Gefitinib

Name: Gefitinib
SKU: PI184475352
Rating: 5 (1 reviews)

Catalog NumberPI184475352

CAS Number184475-35-2

CategoryFeatured APIs

Gefitinib is an EGFR inhibitor, like erlotinib, which interrupts signaling through the epidermal growth factor receptor (EGFR) in target cells. Therefore, it is only effective in cancers with mutated and overactive EGFR, but resistances to gefitinib can arise through other mutations.

Product Details

Synonyms	ZD1839
Molecular Formula	C22H24ClFN4O3
Molecular Weight	446.90
Therapeutic Category	Anti-Cancer
CEP/DMF/GMP	CEP, USDMF, NMPA DMF
Uses	Gefitinib is used as first-line therapy to treat non-small cell lung carcinoma (NSCLC) that meets certain genetic mutation criteria.
Mechanism Of Action	Gefitinib is an inhibitor of the epidermal growth factor receptor (EGFR) tyrosine kinase that binds to the adenosine triphosphate (ATP)-binding site of the enzyme. EGFR is often shown to be overexpressed in certain human carcinoma cells, such as lung and breast cancer cells. Overexpression leads to enhanced activation of the anti-apoptotic Ras signal transduction cascades, subsequently resulting in increased survival of cancer cells and uncontrolled cell proliferation. Gefitinib is the first selective inhibitor of the EGFR tyrosine kinase which is also referred to as Her1 or ErbB-1. By inhibiting EGFR tyrosine kinase, the downstream signaling cascades are also inhibited, resulting in inhibited malignant cell proliferation.

Download COA Download MSDS

Case Study

Synergistic Enhancement of Gefitinib Efficacy in Gefitinib-Resistant NSCLC through Ginsenoside CK

Synergistic anticancer effects of ginsenoside CK and gefitinib against gefitinib-resistant NSCLC by regulating the balance of angiogenic factors through HIF-1α/VEGF Song X, et al. Toxicology and Applied Pharmacology, 2024, 486, 116938.

Gefitinib is commonly used for the treatment of non-small cell lung cancer (NSCLC). However, both primary and acquired resistance to gefitinib present significant challenges to its clinical efficacy. Recent studies have highlighted the potential of ginsenoside CK, a bioactive metabolite derived from ginsenosides, in overcoming this resistance. In both in vitro and in vivo models of gefitinib-resistant NSCLC, ginsenoside CK was shown to significantly enhance the anti-cancer activity of gefitinib, improving proliferation inhibition, apoptosis induction, and migration suppression.
The mechanism underlying this synergistic effect involves the modulation of angiogenic factors. Specifically, co-treatment with ginsenoside CK was found to down-regulate key signaling pathways, particularly the HIF-1α/VEGF axis, which is critical for tumor angiogenesis. The combination therapy reduced the expression of pro-angiogenic factors such as HIF-1α, VEGF, FGF, and MMP2/9 while simultaneously enhancing anti-angiogenic factors like PF4. This shift in the balance of angiogenic factors not only suppressed the angiogenic potential of tumor cells but also promoted the normalization of tumor vasculature, improving the overall tumor microenvironment.
In vivo, the combination therapy of ginsenoside CK and gefitinib led to a significant increase in tumor inhibition rate (70.97%) compared to gefitinib monotherapy (32.65%). These findings suggest that ginsenoside CK can effectively sensitize NSCLC to gefitinib, offering a promising therapeutic strategy to combat gefitinib resistance.

* Our products are for research use only.

Gefitinib

Synergistic Enhancement of Gefitinib Efficacy in Gefitinib-Resistant NSCLC through Ginsenoside CK

Get in Touch