BMS-911543 JAK2 inhibitor
- Known as:
- BMS-911543 JAK2 suppressor
- Catalog number:
- a-1175
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ActivBio Active Biochem
- Gene target:
- BMS-911543 JAK2 inhibitor
Related genes to: BMS-911543 JAK2 inhibitor
- Gene:
- JAK2 NIH gene
- Name:
- Janus kinase 2
- Previous symbol:
- -
- Synonyms:
- JTK10
- Chromosome:
- 9p24.1
- Locus Type:
- gene with protein product
- Date approved:
- 1992-04-16
- Date modifiied:
- 2019-04-23
Related products to: BMS-911543 JAK2 inhibitor
Related articles to: BMS-911543 JAK2 inhibitor
- Sepsis-induced cardiomyopathy (SICM) contributes greatly to high mortality in critically ill patients. Accumulating evidence indicates that miRNAs play key roles in sepsis-related organ injury. This work investigated the function and molecular mechanism of miR-454-3p in SICM, along with its potential clinical utility. A total of 100 healthy controls and 210 sepsis patients were enrolled. Sepsis patients were categorized into non-cardiomyopathy group (non-CM, n=105) and SICM group (n=105). Receiver operating characteristic (ROC) curve analysis, multivariate logistic regression, and Cox regression were performed to assess the clinical value of miR-454-3p. In vitro functional experiments were conducted using LPS-stimulated AC16 cardiomyocytes. The dual-luciferase reporter assay verified the targeting relationship between miR-454-3p and STAT3. miR-454-3p expression decreased progressively from healthy controls to non-CM patients and further to SICM patients. miR-454-3p demonstrated good diagnostic performance for SICM. Multivariate analysis identified miR-454-3p as both an independent protective factor against SICM and an independent predictor of favorable prognosis. Cellular experiments revealed that miR-454-3p directly binds to the 3'UTR of STAT3 and suppresses STAT3 expression. Functional assays indicated that miR-454-3p attenuates LPS-induced cardiomyocyte apoptosis, inflammation, and oxidative stress, whereas STAT3 overexpression reverses these protective phenotypes. Furthermore, western blot analysis showed that miR-454-3p inhibits activation of the JAK2/STAT3/NF-κB inflammatory cascade. In vitro assays suggest that miR-454-3p alleviates LPS-triggered cardiomyocyte damage by negatively regulating STAT3 and suppressing the JAK2/STAT3/NF-κB inflammatory cascade. Our single-center observational data indicate that circulating miR-454-3p correlates independently with SICM incidence and 28-day all-cause mortality, implying its potential value as a candidate diagnostic and prognostic biomarker for SICM. Nevertheless, correlational findings from this cross-sectional cohort cannot confirm causal relationships, and large-scale multicenter prospective cohorts are needed for external validation to verify its clinical utility. - Source: PubMed
Publication date: 2026/10/03
Sha ZimoHou TianzhichaoZhou TaojieBao YangyangWei YueLing TianyouWu Liqun - Chronic obstructive pulmonary disease (COPD) is asyndrome characterized by airflow limitation, and its pathogenesis is not fully understood. This study intends to conduct a systematic analysis of the key cellular and metabolic remodeling mechanisms involved in the occurrence and development of COPD. A murine COPD model was established and analyzed by histopathology, molecular assays, scRNA-seq, and targeted metabolomics to investigate pulmonary inflammation, microenvironment changes, cellular composition, and signaling dysregulation. Furthermore, CCAAT enhancer-binding protein β (Cebpb) was knocked down in M1-polarized macrophages to assess its role in gene expression and energy metabolism reprogramming. The results showed that pulmonary inflammation was increased in COPD mice, with elevated inflammatory cell infiltration, pro-inflammatory cytokine upregulation, and enhanced M1 macrophage polarization. Specifically, scRNA-seq revealed immune cell landscape remodeling, with T cells as central intercellular mediators. Additionally, macrophage differentially expressed genes were enriched in energy metabolism pathways, including ribosome and oxidative phosphorylation. Moreover, targeted metabolomics demonstrated substantial metabolic