FGFR2
- Known as:
- FGFR2
- Catalog number:
- Y214020
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- FGFR2
Related genes to: FGFR2
- Gene:
- FGFR2 NIH gene
- Name:
- fibroblast growth factor receptor 2
- Previous symbol:
- KGFR, BEK, CFD1, JWS
- Synonyms:
- CEK3, TK14, TK25, ECT1, K-SAM, CD332
- Chromosome:
- 10q26.13
- Locus Type:
- gene with protein product
- Date approved:
- 1991-05-09
- Date modifiied:
- 2019-04-23
Related products to: FGFR2
Related articles to: FGFR2
- Metabolic dysfunction-associated steatotic liver disease (MASLD) and advanced fibrotic stages are significant contributors to cirrhosis and liver-related mortality, yet no therapies directly target fibrosis in the later stages of the disease. Fibroblast growth factor 10 (FGF10) facilitates epithelial repair, yet its function and epithelial receptor requirements in chronic liver fibrogenesis are unclear. - Source: PubMed
Yang XuanxinDong QingqingMa JiayingYan YaweiPeng ShuangyanWu QiqiWang HuanZhang TingtingZhang PanyuJiang ZelongLu ChaoLi LeYou XinyiXu YuandongBanda JoshuaMu ZhixiangZheng MinghuaLi XiaokunHui QiYu BingjieWang Xiaojie - Tinengotinib is a spectrum-selective multi-kinase inhibitor targeting FGFR1-3, JAK1/2, VEGFRs, and Aurora A/B kinases. This phase Ib/II clinical trial (NCT05253053) evaluated tinengotinib as monotherapy (Arm A, n = 53, in Chinese patients with advanced solid tumors) and in combination with atezolizumab (Arm B, n = 31, in patients with advanced biliary tract cancer). Each arm comprised a dose-escalation phase with standard 3 + 3 design (phase Ib) followed by a dose-expansion phase (phase II). The primary endpoints of the phase Ib were safety, tolerability, dose-limiting toxicity (DLT), maximum tolerated dose (MTD), and dose selection for expansion, with secondary endpoints of efficacy (phase II) and pharmacokinetics. The trial met pre-specified primary endpoints: tinengotinib was well tolerated without DLTs, and MTD was not reached. Tinengotinib demonstrated antitumor activity both as monotherapy (objective response rate [ORR]: 16.7% in Arm A) and combined with atezolizumab (ORR: 22.6% in Arm B). In predefined exploratory subgroup analysis, notable efficacy was observed in cholangiocarcinoma (ORR: 30.8% in Arm A [n = 13]; 25.0% in Arm B [n = 28]). Tinengotinib monotherapy achieved favorable response in cholangiocarcinoma harboring FGFR2 fusion progressing on prior FGFR inhibitor (ORR: 66.7%). In patients with cholangiocarcinoma previously treated with immune checkpoint inhibitors (n = 20), the combination regimen achieved an ORR of 20.0% and a disease control rate of 75.0%. These findings support further development of tinengotinib, both as monotherapy and in combination with immunotherapy. - Source: PubMed
Publication date: 2026/05/11
Zhang PanpanNiu ZuoxingGuo HongqianZhang MiaoJiang ShusuanCao BaoshanHe ChaohongHou XinfangZhang JianYuan JiajiaZhu YujiaYu YingyingSun CaixiaPeng PengFan JeanGong JifangZhou JunShen Lin - Fibroblast growth factor receptor 2 (FGFR2) has emerged as a highly promising therapeutic target due to its critical role in the pathogenesis and progression of endometriosis. To date, a variety of FGFR2 inhibitors have exhibited remarkable therapeutic efficacy against endometriosis in both preclinical studies and clinical trials. However, these small-molecule inhibitors suffer from drawbacks including poor targeting ability and high toxicity, and their direct administration has consequently limited their further clinical applications. In this study, a rationally designed hydrogenator, Nap-Phe-Phe-Phe-Asp-Asp-Asp-Tyr-OH (NapY), was co-assembled with the FGFR2 inhibitor AZD4547 (AZD) to construct an FGFR2-responsive hydrogel, aiming to achieve precise targeted therapy for endometriosis. Under the specific phosphorylation by FGFR2 which is