CD44 Biotin
- Known as:
- CD44 Biotin
- Catalog number:
- ANT-243
- Product Quantity:
- 500µg
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- CD44 Biotin
Related genes to: CD44 Biotin
- 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 Biotin
Related articles to: CD44 Biotin
- Glioblastoma multiforme (GBM) is a lethal and fast-growing brain cancer that is difficult to treat with standard medical interventions. GBM tumors often overexpress cyclin-dependent kinase 9, in complex with cyclin T1, and thus, it represents a promising target for therapeutic intervention. In this study, we employed a structure-based virtual screening approach for a curated library of 6,059 bis-pyridyl compounds from PubChem to identify potential CDK9/T1 inhibitors. Subsequent ADP-Glo assay led to the identification of GNE-3511 as a potent CDK9/T1 inhibitor with an IC of 0.064 μM. GNE-3511 also inhibited CDK7/cyclin H with an IC of 0.12 μM. In U-87 MG and T98G glioblastoma cells, GNE-3511 exhibited cytotoxicity with a GI of 3.4 and 5.0 μM, inducing G2/M phase cell cycle arrest and promoting early apoptosis. Treatment with GNE-3511 significantly reduced the expression of the anti-apoptotic markers BCL-2, SURVIVIN and drug resistance markers ( and ) in a dose-dependent manner, and downregulated glioma stem cell population/markers (, CD90, or CD133 and ) and sphere formation abilities. Oral administration of GNE-3511 at 20 mg/kg (twice daily) demonstrated significant anti-tumor efficacy and improved survival in both U-87 MG and T98G xenograft/orthotopic mouse models. Collectively, these findings highlight GNE-3511 as a promising lead candidate for the development of GBM therapeutics. - Source: PubMed
Publication date: 2026/05/14
Pr Nithya SreeSomarowthu TejaswiS JeyasankariKuncha MadhusudhanaAndugulapati Sai BalajiBharate Sandip B - Kidney stones (KS) represent a complex and globally prevalent disease; however, the mechanisms underlying their formation are not fully understood. Inflammatory responses and crystal aggregation are recognized as critical factors in KS pathogenesis. Interleukin-6 (IL-6) is widely recognized as an inflammatory mediator; however, its precise contribution to calcium oxalate (CaOx) KS formation has not been fully elucidated. This study aimed to explore the detailed mechanism through which IL-6 influences CaOx KS formation. To achieve this, a rat model for CaOx nephrolithiasis was developed by administrating drinking water containing 1% ethylene glycol (EG). Concurrently, an in vitro model of cellular injury was established by treating human renal proximal tubular epithelial cells (HK-2) with calcium oxalate monohydrate (COM) crystals. Employing various molecular biology and immunological techniques, the specific role of IL-6 in the formation of CaOx stones was comprehensively examined. The data indicated significantly elevated IL-6 expression in both in vivo and in vitro models of CaOx KS. Increased IL-6 exacerbated inflammatory responses during stone formation, triggered activation of the p38 MAPK signaling pathway, and promoted higher expression levels of osteopontin (OPN) and CD44. These molecular alterations enhanced adhesion between renal tubular epithelial cells (RTECs) and crystals, consequently facilitating crystal aggregation, nucleation, and accelerating overall stone formation. In summary, the study illustrates that IL-6 accelerates CaOx KS development through activation of the p38 MAPK signaling pathway, amplifying inflammation, and promoting crystal-cell adhesion. Thus, IL-6 emerges as a promising therapeutic target for interventions in CaOx nephrolithiasis. - Source: PubMed
Publication date: 2026/05/14
Liang FujieGuo FuYouHan ZepingXiang YouGuan XiaoFengWang Xiang - Metabolic reprogramming is a pivotal driver of tumor microenvironment (TME) remodeling and colorectal cancer (CRC) progression. However, the spatial organization of glycolysis heterogeneity and the molecular drivers maintaining the malignant high-glycolytic state remain poorly understood. - Source: PubMed
