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clobetasol (clobetasol, Mipharm / Dermovate / Dermoval)

✓ Approved

Pierre Fabre S.A. · NR3C1 · 小分子

什么是 clobetasol?

clobetasol 是一种小分子,由Pierre Fabre S.A.研发。该药已获批,用于治疗相关适应症,给药途径:Topical。

药物档案

商品名clobetasol, Mipharm, Dermovate, Dermoval
公司Pierre Fabre S.A.
药物类别小分子
分子靶点NR3C1
给药途径Topical
状态Approved

作用机制

分子靶点

clobetasol 作用于 1 个分子靶点:

NR3C1nuclear receptor subfamily 3 group C member 1 (GR, GCCR)
需要更深入的分析?Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

clobetasol 针对 4 个适应症,涉及 1 个治疗领域。

治疗领域疾病/病症分期
Skin and subcutaneous tissue disordersDermatitis allergic✓ Approved
Skin and subcutaneous tissue disordersDermatitis atopic✓ Approved
Skin and subcutaneous tissue disordersPsoriasis✓ Approved
Skin and subcutaneous tissue disordersSeborrhoeic dermatitis✓ Approved

相关研究文献

PubMedPopulation health management2026-10-26

Expanding Primary Care-Based Echocardiography Access in a Value-Based Care Network: Impact on Heart Failure Detection, Utilization, and Spending.

Wolf Philip P, Howell Scott S, Avery Samantha S, Mackenzie Andrew A et al.

This retrospective observational study assessed whether expanding primary care-based echocardiography access within a rural Pennsylvania value-based care network was associated with differences in heart failure (HF) diagnosis patterns, health care utilization, and spending compared with internal controls and a state-level benchmark. Eligibility, medical, and pharmacy claims were analyzed from 2 sources: third-party payers covering the primary care network and Merative's MarketScan Medicare data as a state-level reference. Members with HF-related risk factors were identified using diagnosis codes and followed for 12 months after index risk factor documentation, and the inverse probability of treatment weighting was used, incorporating age, sex, risk score, HF risk-factor category, and eligibility duration to address baseline demographic and clinical differences. Among members with HF risk factors, 21.0% of internal study members received an incident HF diagnosis compared with 13.7% of MarketScan members (P < 0.01). Internal cohort diagnoses were less likely to occur in inpatient (IP) settings than MarketScan diagnoses (0.53% vs. 10.2%; P < 0.01) and occurred after longer intervals from risk factor documentation (202 vs. 142 days; P < 0.01). Among diagnosed members, the internal cohort had lower HF-related IP admissions (21 vs. 28 per 1,000 member-years; P < 0.01), fewer HF-related emergency department visits (34 vs. 49 per 1000 member-years; P < 0.01), and lower average monthly spending ($1,937 vs. $2,826; P < 0.01). These findings suggest that expanding primary care-based echocardiography access in a rural value-based care setting was associated with greater HF detection, more outpatient-based diagnosis, and lower downstream acute care use and spending, broadly applicable to health systems and payers investing in diagnostics.

PMID 42928563
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PubMedNeurorehabilitation and neural repair2026-10-26

Comparative Efficacy of Noninvasive Neuromodulation in Patients with Disorders of Consciousness: A Systematic Review and Network Meta-Analysis of Randomized Controlled Trials.

Huang Liyi L, Wang Lu L, Ye Saiqing S, Sun Xin X et al.

To evaluate the efficacy of various noninvasive neuromodulation in restoring consciousness in patients with disorders of consciousness (DoC) through a network meta-analysis and identify the optimal noninvasive neuromodulation strategies. Systematic review and network meta-analysis. A comprehensive and systematic literature search was conducted for this study, encompassing several authoritative databases, including PubMed, Web of Science, EMBASE, the Cochrane Library, and ClinicalTrials.gov. This study adhered to the PRISMA-Network Meta-Analysis guidelines and was registered with PROSPERO (CRD420251018090). Literature screening, data extraction, and bias assessment (using the PEDro scale) were performed independently by 2 reviewers. A Bayesian framework-based network meta-analysis was conducted using the GeMTC package in R. Treatment rankings were determined using the surface under the cumulative ranking curve. A total of 41 studies were included, of which 19 were used for quantitative analysis. For Coma Recovery Scale-Revised (CRS-R), high frequencies-repetitive transcranial magnetic stimulation-primary motor cortex (HF-rTMS-M1) demonstrated the most pronounced effect (MD = 7.1; 95% CI = 2.6-11), followed by right median nerve electrical stimulation (RMNS) plus HF-rTMS-dorsolateral prefrontal cortex (DLPFC) (MD = 5.0; 95% CI = 2.6-7.5) and RMNS (MD = 3.0; 95% CI = 1.1-4.9). For Glasgow Coma Scale (GCS), subgroup analysis by etiology indicated that both HF-rTMS-DLPFC and HF-rTMS-M1 significantly improved CRS-R and GCS scores in patients with traumatic brain injury-related disorders of consciousness. The included studies generally demonstrated low risk of bias and the analysis model showed minimal heterogeneity (I2 < 5%), supporting the robustness of these findings. HF-rTMS-M1 and RMNS plus HF-rTMS-DLPFC, RMNS, HF-rTMS-DLPFC, and tDCS have shown positive signals in patients with DoC. The duration of the disorder and underlying etiology may influence the effectiveness of different noninvasive neuromodulation techniques in DoC. Given the marked heterogeneity of DoC and the limitations of the present study, these findings should be interpreted as hypothesis-generating observations rather than universally applicable conclusions. Further high-quality randomized controlled trials (RCTs) are warranted to provide robust evidence on the most suitable neuromodulation approaches for different DoC populations and to evaluate their long-term efficacy.

