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- Safety Data Sheet
Catalog #: Product Name: 100-1601 Anti-Mouse CD4 Antibody, Clone GK1.5 Catalog #: 100-1601 Product Name: Anti-Mouse CD4 Antibody, Clone GK1.5 - ReferenceS. Trushin et al. (Sep 2025) eBioMedicine 120 4
Therapeutic assessment of a novel mitochondrial complex I inhibitor in in vitro and in vivo models of Alzheimer's disease
Despite recent approval of monoclonal antibodies that reduce amyloid (Aβ) accumulation, the development of disease-modifying strategies targeting the underlying mechanisms of Alzheimer's disease (AD) is urgently needed. We demonstrate that mitochondrial complex I (mtCI) represents a druggable target, where its weak inhibition activates neuroprotective signalling, benefiting AD mouse models with Aβ and p-Tau pathologies. Rational design and structure‒activity relationship studies yielded mtCI inhibitors profiled in a drug discovery funnel designed to address safety, selectivity, and efficacy. The lead compound C458 is highly protective against Aβ toxicity, has favourable pharmacokinetics, and minimal off-target effects. C458 exhibited excellent brain penetrance, activating neuroprotective pathways with a single dose. Preclinical studies in APP/PS1 mice were conducted using functional tests, metabolic assessment, in vivo 31 P-NMR spectroscopy, blood cytokine panels, ex vivo electrophysiology, and Western blotting. Chronic oral administration improved long-term potentiation, reduced oxidative stress and inflammation, and enhanced mitochondrial biogenesis, antioxidant signalling, and cellular energetics. Efficacy against Aβ and p-Tau was confirmed in human organoids. These studies provide further evidence that the restoration of mitochondrial function in response to mild energetic stress represents a promising disease-modifying strategy for AD. This research was supported by grants from NIH AG 5549-06, NS1 07265, AG 062135, UG3/UH3 NS 113776, and ADDF 291204 (all to ET); U19 AG069701 (to TK); the Alzheimer’s Association Research Fellowship grant 23AARF-1027342 (to TKON).Catalog #: Product Name: 08570 STEMdiff™ Cerebral Organoid Kit Catalog #: 08570 Product Name: STEMdiff™ Cerebral Organoid Kit Safety Data SheetCatalog #: Product Name: 100-1600 Anti-Human CD80 (B7-1) Antibody, Clone 2D10.4, APC Catalog #: 100-1600 Product Name: Anti-Human CD80 (B7-1) Antibody, Clone 2D10.4, APC ReferenceA. Chakraborty et al. (Aug 2025) International Journal of Molecular Sciences 26 17Cholesterol Regulates Airway Epithelial Cell Differentiation by Inhibiting p53 Nuclear Translocation
Cholesterol is an essential plasma membrane component, and altered cholesterol metabolism has been linked to cholesterol accumulation in the airways of COPD and cystic fibrosis patients. However, its role in airway epithelial differentiation is not well understood. Tandem mass spectrometry-based proteomic analysis of differentiating primary human bronchial epithelial cells (phBECs) revealed an overall inhibition of the cholesterol biosynthesis pathway. We hypothesized that excess cholesterol impairs the differentiation of phBECs into a fully functional bronchial epithelium. PhBECs were differentiated in the presence of 80 µM cholesterol for 21 days, the main airway cell type populations monitored using qRT-PCR and immunofluorescent stainings, and epithelial barrier integrity was analyzed via transepithelial electrical resistance measurements. Chronic cholesterol exposure led to a significant increase in CC10 + secretory cells at the expense of ciliated cells. Pathway enrichment analysis suggested the tumor protein p53 as a master regulator of genes during normal differentiation of phBECs. Chronic cholesterol exposure drastically impaired the nuclear translocation of p53. Our findings suggest that this inhibition underlies the cholesterol-induced expansion of CC10 + secretory cell populations at