gefitinib

Gefitinib (ZD1839) is an EGFR first-generation inhibitor with oral activity that inhibits the EGFR 19 Del and L858R mutations. Gefitinib has antitumor activity and is used for the treatment of EGFR-mutated non-small-cell lung cancers. Gefitinib administration RESULTS in the development of the EGFR C797S resistance mutation.

Gefitinib is an EGFR tyrosine kinase inhibitor, with IC50 of 2-37 nM in NR6wtEGFR cells. Gefitinib D8 is a deuterium labeled Gefitinib.

Gefitinib is an EGFR tyrosine kinase inhibitor, with IC50 of 2-37 nM in NR6wtEGFR cells. Gefitinib N-oxide is the N-oxide derivative of Gefitinib.

Gefitinib hydrochloride (ZD-1839 hydrochloride) is an orally active selective and potent tyrosine kinase (EGFR) inhibitor. Gefitinib hydrochloride exhibits antitumor activity, selectively inhibits EGF-stimulated tumor cell growth, induces cellular autophagy, improves lung dysfunction, and inhibits inflammation. Gefitinib hydrochloride has antitumor activity, selectively inhibits EGF-stimulated tumor cell growth, induces cellular autophagy, ameliorates lung dysfunction, and inhibits the progression of inflammation and fibrosis.

O-Desmethyl gefitinib inhibits EGFR (IC50: 36 nM in subcellular assays). In human plasma, O-Desmethyl gefitinib is an active metabolite of Gefitinib. The formation of O-desmethyl gefitinib is dependent on the CYP2D6 activity.

MC-Sq-Cit-PAB-Gefitinib is a potent antitumor drug-linker conjugate for Antibody-Drug Conjugates (ADC), utilizing Gefitinib—an EGFR tyrosine kinase inhibitor—connected through the MC-Sq-Cit-PAB ADC linker.

O-Desmethyl gefitinib D8 is a deuterium labeled O-Desmethyl gefitinib that is an active metabolite of Gefitinib in human plasma.

Gefitinib impurity 1 is a compound derived from Gefitinib, a potent and selective EGFR tyrosine kinase inhibitor (IC 50 = 33 nM). This orally active compound selectively inhibits tumor cell growth stimulated by EGF (IC 50 = 54 nM) and inhibits EGFR autophosphorylation induced by EGF in tumor cells. Additionally, Gefitinib induces autophagy and exhibits antitumor activity.

Gefitinib-based PROTAC 3, which connects an EGFR binding element to a VHL 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 mutation) cells, respectively[1].

Gefitinib dihydrochloride is a potent, selective, orally active EGFR tyrosine kinase inhibitor (IC50: 33 nM). Gefitinib dihydrochloride selectively inhibits EGF-stimulated tumor cell growth with an IC50 value of 54 nM and blocks EGFR autophosphorylation in EGF-stimulated tumor cells. Gefitinib dihydrochloride induces autophagy and apoptosis, and can be used in studies of cancer-related diseases such as lung and breast cancer.

Gefitinib analog III (4-((3-Chloro-4-fluorophenyl)amino)-7-methoxyquinazolin-6-yl acetate) has potential anti-inflammatory and anti-tumor activity and can be used to study its interactions and activity in organisms.

Gefitinib impurity 5 is a useful organic compound for research related to life sciences. The catalog number is T65585 and the CAS number is 199327-61-2.

Gefitinib impurity 2 is a useful organic compound for research related to life sciences and the catalog number is T67092.

Gefitinib N-oxide hydrochloride, an N-oxide derivative of Gefitinib, acts as an EGFR tyrosine kinase inhibitor. Demonstrating an IC50 range of 2-37 nM in NR6wtEGFR cells, it emphasizes its efficacy in inhibiting the enzymatic activity of EGFR [1] [2].

