CXCR4 (N-Terminus) Peptide
- Known as:
- CXCR4 (N-Terminus) Peptide
- Catalog number:
- 1009P
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- CXCR4 (N-Terminus) Peptide
Ask about this productRelated genes to: CXCR4 (N-Terminus) Peptide
- Gene:
- CXCR4 NIH gene
- Name:
- C-X-C motif chemokine receptor 4
- Previous symbol:
- -
- Synonyms:
- LESTR, NPY3R, HM89, NPYY3R, D2S201E, fusin, HSY3RR, NPYR, CD184
- Chromosome:
- 2q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-17
- Date modifiied:
- 2019-04-23
Related products to: CXCR4 (N-Terminus) Peptide
Related articles to: CXCR4 (N-Terminus) Peptide
- Ovarian cancer (OC) remains a malignancy characterized by obscure risk factors and unfavorable prognosis. While 3-tert-butyl-4-hydroxyanisole (3-BHA) is suspected of exerting toxic effects on ovarian health, the precise molecular mechanisms underlying its impact remain elucidated. This study aims to systematically investigate the potential pathogenic mechanisms of 3-BHA in the progression of OC.Integrated transcriptomic data from the GEO database (GSE18520 and GSE40595) were analyzed. A synergistic computational framework was employed, incorporating Differentially Expressed Genes (DEGs) identification, Weighted Gene Co-expression Network Analysis (WGCNA), multiple machine learning algorithms, and SHapley Additive exPlanations (SHAP) analysis to achieve high-interpretability feature selection.Five hub genes-CXCR4, CCL7, CXCL8, CXCR2, and CX3CL1-were identified, all demonstrating robust diagnostic efficacy with AUC values of 0.911, 0.882, 0.823, 0.772, and 0.837, respectively. Prognostic profiling via GEPIA3 highlighted CXCR2 overexpression as a potential critical biomarker driving poor clinical outcomes in OC. Furthermore, molecular docking validated the strong binding affinity of 3-BHA with CX3CL1 and CXCR2. Subsequent 100 ns molecular dynamics simulations and thermodynamic stability assessments confirmed the structural stability of the 3-BHA-CXCR2 complex.By integrating bioinformatics and computational toxicology, this study deciphers the potential mechanistic landscape through which 3-BHA influences OC. These findings not only refine the toxicological understanding of 3-BHA but also provide novel candidates for early diagnosis and prognostic risk stratification in OC. - Source: PubMed
Publication date: 2026/05/03
Shi YifeiNiu DongJin Chunhui - Covalent Bruton tyrosine kinase (BTK) inhibitors have advanced the treatment of Waldenström macroglobulinaemia; however, the occurrence of progression, intolerance, and acquired resistance are not fully understood. We aim to report on the safety and activity of pirtobrutinib (a highly selective, non-covalent BTK inhibitor) in patients with relapsed or refractory Waldenström macroglobulinaemia, including those who received previous covalent BTK inhibitors as part of the phase 1/2 BRUIN trial. - Source: PubMed
Palomba M LiaPatel Manish REyre Toby AJurczak WojciechLewis DavidGastinne ThomasMa ShuoCohen Jonathon BPatel KrishBrown Jennifer RScarfò LydiaMunir TalhaLech-Maranda EwaHoffmann Marc SUjjani Chaitra SFakhri BitaWang Michael LIzutsu KojiNagai HirokazuTam Constantine SRhodes Joanna MVose JulieMcKinney MatthewGerson James NBarve Minal AKuss BryoneKoh YoungilBarrett AislingTreon Steven PCastillo Jorge JSeymour John FRuppert Amy SMcNeely Samuel CWalgren Richard ATsai Donald EBao KatherineNair BinojWoyach JenniferCheah Chan Y - Major Depressive Disorder (MDD) is characterized by heterogeneous pathogenesis that extends beyond traditional monoamine deficits. A paradigm shift is recognizing neuroinflammation as a central, critical driver of both illness onset and resistance to treatment. The CXCL12/CXCR4 system is traditionally associated with immune cell trafficking, but increasing evidence reveals its powerful regulatory role in neuropsychiatric disorders. We performed a comprehensive synthesis demonstrating that CXCL12/CXCR4 axis acts as a direct molecular modulator of neurotransmission, neuroplasticity, and glial cell signaling. Specifically, this axis can modulate a multiple molecular pathways linked with the glutaminergic, GABAergic, and serotonergic systems, and mediating neuroplasticity and glial cell function. Functionally, CXCL12/CXCR4 axis has twofold character - it can strengthen neurotoxic processes through overactivation of NMDAR and excessive Ca2+ influx. On the other hand, it can also play protective role by preventing excitotoxicity, supporting neurogenesis, enhancing GABA synthesis, and dendritic spines stabilization. This review focuses on identifying potential mechanisms across in vitro, animal, and human studies to establish the CXCL12/CXCR4 axis as a powerful biomarker and, critically, an unexploited therapeutic target. - Source: PubMed
Publication date: 2026/04/30
Grzybowska KingaCzarny PiotrKołodziej ŁukaszWigner-Jeziorska PaulinaSzemraj JanuszGałecki PiotrSu Kuan-PinŚliwiński Tomasz - Chemokine receptor 4 (CXCR4) is a clinically significant G protein-coupled receptor implicated in HIV-1 entry, cancer progression, immune regulation, and metastatic dissemination, making it an attractive therapeutic target. This study employed an integrated computational and experimental framework to identify novel small-molecule CXCR4 inhibitors. A curated dataset of 608 compounds from peer-reviewed literature and patents was used to train machine-learning classification models. Decision Tree, Logistic Regression, and AdaBoost models showed balanced performance across key metrics, and external validation on 2146 in-house compounds identified 44 consensus CXCR4 inhibitors. Molecular docking analyses suggested favorable binding modes and key interactions comparable to those predicted for the reference inhibitor IT1t. One hundred-nanosecond molecular dynamics simulations indicated stable CXCR4-ligand complexes, with equilibration occurring within approximately 20 ns and backbone RMSD values maintained between 4 and 8 Å. MM/GBSA free-energy calculations demonstrated favorable energetics, with IS00622 exhibiting the strongest affinity (-70 kcal/mol), followed by IT1t, IS00998, and IS00179. In vitro assays identified IS00127 as a promising lead, showing strong antiproliferative activity against MDA-MB-231 cells and minimal toxicity toward HEK293 cells. ELISA assays confirmed dose-dependent CXCR4 downregulation with negligible effects on CXCR7, indicating high functional selectivity. Overall, this integrative strategy accelerates the discovery of potent, selective CXCR4 inhibitors for translational research. - Source: PubMed
Publication date: 2026/04/30
Wani Mushtaq AhmadKumari PoojaIrshad FaisalGupta YashiGupta MonikaGoswami AnindyaAhmed ZabeerNargotra Amit - Uveal melanoma (UVM) is a highly aggressive intraocular malignancy with limited treatment options and a poor prognosis, particularly following metastasis. Oxidative stress plays a complex, dual role in tumor progression, but the regulatory roles of long non-coding RNAs (lncRNAs) in the oxidative stress response within UVM remain largely unexplored. The objective of this study was to investigate the regulatory mechanism of the lncRNA MIAT/miR-4306/CXCR4 axis in modulating oxidative stress and apoptosis in uveal melanoma (UVM), and to develop an oxidative stress-related prognostic gene signature. - Source: PubMed
Publication date: 2026/04/29
Wu YueZhao YubaoCao RunyanHu MenghanCai XiaoyanWang Yong