the expense of ciliated cells. In conclusion, we identify cholesterol as an important regulator of normal bronchial epithelial cell differentiation through inhibition of p53 nuclear translocation.Catalog #: Product Name: 05001 PneumaCult™-ALI Medium 05040 PneumaCult™-Ex Plus Medium Catalog #: 05001 Product Name: PneumaCult™-ALI Medium Catalog #: 05040 Product Name: PneumaCult™-Ex Plus Medium Safety Data SheetCatalog #: Product Name: 100-1599 Anti-Human CD80 (B7-1) Antibody, Clone 2D10.4, PE Catalog #: 100-1599 Product Name: Anti-Human CD80 (B7-1) Antibody, Clone 2D10.4, PE ReferenceT. Nosaka et al. (Aug 2025) Cancers 17 17Clinical Significance of CD90(+) Circulating Tumor Cells as Dynamic Biomarkers in Unresectable Hepatocellular Carcinoma Treated with Atezolizumab/Bevacizumab and Lenvatinib
Atezolizumab plus bevacizumab and lenvatinib are standard treatments for unresectable hepatocellular carcinoma; however, tumor markers such as alpha-fetoprotein and des-gamma-carboxy prothrombin have a limited ability to reflect treatment responses. Circulating tumor cells are non-invasive biomarkers associated with cancer stemness and treatment resistance. We assessed circulating tumor cell subsets expressing cancer stem cell markers (CD90, epithelial cell adhesion molecule, CD133, vimentin) using multiparametric flow cytometry at early and maximal response phases in patients receiving atezolizumab plus bevacizumab or lenvatinib. Early decreases in CD90-positive circulating tumor cells after therapy initiation were associated with tumor shrinkage and longer progression-free survival in both groups, as well as prolonged overall survival in the atezolizumab plus bevacizumab group. At maximal response, changes in CD90-positive circulating tumor cells reflected tumor burden more accurately than alpha-fetoprotein or des-gamma-carboxy prothrombin. These findings highlight the potential of CD90-positive circulating tumor cells to become dynamic biomarkers in systemic therapy for unresectable hepatocellular carcinoma.Catalog #: Product Name: 15122 RosetteSepâ„¢ Human CD45 Depletion Cocktail Catalog #: 15122 Product Name: RosetteSepâ„¢ Human CD45 Depletion Cocktail ReferenceW. Yang et al. (Aug 2025) Cancers 17 17A Polyomavirus-Positive Merkel Cell Carcinoma Mouse Model Supports a Unified Origin for Somatic and Germ Cell Cancers
Cancer research has long focused on mutations in normal body cells, but this approach has not produced major breakthroughs for most cancers. Our study explores a different concept that some aggressive cancers may actually arise from early reproductive cells called primordial germ cells, which normally develop into eggs and sperm. We created a new experimental model showing how a virus can transform human primordial germ cell-like cells into virus-positive Merkel cell carcinoma, a rare but deadly skin cancer. This model shows that cancers can emerge through changes in developmental states rather than relying solely on genetic mutations. By linking cancer development to early germ cells, our findings suggest a unifying explanation for both germ cell cancers and body cancers. This new perspective may guide more effective approaches to study, diagnose, and treat cancer by focusing on early human development rather than only DNA mutations and later developmental stages.Catalog #: Product Name: 05872 ¸é±ð³¢±ð³§¸éâ„¢ Catalog #: 05872 Product Name: ¸é±ð³¢±ð³§¸éâ„¢ Safety Data SheetCatalog #: Product Name: 100-1598 Anti-Mouse CD45.2 Antibody, Clone 104, APC Catalog #: 100-1598 Product Name: Anti-Mouse CD45.2 Antibody, Clone 104, APC ReferenceK. Chang et al. (Sep 2025) Nature Communications 16Modulating the PPARγ pathway upregulates NECTIN4 and enhances chimeric antigen receptor (CAR) T cell therapy in bladder cancer