Publication date: 2026/04/28
Yang FengmingBian YinuoJin YuqiTan YinuoLao TianhaoYang JieChen Hua - Lung cancer is still the most common cause of cancer fatalities around the world. To address these issues, we fabricated a cisplatin-containing hyaluronic acid-modified Fe-MOF that was designed to release drugs in response to changes in pH and actively target lung cancer cells. The incorporation of HA, which specifically binds to CD44 receptors that are overexpressed on the surface of lung cancer cells, improves cellular uptake and therapeutic effectiveness. The pH-dependent behavior is confirmed by drug release experiments, demonstrating little cisplatin release at physiological pH and enhanced release within the acidic tumor microenvironment. Cytotoxicity studies showed that HA/Fe-MOF/CP is more effective against A549 lung cancer cells than free cisplatin (82.72% inhibition at 50 µM and IC = 17.3 ± 0.5 µM). HA/Fe-MOF/CP showed less toxicity to normal BEAS-2B cells (85.34% viability and IC > 40 µM), while free cisplatin showed more toxicity to BEAS-2B cells (23.16% inhibition and IC > 40 µM). The uncoated Fe-MOF/CP inhibited A549 cells by 76.42% (IC = 22.4 ± 0.3 µM), which indicates a moderate level of effectiveness. Fe-MOF has been altered a significant effect on cancer cells (60.41% inhibition and IC = 35.6 ± 0.5 µM) and worked well with BEAS-2B cells (89.31% viability). - Source: PubMed
Publication date: 2026/05/12
Saleem AmmarKhan Komal ZamanFayad EmanZaib AurangAbbas GhazanfarBinjawhar Dalal NasserJunaid AliAshiq Muhammad NaeemShafiq ZahidQin Hua Li - In the pathogenesis of ulcerative colitis, inflammatory responses, mucosal injury, and gut dysbiosis form a mutually reinforcing network that perpetuates disease progression. Current clinical interventions can rarely modulate these pathological modules simultaneously, underscoring the urgent need for more effective therapeutic strategies. Here, we report a dual-functional nanotherapy that couples aryl hydrocarbon receptor (AhR) activation with on-site reactive oxygen species (ROS) scavenging. An amphiphilic copolymer, HA-TK-LA (HTL), was synthesized by grafting lipoic acid (LA) to hyaluronic acid (HA) via a ROS-cleavable thioketal (TK) linker. The copolymer self-assembles into ~130-nm nanoparticles that encapsulate the natural AhR ligand indole-3-acetic acid (IAA) with a high loading efficiency of 73%. The resulting IAA@HTL nanoparticles exhibit ROS/glutathione-triggered drug release and are actively taken up by inflamed intestinal epithelial cells and M1 macrophages through CD44-mediated endocytosis, leading to suppressed epithelial apoptosis and macrophage repolarization toward an anti-inflammatory phenotype. In dextran sulfate sodium-induced murine colitis, IAA@HTL specifically accumulates in the inflamed colon and markedly alleviates disease activity. Mechanistically, IAA and LA released from the nanoparticles synergistically activate aryl hydrocarbon receptor/cytochrome P450 family 1 subfamily A member 1 and nuclear factor erythroid 2-related factor 2/heme oxygenase-1 signaling, skew macrophages toward an anti-inflammatory state, dampen proinflammatory cytokine release, and reinforce the mucosal barrier by up-regulating tight-junction proteins and interleukin-22 secretion. As inflammation subsides and mucosal integrity is restored, the gut microbiota gradually returns to homeostasis. Collectively, this study establishes a ROS-scavenging and AhR-activating nanodelivery system that achieves a "one-stone-three-birds" outcome-attenuating inflammation, repairing mucosa, and rebalancing microbiota-providing new experimental evidence and theoretical support for ulcerative colitis therapy. - Source: PubMed
Publication date: 2026/05/12
Dong KaiGuan ZelinWang DanyangSun JinyaoZhang YingYou CuiyuXing Yuanming