PMID 42928473
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PubMedCirculation research2026-10-26

CCR2-Dependent Myeloid Cell Recruitment Links Post-MI Heart Failure to Pulmonary Hypertension.

Gillan Jonathan L JL, Kamp Justus J, Kucherenko Mariya M MM, Winkler Annika A et al.

Pulmonary hypertension due to left heart disease (PH-LHD) is a common complication of myocardial infarction (MI) and heart failure (HF). Myeloid inflammation is a major hallmark of both the local cardiac and systemic post-MI response, with resident and recruited monocyte-derived macrophages orchestrating each step of the ensuing inflammatory cascade, from clearance of dead cardiomyocytes to scar tissue formation. Similarly, myeloid inflammation is a key feature of the PH lung, driving remodeling of small pulmonary vessels. We thus hypothesized that MI-induced systemic myeloid inflammation contributes directly to the development of PH-LHD. We assessed expression of inflammatory adhesion molecules, as markers of vascular inflammatory activation and myeloid cell recruitment pathways, in patients with pulmonary arterial hypertension, PH-LHD, as well as in a PH-LHD rat model. We then induced MI and subsequent HF in 8- to 10-week-old female C57BL/6J mice via permanent ligation of the left anterior descending coronary artery. HF mice were then treated with a CCR2 (C-C chemokine receptor 2) antagonist to block monocyte recruitment and the development of PH-LHD was assessed at 6 weeks post-MI by a combination of invasive hemodynamics, flow cytometry, echocardiography, and lung histology. Expression of key inflammatory adhesion molecules, including VCAM1 and SELE, was increased in PH-LHD lungs from humans and rats. Following early post-MI development of HF with reduced ejection fraction, mice exhibited increased numbers of circulating monocytes, lung monocytes, and lung interstitial macrophages, as well as PH-LHD by 6 weeks, characterized by right ventricular hypertrophy, elevated right ventricular pressures, and lung vascular remodeling of small-to-medium-sized pulmonary vessels. Administration of the selective CCR2 antagonist RS102895 from day 10 post-MI to reduce monocyte tissue recruitment attenuated lung vascular remodeling, right ventricular systolic and diastolic pressures, right ventricular hypertrophy, and lung adhesion molecule expression at 6 weeks, compared with vehicle-treated controls, without improving the underlying left-sided HF. This proof-of-concept study demonstrates a causal role for CCR2-dependent myeloid cell recruitment in the progression from MI-induced HF to secondary pulmonary vascular disease.

PMID 42929140
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PubMedIranian journal of biotechnology2026-10-26

Targeting CCR2 and PTPN22 Genes for Post-Infarct Heart Failure Therapy: A Network-based Repurposing of Kuanxiong Aerosol.

Sun Zhifei Z, Wang Rongzhi R, Liu Yingwu Y

Kuanxiong aerosol (KX) has been used in ischemic cardiovascular diseases, but its potential molecular targets and pathway-level associations in post-myocardial infarction heart failure (post-MI HF) remain insufficiently characterized. This study aimed to identify and prioritize putative KX-related molecular targets and signaling pathways associated with post-MI HF by integrating network pharmacology, WGCNA, immune infiltration analysis, and transcriptomic correlation analysis. We retrieved KX components from published data, predicted their targets using SwissTargetPrediction, and collected post-MI HF-related genes from GeneCards, OMIM, and DigSee. Using network pharmacology and WGCNA on GSE59867 (80 samples), we screened KX-related targets. Enrichment analyses (KEGG/GSEA) and immune infiltration correlations (ssGSEA) were performed. Key targets were then cross-validated with disease-regulated genes. Among 215 overlapping targets, calcium, HIF-1, and MAPK signaling were top hits. Two targets, CCR2 and PTPN22, showed significant immune-cell correlations (CCR2 with neutrophils: r=0.62, P<0.001; PTPN22 with NK cells: r=0.48, P<0.05). CCR2 also correlated with MIR21 (r=0.59, P=0.00024) and TTN (r=-0.48, P=0.0039). GSEA linked CCR2 to NOTCH and PTPN22 to PPAR signaling. CCR2 and PTPN22 are credible molecular targets for KX in post-MI HF. From a biotechnology standpoint, these findings support developing targeted immunomodulators (e.g., CCR2 antagonists or PTPN22 activity modulators) or engineered aerosol formulations. Further validation in engineered heart tissue models or bioreactor-based assays is needed before clinical translation.

