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.

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.

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.

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.

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.

Anticanceragent 210 (Compound 7a) is a derivative of Gefitinib. It inhibits the proliferation, migration, and colony formation of cancer cells and induces apoptosis in H1299 cells.