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metoprolol ER + hydrochlorothiazide (Selopress Zok / Dutoprol)

✓ Approved

AstraZeneca UK Limited · ADRB1 · 小分子

什么是 metoprolol ER + hydrochlorothiazide？

metoprolol ER + hydrochlorothiazide 是一种小分子，由AstraZeneca UK Limited研发。该药已获批，用于治疗相关适应症，给药途径：Oral (PO)。

药物档案

商品名Selopress Zok, Dutoprol
公司AstraZeneca UK Limited
药物类别小分子
分子靶点ADRB1
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, AstraZeneca UK Limited

作用机制

分子靶点

metoprolol ER + hydrochlorothiazide 作用于 1 个分子靶点：

ADRB1adrenoceptor beta 1 (B1AR, RHR)
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

metoprolol ER + hydrochlorothiazide 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Vascular disordersHypertension✓ Approved

相关研究文献

PubMedPolymers2026-10-27

Enhancing the Electrorheological Effect of Crosslinked Poly(ionic liquid)s by Copolymerizing with Acrylonitrile.

Liu Yuchi Y, Li Yu Y, Pang Haoming H, Yin Jianbo J

Poly(ionic liquid)s (PILs) are polyelectrolytes that can produce a strong anhydrous electrorheological (ER) effect, which overcomes the limitation of the hydrous ER effect of classic polyelectrolytes. Crosslinking PILs can further broaden the working temperature range of the ER effect of PILs by increasing or eliminating the glass transition temperature. However, the crosslinked network also easily restricts the ion movement and decreases the interfacial polarization and ER effect of PILs. In this paper, we propose a chemical way to enhance the ion movement and ER effect through the copolymerization of crosslinked PILs with polar acrylonitrile (AN). The structure of the obtained copolymers was characterized by different techniques; the dielectric properties of the copolymer particles in suspensions were analyzed by dielectric spectroscopy, and the ER effect of suspensions of copolymer particles was measured by a rheometer under electric fields. It showed that the copolymerization of crosslinked PILs with an appropriate small amount of AN could enhance the ER effect, which originates from the enhancement of the interfacial polarization rate of crosslinked PILs due to the decrease in the activation energy of ions by polar AN copolymerization.

PMID 42942703
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PubMedBehavioral sciences (Basel, Switzerland)2026-10-27

Emotion Regulation and Brain Mechanisms: A Transdiagnostic Perspective on Neural Circuits, Individual Differences, and Clinical Translation.

Carvalho Sandra S

Emotion regulation (ER) difficulties are now firmly established as a transdiagnostic feature of psychiatric and stress-related disorders. Large-scale meta-analyses published in 2026 confirmed ER impairments across fifteen diagnostic categories, shifting the key question from whether ER is transdiagnostic to how this knowledge can inform diagnosis and treatment. This Perspective argues that ER should be conceptualized as a transdiagnostic neurocognitive dimension rather than a disorder-specific deficit. To support this view, three complementary studies are integrated: neuroimaging studies of prefrontal-limbic and large-scale brain networks involved in cognitive reappraisal; evidence of ER-related neural alterations across mood, anxiety, trauma-related, personality, and addictive disorders; and research on individual differences and neuromodulation that explain variability in regulatory capacity and treatment response. ER is framed within a broader executive-function model, operating as a "hot" executive process alongside "cool" cognitive-control functions. Building on this evidence, a Layered Transdiagnostic Model of Emotion Regulation (LTM-ER) is proposed. The model includes a shared transdiagnostic core circuit (Layer 1), disorder-specific neural signatures (Layer 2), and individual moderators such as developmental history, dispositional traits, regulatory strategies, and stimulation parameters (Layer 3). Five testable predictions are derived from the model, highlighting how multimodal biomarkers and personalized interventions may advance precision approaches to emotion dysregulation across psychiatric disorders.

