CD44
- Known as:
- CD44
- Catalog number:
- ANT-242
- Product Quantity:
- 500µg
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- CD44
Ask about this productRelated genes to: CD44
- Gene:
- CD44 NIH gene
- Name:
- CD44 molecule (Indian blood group)
- Previous symbol:
- MIC4, MDU2, MDU3
- Synonyms:
- IN, MC56, Pgp1, CD44R, HCELL, CSPG8
- Chromosome:
- 11p13
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2019-04-23
Related products to: CD44
Related articles to: CD44
- Glioblastoma (GBM) is the most common adult primary brain malignancy. Recent studies demonstrate that temozolomide (TMZ) facilitates the persistence of quiescent glioma stem cells (GSCs), which are responsible for GBM recurrence. An ideal therapy should eradicate both proliferating cells and GSCs. Abexinostat (Abx), a histone deacetylase inhibitor, was identified through connectivity mapping to target the specific GBM signature. Here, we demonstrate the anti-proliferative effect of Abx on both differentiated cells and GSCs. - Source: PubMed
Publication date: 2026/08/19
Perumalsamy BalajiVengoji RaghupathyThiraviyam AnandRamireddy IndumatiYadav PoonamShah AshuMallya KavitaSalehi AfshinKumar SushilJain ManeeshPonnusamy Moorthy PBatra Surinder KShonka Nicole - Cancer stem cells (CSCs) drive chemoresistance, metastasis, and relapse in triple-negative breast cancer (TNBC), yet a comprehensive synthesis of targeted therapy evidence remains lacking. We systematically searched PubMed, Scopus, and Web of Science (2010-2025) and pooled effect sizes from 12 eligible studies (540 TNBC samples) using a random-effects model per PRISMA 2020 guidelines. CSC-targeted therapies significantly reduced CSC viability (SMD = -1.12; 95% CI: -1.45 to -0.79; p < 0.001), with combination approaches showing superior efficacy, moderate heterogeneity (I = 52%), and no publication bias, supporting further clinical trials to validate these promising preclinical strategies. - Source: PubMed
Publication date: 2026/08/19
Rebai OlfaAmri MohamedFattouch Sami - Alveolar microenvironment-driven macrophage polarization critically influences chronic obstructive pulmonary disease (COPD) progression. Nuclear factor erythroid 2-related factor 2 (NRF2), a key transcription factor, regulates macrophage polarization, suppresses inflammation, and promotes cellular repair. However, its role in macrophage-mediated inflammation and metabolic regulation, particularly hyaluronic acid (HA)-related remodeling, remains incompletely defined. This study investigates a novel dimension of NRF2 in COPD pathogenesis through macrophage-specific modulation, aiming to uncover its previously unrecognized mechanism. - Source: PubMed
Publication date: 2026/08/14
Bai GeWang JiaqiWen QianmeiHuang YuningLi HaiqingXu YanhuiLiu YiyiYi ErkangWu FanCui JiedaMei XinyueZhang YuxiaZhou YuminSun RuitingRan Pixin - Oral squamous cell carcinoma (OSCC) remains highly lethal and is driven, in part, by chronic NF-κB-mediated inflammation. Sorafenib, a multikinase inhibitor of RAF/VEGFR/PDGFR, can suppress these pathways, but its clinical utility is limited by hydrophobicity, toxicity, and poor tumor penetration. We engineered hyaluronic acid-coated niosomes encapsulating sorafenib (SOR@Nio/HA) to enable CD44-targeted delivery to OSCC cells. - Source: PubMed
Wu TingLi YongshuoWang ZixianGuo Bin - Cyclophosphamide is widely used in oncology, autoimmune disorders, and transplantation-related conditioning or post-transplant immunosuppression. However, its therapeutic value is limited by hematopoietic and lymphoid toxicity, including leukopenia, neutropenia, anemia, thrombocytopenia, bone marrow suppression, thymic injury, and prolonged impairment of T-cell recovery. These effects may occur after pulsed intravenous administration, high-dose regimens used in transplantation or severe refractory disease, and continuous low-dose/metronomic exposure. Therefore, there is a medical need for pharmacological agents capable of compensating cyclophosphamide-induced hematopoietic and lymphopoietic suppression without causing uncontrolled stimulation of early progenitor cells. - Source: PubMed
Publication date: 2026/08/03
Ten AsselBaktybayeva LayilyaKoshetova ZhanargulKoizhaiganova RaushanDaulet GuldanaZharkynbek TolganayYu Valentina