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ketoprofen SR

✓ Approved

Ethypharm Corp. · PTGS1 · 小分子

什么是 ketoprofen SR？

ketoprofen SR 是一种小分子，由Ethypharm Corp.研发。该药已获批，用于治疗相关适应症，给药途径：Unknown。

药物档案

公司Ethypharm Corp.
药物类别小分子
分子靶点PTGS1, PTGS2
给药途径Unknown
状态Approved
来源： ClinicalTrials.gov, Ethypharm Corp.

作用机制

分子靶点

ketoprofen SR 作用于 2 个分子靶点：

PTGS1prostaglandin-endoperoxide synthase 1 (COX3, PCOX1)
PTGS2prostaglandin-endoperoxide synthase 2 (GRIPGHS, hCox-2)
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

ketoprofen SR 针对 2 个适应症，涉及 2 个治疗领域。

治疗领域疾病/病症分期
Gastrointestinal disordersAbdominal pain✓ Approved
Hepatobiliary disordersHepatitis✓ Approved

相关研究文献

PubMedJournal of pineal research2026-09-10

Melatonin Inhibits Metastasis of Sunitinib-Resistant Renal Cell Carcinoma Cells Via the GRP78/p38/CTSD Expression.

Huang Po-Yu PY, Hsieh Yi-Hsien YH, Chen Yong-Syuan YS, Hung Tung-Wei TW et al.

Sunitinib resistance contributes to poor outcomes in advanced renal cell carcinoma (RCC). This study investigated the anti-metastatic effects and underlying mechanisms of melatonin in sunitinib-resistant (SR)-RCC. Melatonin significantly inhibited the migration and invasion of A498-SR and Caki-1-SR cells. SR-RCC cells exhibited elevated CTSD expression, impaired endoplasmic reticulum (ER) stress signaling with reduced GRP78 and IRE1α, and enhanced p38 MAPK activation, all of which were reversed by melatonin. Silencing p38 MAPK further potentiated the inhibitory effects of melatonin on cell migration and invasion. Mechanistically, CTSD expression was regulated through both GRP78/p38 MAPK-mediated ER stress. In vivo, melatonin markedly reduced lung metastasis of Caki-1-SR cells without causing significant toxicity to major organs. Collectively, these findings demonstrate that melatonin inhibited the metastatic potential of SR-RCC by decreasing CTSD expression, restoring ER stress response, and decreasing p38 MAPK expression, supporting its potential as an anti-metastatic therapeutic agent for SR-RCC.

PMID 42720349
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PubMedMaterials horizons2026-09-10

Tunable A-site crystal-field modulation enables ultra-sensitive, multi-channel lanthanide thermometry in low-phonon halide lattices.

Xin Yuxiang Y, Wang Jianru J, Xiao Xiachu X, Yang Yutao Y et al.

The development of high-performance lanthanide-based fluorescence-intensity-ratio (FIR) thermometers is limited by the lack of a continuously tunable, qualitative guided crystal-field design principle. Most systems still rely on empirical host-dopant screening, and the correlation among lattice geometry, crystal-field strength, energy gap (ΔE), and thermometric sensitivity (Sr) remains unclear. Here, we establish an A-site lattice-site engineering strategy in APb2Cl5 (A = Na, K, Rb, Cs and solid solutions), where the A-site ionic radius acts as a single tunable parameter to regulate local geometry, crystal-field strength, and ΔE. Mapping from Na+ to Cs+ identifies an optimal K-Rb-Cs regime enabling linear tuning of ΔE and Sr, while excessive lattice contraction near the Na boundary suppresses luminescence and disrupts thermal coupling, revealing that ΔE enhances Sr only within a finite, lattice-defined window. Owing to the ultra-low phonon energy of the Pb-Cl lattice, Er3+/Yb3+-doped KPb2Cl5 nanoparticles (NPs) exhibit strong upconversion (UC), including the 490 nm 4F7/2 band, and achieve record Sr values of 33.6% K-1 at 78 K and 2.3% K-1 at 298 K, enabling cross-validated thermometry from 78-418 K. Extending this framework to Nd3+ enables 808 nm excitation and visible/near infrared (NIR) dual-mode thermometry with Sr up to 21.7% K-1. This work establishes a general route for high-performance optical nanothermometers.

PMID 42720040
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PubMedThe Journal of physiology2026-09-10

Intracellular mechanosensation in intestinal smooth muscle: Piezo1 complexes amplify signalling beyond the surface.

Bautista Geoanna M GM, Manning Declan D, Lieu Emily C EC, Ugochukwu Stephanie I SI et al.