PMID 42928728
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PubMedHeart failure reviews2026-10-26

Heart failure with supranormal ejection fraction: is it the new Ariadne's string?

Katsi Vasiliki V, Maragkoudakis Spyridon S, Lilikaki Gabriella G, Marketou Maria M et al.

Heart failure with supranormal ejection fraction (HFsnEF) is an emerging and incompletely characterized phenotype within the heart failure (HF) spectrum. Although no universally accepted LVEF threshold for HFsnEF has been established and different definitions have been used across published studies, for the purposes of this review HFsnEF is operationally defined as HF with a left ventricular ejection fraction (LVEF) > 65%. Importantly, a supranormal LVEF should not be interpreted as evidence of enhanced ventricular performance. Patients with HFsnEF may exhibit smaller left ventricular (LV) volumes, concentric remodeling, increased myocardial stiffness, impaired longitudinal deformation, reduced stroke volume and preload reserve, and elevated filling pressures, particularly during exercise. HFsnEF is unlikely to represent a single disease entity; rather, it encompasses heterogeneous pathophysiological substrates and clinical phenotypes, including hypertensive and cardiometabolic remodeling, valvular heart disease, hypertrophic cardiomyopathy (HCM), transthyretin cardiac amyloidosis (ATTR-CM), and other conditions associated with hyperdynamic ventricular function. Accordingly, the diagnostic evaluation should extend beyond recognition of an elevated LVEF and systematically identify the underlying phenotype and potentially treatable causes through comprehensive echocardiography, myocardial deformation imaging, cardiac magnetic resonance, disease-specific testing, and exercise or invasive hemodynamic assessment when indicated. Therapeutic evidence specific to HFsnEF remains limited. No randomized clinical trial has specifically evaluated conventional HF pharmacotherapy in a population prospectively defined by LVEF > 65%; therefore, evidence for conventional HF and cardiometabolic therapies is derived predominantly from broader HFpEF populations or subgroup analyses and should be regarded as indirect rather than definitive evidence for HFsnEF. In contrast, recognition of specific underlying diseases, particularly ATTR-CM, HCM, and significant valvular heart disease, may permit evidence-based disease-specific treatment. This review summarizes the epidemiology, pathophysiology, and clinical phenotypes of HFsnEF and proposes a practical phenotype-guided approach to diagnosis and management. Standardized definitions and prospective trials specifically addressing patients with LVEF > 65% are needed to establish evidence-based therapeutic strategies for this population.

PMID 42928386
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PubMedDentistry journal2026-10-26

Effect of Surface Treatment Protocols on Nanoindentation-Derived Mechanical Properties and Wettability of Hybrid CAD/CAM Materials.

Todorović Miloš M, Petrović Bojan B, Vulović Stefan S, Malivuk Nastasija N et al.

Background/Objectives: Hybrid CAD/CAM materials combine ceramic and polymeric phases, so conditioning protocols developed for glass-ceramics may not transfer to them. Because wettability and near-surface mechanics are usually studied separately, this study measured both to test whether conditioning trades one for the other. Methods: Edelweiss C-Block, Lava Ultimate, Vita Enamic and Cerasmart 270 specimens were left untreated or treated with 9% hydrofluoric acid (HF) for 60 s, sandblasting (50 µm Al2O3, 1 bar) or silane. Static water contact angle (sessile drop; 90 readings per group) and hardness, elastic modulus and maximum penetration depth (nanoindentation at 30 mN, Oliver-Pharr; 17-25 valid indentations per group) were compared with controls using Welch's t-tests with Holm correction. Results: Control contact angles (45.1-60.4°) fell to 6.3-18.1° after sandblasting and 8.8-32.5° after silanization; HF lowered them to 17.9-38.0° in three materials but raised Lava Ultimate's from 48.4° to 58.1°. Sandblasting caused the largest mechanical losses in every material (hardness reduced by >90%, penetration depth up to 7.9-fold); HF reduced hardness by 58-98%. Silanization preserved 93-97% of control hardness in Lava Ultimate and Cerasmart 270 and gave Vita Enamic its lowest contact angle. Conclusions: Improved wettability and preserved near-surface mechanics were not mutually exclusive, and responses depended on microstructure. Bond strength was not measured, so these findings should guide, not replace, bonding studies.

PMID 42930416
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