With the approval of the antibody-drug conjugate enfortumab vedotin (EV), NECTIN4 has emerged as a bona fide therapeutic target in urothelial carcinoma (UC). Here, we report the development of a NECTIN4-directed chimeric antigen receptor (CAR) T cell, which exhibits reactivity across cells expressing a range of endogenous NECTIN4, with enhanced activity in high expressors. We demonstrate that the PPARγ pathway, critical for luminal differentiation, transcriptionally controls NECTIN4 , and that the PPARγ agonist rosiglitazone primes and augments NECTIN4 expression, thereby increasing sensitivity to NECTIN4-CAR T cell-mediated killing. NECTIN4-CAR T cells have potent anti-tumor activity even against EV resistant cells, which largely retain NECTIN4 expression, including in a post-EV biopsy cohort. Our results elucidate a therapeutically actionable mechanism that UC cells use to control NECTIN4 expression and suggest therapeutic approaches that leverage PPARγ agonists for rational combinations with NECTIN4-targeting agents in UC, as well as future potential treatment options for EV-refractory patients. Subject terms: Bladder cancer, Cancer immunotherapy, Cancer therapeutic resistance, Oncology, Bladder cancerCatalog #: Product Name: 10981 ±õ³¾³¾³Ü²Ô´Ç°ä³Ü±ô³Ùâ„¢-³Ý¹ó T Cell Expansion Medium 100-0956 ±õ³¾³¾³Ü²Ô´Ç°ä³Ü±ô³Ùâ„¢-³Ý¹ó Catalog #: 10981 Product Name: ±õ³¾³¾³Ü²Ô´Ç°ä³Ü±ô³Ùâ„¢-³Ý¹ó T Cell Expansion Medium Catalog #: 100-0956 Product Name: ±õ³¾³¾³Ü²Ô´Ç°ä³Ü±ô³Ùâ„¢-³Ý¹ó Safety Data SheetCatalog #: Product Name: 100-1597 Anti-Mouse CD45.2 Antibody, Clone 104, FITC Catalog #: 100-1597 Product Name: Anti-Mouse CD45.2 Antibody, Clone 104, FITC ReferenceE. Yamashita et al. (Sep 2025) The FASEB Journal 39 17Red Blood Cellâ€Mediated Enhancement of Hematopoietic Stem Cell Functions via a Hes1â€Dependent Pathway
In bone marrow, cell numbers are balanced between production and loss. After chemotherapy, blood cell counts decrease initially but later recover as hematopoietic progenitor cells expand, although the mechanisms underlying this recovery are still unclear. We investigated the influence of red blood cells (RBCs) on hematopoietic stem cell (HSC) function during bone marrow recovery. Following chemotherapy, RBC concentrations in bone marrow peaked on day 5 posttreatment, coinciding with the recovery of hematopoiesis. Coculture of HSCs with RBCs resulted in a significant increase in hematopoiesis. Direct contact between RBCs and HSCs was essential for enhancement of hematopoiesis, and HSCs precultured with RBCs resulted in greater numbers of donorâ€derived mature hematopoietic cells after transplantation. RNAâ€sequencing analysis showed that Hes1 was the most significantly upregulated transcription factor in RBC coculture, and the response to RBCâ€induced hematopoiesis of Hes1â€deficient HSCs was reduced. These findings imply a role of RBCs and Hes1 in the enhancement of hematopoietic recovery following bone marrow stress.Catalog #: Product Name: 03436 MethoCultâ„¢ SF M3436 Catalog #: 03436 Product Name: MethoCultâ„¢ SF M3436 ReferenceM. Nakagawa et al. (Sep 2025) Scientific Reports 15MDM4 enables efficient human iPS cell generation from PBMCs using synthetic RNAs
If iPS cells can be established easily and efficiently using freshly collected blood cells, it will enhance regenerative and personalized medicine. While reports of iPS derivation from blood-derived endothelial progenitor cells using RNA have been documented, none have been reported from peripheral blood-derived mononuclear cells (PBMCs). In this study, we established a method to generate iPS cells from PBMCs using synthetic RNAs and found that MDM4, which suppresses p53, improved reprogramming efficiency. Subject terms: Reprogramming, Induced pluripotent stem cellsCatalog #: Product Name: 09600 StemSpanâ„¢ SFEM 09605 StemSpanâ„¢ SFEM II Catalog #: 09600 Product Name: StemSpanâ„¢ SFEM Catalog #: 09605 Product Name: StemSpanâ„¢ SFEM II Items 433 to 444 of 14067 total
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