Mc-Val-Cit-PAB-Gefitinib chloride is a conjugate agent-linker for antibody-drug conjugates (ADCs) that combines Gefitinib, an epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor, with the proprietary ADC linker Mc-Val-Cit-PAB [1].

N3-PEG8-Phe-Lys-PABC-Gefitinib is an antibody-drug conjugate (ADC) agent-linker complex exhibiting potent antitumor activity. It incorporates the orally active EGFR tyrosine kinase inhibitor Gefitinib, tethered by the cleavable linker N3-PEG8-Phe-Lys-PABC. As a click chemistry reagent, it features an azide group facilitating copper-catalyzed azide-alkyne cycloaddition (CuAAC) with alkyne-bearing molecules. Additionally, it can engage in strain-promoted alkyne-azide cycloaddition (SPAAC) with compounds presenting DBCO or BCN groups.

Gefitinib-d6 is a deuterated compound of Gefitinib. Gefitinib has a CAS number of 184475-35-2. Gefitinib is an EGFR tyrosine kinase inhibitor and can inhibit Tyr1173, Tyr992, Tyr1173 and Tyr992 (IC50s: 37 37 26 57 nM).

MS 154 is a potent and selective cereblon-recruiting Degrader (PROTAC®) of mutant epidermal growth factor receptor (EGFR), comprising a cereblon-binding moiety joined by a linker to gefitinib(Iressa). MS 154 decreases EGFR protein levels, inhibits downstream signaling in and inhibits proliferation of mutant EGFR-bearing lung cancer cells (DC50values are 11 and 25 nM in HCC-827 and H3255 cells, respectively; Dmax> 95% at 50 nM), but not in WT-EGFR-bearing ovarian and lung cancer cells lines. Bioavailable in mice following ip administration.

MS 39 is a highly effective, highly affinity and selective depressant of mutant epidermal growth factor receptor (EGFR) with high efficiency, high affinity and selectivity. MS 39, conjured by gefitinib to VHL ligand via a linker, effectively induced the degradation of mutant EGFR (DC50 values in HCC827(exon 19 del) and H3255 (L858R mutation) lung cancer cell lines were 5 nM and 3.3 nM, respectively). However, there was no significant effect in wild-type EGFR cell lines with concentrations up to 10 μM. MS 39 inhibited the proliferation of H3255 lung cancer cells in vitro and was bioavailable in mice after administration.

Sapitinib (AZD-8931) , a reversible, ATP competitive inhibitor of EGFR(IC50=4 nM), ErbB2(IC50=3 nM) and ErbB3(IC50=4 nM), is more effective over Gefitinib or Lapatinib against NSCLC cell, 100-fold more specific for the ErbB family over MNK1 and Flt.

EGFR-IN-1, an orally active and irreversible selective inhibitor targeting L858R T790M mutant EGFR, exhibits strong antiproliferative and antitumor activity, particularly against H1975 cells and first line mutant HCC827 cells. This compound potently inhibits Gefitinib-resistant EGFR L858R T790M mutations with a 100-fold selectivity over the wild-type EGFR.

FAAH-IN-2 (O-Desmorpholinopropyl Gefitinib) is a potent inhibitor of FAAH (fatty acid amide hydrolase).

WK88-1, an inhibitor of Hsp90, effectively induces the degradation of various oncogenic signaling molecules, including EGFR, ErbB2, and ErbB3, in the gefitinib-resistant H1975 cell line. This leads to subsequent growth arrest and apoptosis.

TrxR EGFR-IN-1 (Compound L1Au2) is a TrxR EGFR inhibitor with activity against both gefitinib-sensitive and -resistant lung cancer, effectively suppressing tumor proliferation and promoting apoptosis. It enhances GPX4 degradation through autophagosome-lysosome and proteasome pathways, leading to ferroptosis. Additionally, it induces endoplasmic reticulum stress and triggers immunogenic cell death, making it applicable for studies on gefitinib-resistant lung cancer.