Mechanosensation is fundamentally viewed as a plasma membrane phenomenon. We challenge this paradigm by introducing intracellular mechanosensation in intestinal smooth muscle. We hypothesized that a distinct, organelle-based signalling axis exists to amplify mechanotransduction from the inside out. To test this we investigated whether Piezo1, a canonical plasma membrane (PM) mechanosensor, also operates within the cell. Using tissue-level wire myography, high-resolution confocal microscopy, proximity ligation assays and patch-clamp electrophysiology on freshly dissociated cells, we identified a previously uncharacterized Piezo1-RyR-BKCa signalling axis in small intestinal smooth muscle cells (SMC). This intracellular mechanism relies on a nanoscale signalling complex (<40 nm) comprising an intracellular sensor (intra-Piezo1) and an amplifier (ryanodine receptor, RyR), coupled with a PM effector (large-conductance, Ca2+-activated K+ channels, i.e., BKCa channels). Activating this intracellular complex generated paxilline-sensitive outward currents independent of extracellular Ca2+ and dependent on internal SR Ca2+ stores, consistent with intrinsic organellar mechanotransduction. Within this complex intra-Piezo1 and RyR are positioned to operate as a coupled SR Ca2+ release unit that activates BK channels at SR-PM junctions, driving potent membrane hyperpolarization that reduces smooth muscle contractility, revealing the intra-Piezo1 complex as a molecular brake on excitation. These findings support a model in which mechanotransduction is not confined to the cell surface. Instead a specialized sensor-amplifier-effector complex originating at intracellular organelles amplifies cellular sensitivity to physical force, providing a critical gain-control system that restrains smooth muscle excitability and regulates gastrointestinal (GI) motility. KEY POINTS: This study advances a framework in which intracellular organelles contribute to mechanosensory signalling in gastrointestinal (GI) smooth muscle cells, complementing plasma membrane mechanisms. Piezo1 is predominantly intracellular in intestinal smooth muscle, where this pool, intra-Piezo1, forms a nanoscale signalling complex on the sarcoplasmic reticulum (SR) that positions it within <40 nm of RyR and of sarcolemmal large-conductance, Ca2+-activated K+ (BKCa) channels. Electrophysiological recordings show that this 'sensor-amplifier-effector' mechanism generates potent paxilline-sensitive hyperpolarizing currents that depend on SR Ca2+ release and persist without extracellular Ca2+, amplifying the cell's response to mechanical stress when intra-Piezo1 is activated from the inside out. Activation of this intra-Piezo1-mediated axis significantly dampens smooth muscle contractility, acting as a molecular 'brake' that supports the stretch-induced-relaxation feedback mechanism essential for intestinal function.

PMID 42717762
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PubMedBiomedical reports2026-09-10

Tafolecimab mitigates ox-LDL-induced macrophage foam cell formation and inflammation by modulating SR-A/ABCG1 expression and inhibiting the NF-κB/MAPK pathways.

Yu Xinyi X, Liu Xiaodan X, Dang Yuanye Y, Liu Ruoxuan R

Macrophage foam-cell formation, triggered by excessive uptake of oxidized low-density lipoprotein (ox-LDL) and subsequent intracellular lipid accumulation, represents a critical pathological event in atherosclerotic plaque initiation that drives localized inflammatory responses. The present study investigated the effects of tafolecimab on ox-LDL-induced foam-cell formation and inflammatory responses in murine macrophages, and further explored the underlying molecular mechanisms. Foam-cell models were established by exposing RAW264.7 cells to 100 µg/ml ox-LDL for 24 h. The study groups included a blank control group, a model group, low-, medium- and high-dose tafolecimab groups (5, 10 and 20 µmol/l, respectively), and a positive control group treated with evolocumab. Intracellular lipid accumulation and cholesterol levels were evaluated using Oil Red O staining and a low-density lipoprotein-cholesterol (LDL-C) assay kit. Western blot analysis was performed to determine the expression of cholesterol metabolism-related proteins [class A scavenger receptor (SR-A) and ATP-binding cassette subfamily G member 1 (ABCG1)] and key components of the nuclear factor-κB (NF-κB)/mitogen-activated protein kinase (MAPK) signaling pathways (NF-κB p65 and phosphorylated p38). The concentrations of the inflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the cell supernatant were quantified by enzyme-linked immunosorbent assay. Compared with the blank control, ox-LDL treatment markedly increased intracellular lipid-droplet accumulation and LDL-C content, confirming the successful establishment of a foam-cell model. In vitro, compared with the model group, tafolecimab reduced intracellular lipid accumulation and cholesterol content in a dose-dependent manner (P<0.001). In addition, tafolecimab significantly decreased the expression of the cholesterol influx receptor SR-A while increasing that of the cholesterol efflux transporter ABCG1 (P<0.001). Furthermore, it effectively inhibited the phosphorylation of NF-κB p65 and MAPK p38, which was accompanied by reduced secretion of TNF-α and IL-6 (P<0.001). The present results indicate that tafolecimab inhibits ox-LDL-induced macrophage foam-cell formation and inflammatory responses, likely by modulating the balance between SR-A-mediated cholesterol influx and ABCG1-mediated cholesterol efflux in favor of cholesterol efflux, and by inhibiting NF-κB and MAPK pathway activation.