highly expressed in endometriotic lesions, Nap-Y in Gel Y/AZD is phosphorylated and converted into a hydrophilic product, Nap-Phe-Phe-Phe-Asp-Asp-Asp-Tyr(H₂PO₃)-OH (Nap-Yp). This process further triggers the disassembly of the hydrogel, enabling the responsive release of AZD. In vitro experimental results demonstrated that the sustained release of AZD from Gel Y/AZD could effectively suppress the viability, migration and invasion of 12Z-FGFR2 cells by inhibiting the expression of FGFR2 and the phosphorylation levels of its downstream signaling pathway molecules. In vivo studies confirmed that compared with endometriosis model mice treated with free AZD, those treated with Gel Y/AZD exhibited significantly superior inhibitory effects on the growth and metastasis of ectopic lesions. It is anticipated that this research will expect to be applied in the clinical treatment of endometriosis in the near future. - Source: PubMed
Publication date: 2026/05/09
Ma PanmeiWang ShenZhang XierLi NanaXu LuHuang AnZhan WenjunZhao GuangfengLiu DanSun JiawenLiang GaolinWeng Qiao - Hypospadias is a common congenital malformation with a complex etiology involving genetic susceptibility and environmental factors. MicroRNAs (miRNAs), as epigenetic modulators, are hypothesized to bridge these factors by regulating genes essential for urogenital development. The aim of this study was to investigate the expression profiles of specific miRNAs associated with AR, ESR1, and FGFR2 genes in both tissue and systemic circulation (blood) of children with hypospadias compared to healthy controls, to evaluate their potential as epigenetic footprints. - Source: PubMed
Publication date: 2026/04/27
Yildiz SadettinSezginer Guler HazalInanc IremAtli EnginKorkmaz SelcukAvlan Dincer - Gastric cancer (GC) remains a leading cause of cancer-related mortality globally and is characterized by significant inter- and intra-tumoral heterogeneity, which poses major challenges to effective treatment. Although traditional "one-size-fits-all" chemotherapy regimens have improved outcomes, the prognosis for advanced disease remains poor, necessitating a paradigm shift towards personalized medicine. This review provides a comprehensive synthesis of the current landscape of precision oncology in GC. We systematically analyze the clinical implications of major molecular classification systems, particularly The Cancer Genome Atlas (TCGA) subtypes (EBV-positive, MSI-H, GS, and CIN), and their role in guiding therapeutic stratification. The integration of molecular profiling has revolutionized the management of GC. We discuss the evolution of targeted therapies, ranging from established standards, like HER2 inhibition, to emerging targets, including Claudin18.2 and FGFR2, highlighting their potential of overcoming resistance mechanisms. Furthermore, we evaluate the efficacy of immune checkpoint inhibitors (PD-1/PD-L1 blockade), specifically in the context of high microsatellite instability (MSI-H) and EBV-positive subtypes, where these have demonstrated robust antitumor activity. Beyond tissue-based markers, this article also explores the expanding role of liquid biopsies, including circulating tumor cells (CTCs) and circulating tumor DNA (ctDNA), as non-invasive tools for real-time monitoring of disease progression and therapeutic response. Precision oncology represents a transformative approach in GC, moving beyond histology to a molecularly driven treatment framework. However, realizing its full potential requires addressing challenges related to tumor heterogeneity and drug resistance. Future research must focus on validating novel biomarkers and developing synergistic combination strategies to further improve patient survival. - Source: PubMed
Publication date: 2026/05/09
Hong YanyunWang XiaodongYu HangLiu XiaosunTang Chao