FGF19 Antibody (C-term) Blocking Peptide
- Known as:
- FGF19 Antibody (C-terminus) Blocking Peptide
- Catalog number:
- BP18231b
- Product Quantity:
- 2
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- FGF19 Antibody (C-term) Blocking Peptide
Related genes to: FGF19 Antibody (C-term) Blocking Peptide
- Gene:
- FGF19 NIH gene
- Name:
- fibroblast growth factor 19
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 11q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-06
- Date modifiied:
- 2016-10-05
Related products to: FGF19 Antibody (C-term) Blocking Peptide
Related articles to: FGF19 Antibody (C-term) Blocking Peptide
- Optimal treatment following first-line immunotherapy for advanced hepatocellular carcinoma (HCC) remains uncertain. This study evaluated futibatinib, a pan-FGFR inhibitor, combined with pembrolizumab in previously treated patients with FGF19-expressing HCC. - Source: PubMed
Publication date: 2026/08/25
Tran Nguyen HPalmer Mathias EUlrich AngelaMcCue Shaylene AMahipal AmitMa Wen WeeBabiker Hani MMajeed UmairHalfdanarson Thorvardur RMcWilliams Robert RJin ZhaohuiCarr RyanKankeu Fonkoua Lionel AurelienWashburn LeslieConboy CaitlinGraham Rondell PTorbenson MichaelStarlinger PatrickJethwa Krishan RHallemeier ChristopherRevzin AlexanderThompson Scott MGoenka Ajit HVenkatesh Sudhakar KSonbol Mohamad BBorad Mitesh JBekaii-Saab TaniosGores Gregory JRoberts Lewis RHeimbach Julie KOu Fang-Shu - Fibroblast growth factor 19 (FGF19) signaling is a promising therapeutic target for metabolic diseases and cancers, and several agents targeting the FGF19 signaling are currently undergoing clinical trials. However, as an endocrine FGF, FGF19's organism-wide functions remain vague, which hinders the advancing of FGF19 signaling-based therapies. To systematically explore its systemic effects, we performed a multi-tissue transcriptomic profiling in a FGF19 knock-in mouse model. Sustained FGF19 exposure induced extensive, tissue‑specific transcriptional reprogramming. For instance, lipid metabolic pathways were broadly altered not only in canonical metabolic organs but also in immune‑related tissues including the spleen and thymus. Furthermore, integrated analysis and functional validation demonstrated that FGF19 promoted monocyte/macrophage (Mo/MΦ) migration in an FGFR4‑involved manner, associated with an M2-like polarization state. Moreover, we developed a macrophage‑targeted sustained‑release FGF19 delivery system, which significantly accelerated wound healing and enhanced M2 macrophage infiltration in a murine full‑thickness skin injury model. Overall, our study establishes a multi‑tissue transcriptional atlas of FGF19 action, reveals broad metabolic and immune regulatory responses to sustained human FGF19 exposure in mice, and provides a targeted therapeutic strategy for modulating macrophage. - Source: PubMed
Publication date: 2026/08/22
Xiao YangKuang LiwenHe JuanLiu XudongYi YiSong MiaoyuXia JieZhou YuLei JuanChen YuLiu XiChen JiongmingChen YijiaoZeng XianghuaLi YongshengZhao Huakan - Anti-human epidermal growth factor receptor 2 (HER2) antibody-drug conjugates (ADCs) have revolutionized the treatment for HER2-positive and HER2-low metastatic breast cancer (MBC). However, the comparative efficacy, safety, and molecular predictors of response to various anti-HER2 ADCs remain limited. - Source: PubMed
Publication date: 2026/08/20
Gui XiujuanChen HaizhuZhao JianliLai HongnaLuo SiminChai JieCai YangyangWu WenjingZeng YinduoChen MaojianWang YingYao HeruiDing Linxiaoxiao - Post-pancreatitis diabetes mellitus after acute pancreatitis (PPDM-A) is increasingly recognized as a distinct metabolic complication rather than a simple subtype of type 2 diabetes. This narrative review summarizes current evidence on PPDM-A, with emphasis on terminology, diagnostic timing, epidemiology, pathophysiology, risk factors, clinical phenotypes, screening, prevention, and long-term follow-up. A structured literature search was conducted in PubMed/MEDLINE, Scopus, and Google Scholar to identify relevant studies. PPDM-A may develop after mild, moderately severe, or severe acute pancreatitis, although the risk is greatest in patients with pancreatic necrosis, recurrent attacks, exocrine pancreatic dysfunction, obesity, dyslipidemia, fatty liver disease, metabolic comorbidities, and marked in-hospital glycemic variability. A major diagnostic challenge is distinguishing transient stress hyperglycemia and previously unrecognized diabetes from incident PPDM-A. Formal diagnosis should generally be established no earlier than 90 days after the index episode of acute pancreatitis to minimize misclassification due to transient stress-related dysglycemia. Follow-up assessment should combine fasting plasma glucose and HbA1c, whereas a 75-g oral glucose tolerance test (OGTT) may provide greater sensitivity during early recovery, particularly when HbA1c is unreliable, results are borderline or discordant, or isolated postprandial dysglycemia is suspected. Current evidence indicates that PPDM-A develops through interacting pathogenic domains, including pancreatic endocrine injury with impaired β-cell reserve, metabolic dysregulation characterized by insulin resistance and persistent inflammation, exocrine pancreatic dysfunction with nutritional consequences, and emerging mechanisms involving gut microbiome alterations, bile acid-FGF19 signaling, and extracellular vesicle-mediated communication. Available data support a trajectory-based model in which some patients recover normal glucose metabolism, some develop persistent intermediate dysglycemia, and others progress to overt diabetes over months or years. Structured post-discharge surveillance, risk-stratified follow-up, assessment of exocrine dysfunction, and prevention of recurrent pancreatic injury are essential for improving early detection, reducing diagnostic misclassification, and optimizing long-term clinical outcomes. - Source: PubMed
Publication date: 2026/08/12
Chooklin SergeChuklin Serhii - Traditional risk factors do not fully account for the residual cardiometabolic risk of major adverse cardiovascular events (MACE) in coronary artery disease (CAD). We aimed to identify circulating metabolic signatures associated with MACE susceptibility and uncover potential pathobiological mechanisms underlying the gut-liver-heart axis. - Source: PubMed
Publication date: 2026/08/12
Lin Min-QingWong Chun-KaAu Ka-WingCheung Chloe Yu-YanLau Yee-ManLiao Song-YanLam Karen Siu-LingXu AiminTse Hung-Fat