PMID 42719431
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PubMedTherapeutic advances in hematology2026-09-10

Corticosteroids plus statins in patients with primary immune thrombocytopenia and hyperlipidemia: A multicenter retrospective cohort study.

Hou Xiran X, Zhao Yajing Y, Chen Jian J, Sun Lin L et al.

Hyperlipidemia is prevalent in primary immune thrombocytopenia (ITP) and may exacerbate bleeding severity and compromise treatment responses. Statins possess lipid-lowering and anti-inflammatory properties, but their influence on corticosteroid therapy in ITP patients with hyperlipidemia remains unclear. This study aimed to compare the efficacy and safety of initial corticosteroid therapy between patients with or without concomitant statin use for pre-existing hyperlipidemia in a cohort of newly diagnosed ITP patients. A multicenter retrospective propensity score-matched study. Newly diagnosed ITP patients with pre-existing hyperlipidemia from 9 medical centers were analyzed. Patients were divided into 2 groups based on statin use (statin vs. non-statin). Propensity score matching (PSM) was employed to balance baseline characteristics. Treatment outcomes, including response rates, duration of response (DOR), and safety, were compared. After PSM, 104 patients (52 per group) were included. Baseline characteristics were comparable. Initial response rates were similar between the statin and non-statin groups (67.3% vs. 65.4%, P = 0.836), with the 95% confidence interval (CI) for the between-group risk difference ranging from -15.83% to 19.51%. The median time to response was numerically shorter in the statin group, although this difference did not reach statistical significance (4 [2-8] days vs. 5 [2-12] days, P = 0.054). Notably, the sustained response (SR) rate at 6 months was significantly higher in the statin group compared to the non-statin group (50.0% vs. 30.8%, P = 0.046), with the 95% CI for the between-group risk difference ranging from 0.41% to 36.25%. Kaplan-Meier analysis also demonstrated a significant longer duration of response (DOR) in the statin group (P = 0.044). No serious adverse events were observed in either group during follow-up. In this retrospective, propensity score-matched cohort, concomitant statin use was associated with higher 6-month SR rates and longer DOR in newly diagnosed ITP patients with pre-existing hyperlipidemia, without an apparent increase in serious adverse events. These observational findings warrant further validation in larger, prospective cohorts.

PMID 42719467
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PubMedFrontiers in health services2026-09-10

Exploratory segmentation of selected cardiovascular hospital services in Chile using DRG-based normalized indicators.

Rodríguez José J, Vargas Manuel M, Cos Pilar P, Viveros Andrés A

To assess the use of DRG-based normalized indicators in supporting an exploratory analysis of inter-hospital variation in specific cardiovascular services within the Chilean public system from 2019 to 2023, employing routinely collected administrative data and confining interpretation to descriptive comparisons within the examined sample. The study was designed as descriptive and hypothesis-generating, not to validate hospital performance measures. An analysis was conducted of 141,893 adult discharges from the departments of Cardiology, Cardiovascular Surgery, and Peripheral Vascular Surgery in 54 hospitals within the Chilean public system. Relative throughput, severity, and mortality were summarized into three DRG-based normalized indicators as a function of coded complexity. The hospital-level means were standardized to z-scores prior to principal component analysis. Sampling adequacy for PCA was assessed using the Kaiser-Meyer-Olkin statistic (KMO = 0.6251) and Bartlett's test of sphericity (p = 1.00 × 10-10), which suggested performing exploratory analysis with caution. K-means clustering was then performed on the first two principal components with k = 4, n_init=50, and random_state=42 for reproducibility. Differences (specialty, sex, cluster) in the relative throughput proxy were assessed using the Kruskal-Wallis test and Dunn's post hoc tests. The first two principal components accounted for 86.26% of the variability in the hospital-indicator matrix. K-means clustering resulted in four hospital clusters: cluster 0 (8 hospitals, 14.8%), cluster 1 (8 hospitals, 14.8%), cluster 2 (26 hospitals, 48.1%), and cluster 3 (12 hospitals, 22.2%). Distinct combinations of indicators emerged from the cluster means: cluster 1 had the highest ER (0.9633) and the lowest MR (0.0016), while cluster 3 had low ER (0.2465), high SR (2.3286), and the highest MR (0.0375). Kruskal-Wallis tests indicated significant differences in ER by specialty, sex, and cluster (all p < 0.001). The analysis suggests that DRG-based normalized indicators can be used to explore the segmentation of hospitals providing selected cardiovascular services within the Chilean public system. Their outputs should be interpreted as descriptive and hypothesis-generating rather than as validated measures of hospital efficiency or stand-alone evidence for resource-allocation decisions.

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