alterations in lung tissues and macrophages, particularly in ABC transporters, amino acid metabolism, and the tricarboxylic acid (TCA) cycle. Mechanistically, the Cebpb/janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) axis was strongly activated in COPD lungs and M1-polarized macrophages. Functionally, Cebpb silencing suppressed this pathway activity, macrophage invasion, and M1 polarization, whereas exogenous JAK2/STAT3 activation reversed these effects. Consistently, RNA-seq confirmed that Cebpb regulates macrophage gene expression and metabolic profiles. In conclusion, the Cebpb/JAK2/STAT3 pathway is activated in COPD and promotes progression by driving M1 macrophage polarization and orchestrating downstream metabolic reprogramming. - Source: PubMed
Publication date: 2026/10/03
Mu QingshuangLuo QinYang YeYahefu ReyilaAbudureyimu MairemuguWang QinRuiSheng-Li - The Janus kinase/signal transducer and activator of transcription (JAK-STAT) pathways mediate signaling by multiple cytokines and growth factors critical for inflammation and immune regulation. Povorcitinib (INCB054707) is an oral JAK1 inhibitor designed to achieve high selectivity over JAK2 and minimize off-target hematologic effects. This study comprehensively assessed the in vitro selectivity and potency of povorcitinib relative to the JAK inhibitors upadacitinib, abrocitinib, baricitinib, and tofacitinib. - Source: PubMed
Publication date: 2026/10/02
Wass BrittneyFenix Aidan MZolotarjova NinaMargulis AlexZhang GuofengSales DominicCovington MaryanneSantos Leandro LKanellopoulou ChryssaMacarrón Ricardo - Persistent symptoms suggestive of idiopathic intracranial hypertension despite standard therapy should prompt urgent neuroimaging to exclude cerebral venous sinus thrombosis. When CVST is confirmed without an obvious provoking factor, evaluation for underlying myeloproliferative neoplasms, including JAK2-positive essential thrombocythemia, is essential. - Source: PubMed
Publication date: 2026/09/30
Nafea SarahFarooq TasmiaTaher Md AbuBarros AndreaSoe Kyaw NaingAli FawadThomas Koshy - Alopecia areata (AA) is a common autoimmune disorder characterized by non-scarring hair loss. While traditionally viewed as a T-cell-mediated disease, recent advances have elucidated the central role of the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway in its pathogenesis, establishing a self-sustaining inflammatory loop. The identification of this pathway has transformed AA from a condition with limited therapeutic options to one with targeted biological interventions. Over the past five years, multiple JAK inhibitors have received regulatory approval or shown promising results in clinical trials. Baricitinib, a selective JAK1/JAK2 inhibitor, became the first FDA-approved systemic treatment for severe AA, followed by ritlecitinib, which targets JAK3 and TEC family kinases and deuruxolitinib targeting the JAK1/2. Other agents, including ivarmacitinib, and the topical agent delgocitinib, are under active investigation, offering varying selectivity profiles and routes of administration. Compared with conventional therapies, JAK inhibitors such as baricitinib and ritlecitinib demonstrated therapeutic efficacy rates of 40-50% in Phase III clinical trials. Because head-to-head trials among JAK inhibitors in AA remain lacking, the comparative efficacy discussed in this review is derived primarily from indirect, cross-trial comparisons and network meta-analyses. Despite these remarkable advances, the field currently faces several significant challenges, including variable treatment responses, incomplete hair regrowth in patients with severe AA, potential long-term safety risks, and the absence of validated biomarkers to guide patient selection or predict therapeutic outcomes. Comparative efficacy, treatment challenges, and future directions including combination strategies and biomarker-guided therapy are also discussed to support informed clinical decision-making and highlight unmet needs in AA treatment. - Source: PubMed
Publication date: 2026/09/26
Wu Zhi-XianTang Wei-ZhenXu Hong-YuChen Tong-YuLan Zi-HanYang Yu-HanLiu Run-NingLi Ming-SiChen Hao-WenLiu Tai-HangWang Yong-Heng