T790M mutant selective EGFR inhibitor. EGFR-IN-1 TFA potently inhibits Gefitinib-resistant EGFR L858R, T790M with 100-fold selectivity over wild-type EGFR. EGFR-IN-1 TFA displays strong antiproliferative activity against the H1975 cells and the first line mutant HCC827 cells. Antitumor activity .
    EGFR-IN-1 TFA
  • HY-19617
    EGFR-IN-1

    		EGFR Cancer
    EGFR-IN-1 (compound 24) is an orally active and irreversible L858R/T790M mutant selective EGFR inhibitor. EGFR-IN-1 potently inhibits Gefitinib-resistant EGFR L858R, T790M with 100-fold selectivity over wild-type EGFR. EGFR-IN-1 displays strong antiproliferative activity against the H1975 cells and the first line mutant HCC827 cells. Antitumor activity .
    EGFR-IN-1
  • HY-149508
    Nrf2-IN-3

    		Keap1-Nrf2 Reactive Oxygen Species Cancer
    Nrf2-IN-3 (Compound R16) is a small-molecule NRF2 inhibitor and increases reactive oxygen species (ROS) production. Nrf2-IN-3 selectively binds KEAP1 mutants and restores their NRF2-inhibitory function by repairing the disrupted KEAP1/NRF2 interactions, leading to proteasome-dependent NRF2 degradation in cells. Nrf2-IN-3 sensitizes KEAP1-mutated tumor cells to Cisplatin (HY-17394), Gefitinib (HY-50895), and KEAP1 G333C-mutated xenograft to Cisplatin .
    Nrf2-IN-3

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