PMID 42938519
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PubMedCurrent issues in molecular biology2026-10-27

Dynamics of Endoplasmic Reticulum Stress Responses in Cells with Different Endoplasmic Reticulum Volumes and Senescence States.

Mishina Aleksandra V AV, Pas'ko Alexey Yu AY, Kolesov Dmitry V DV, Kovalenko Lyudmila V LV et al.

The Unfolded Protein Response (UPR) determines cell fate under endoplasmic reticulum (ER) stress, yet its temporal dynamics across different cell types and senescence states re-main poorly understood. In this study, we investigated UPR kinetics in endothelial and T-lymphoblastoid cell lines with distinct ER volumes, as well as in senescent FRSN cells undergoing ER expansion. Variations in ER volume were confirmed via confocal microscopy and flow cytometry. Using the 'gene response time' metric, we demonstrated experimentally and through mathematical modeling that the BiP response kinetics closely correlate with variations in ER volume. Applying this metric to presenescent FRSN cells with a significantly expanded ER, we found that their ER stress response machinery maintained a response time similar to that of exponentially growing FRSN cells, but exhibited a lower amplitude and a prolonged lag phase, leading to chronic ER stress signaling such as a protracted XBP1(S) expression profile. Scanning ion-conductance microscopy (SICM) revealed a significant decrease in the stiffness of the near-surface layer of presenescent cells, reflecting a rarefaction of the actin cortex and possibly cytoplasmic dilution. We propose that this structural remodeling could be associated with active intracellular transport impairment that weakens the temporal 'tethering' of the proteome to the genome upon cellular senescence. Consequently, the stress response machinery fails to scale proportionally with cell enlargement during senescence, creating a state of 'functional dilution'. This prevents enlarged senescent cells from mounting a scaled response, resulting in prolonged stress signaling and increased vulnerability to proteotoxic stress.

PMID 42939565
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PubMedIndian journal of cancer2026-10-27

ESR1 mutations and endocrine resistance in ER-positive breast cancer: Molecular mechanisms, liquid biopsy, and emerging targeted therapies.

Rajendran Ulagarasi U, Sekar Abinaya A, Padmavathy Karthika K, Jethani Priyanka P et al.

Estrogen receptor-positive (ER+)/human epidermal growth factor receptor 2-negative (HER2-) breast cancer is the most common type of breast cancer, and endocrine therapy remains the cornerstone of treatment. This narrative review summarizes the biology of mutations in the ligand-binding domain of the estrogen receptor (ER), the utility of circulating tumor DNA (ctDNA) for detecting these alterations, and the evidence supporting emerging therapies for ESR1 -mutant metastatic disease to provide clinicians with a practical, evidence-based framework for managing patients with the disease. Mutations in the ligand-binding domain of ESR1 , such as Y537S and D538G, lock the receptor in a constitutively active conformation, increasing resistance to aromatase inhibitors and variably affecting sensitivity to selective ER degraders (SERDs). These mutations can be detected non-invasively by longitudinal ctDNA next-generation sequencing, often before radiographic progression is evident, although questions remain regarding optimal assay sensitivity, clonal heterogeneity, and monitoring intervals. Elacestrant, the first oral SERD approved for ESR1 -mutant disease, improved progression-free survival in the phase III EMERALD trial and subsequent trials of oral SERDs, and the proteolysis-targeting chimera vepdegestrant (EMBER-3, SERENA-6, and VERITAC-2) provides further supporting evidence. Other complete ER antagonists and covalent antagonists remain in clinical trials. ESR1 mutation testing and treatment adaptation according to ctDNA are now part of the precision management of ER+/HER2- breast cancer, but more prospective research is required for the best sequencing and monitoring strategies.

PMID 42937403
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PubMedBehavioral sciences (Basel, Switzerland)2026-10-27

Parental Emotion Regulation, Psychological Distress, and Family Involvement in Education Among Chilean Caregivers: An Observed-Variable Analysis.

Fuentes-Vilugrón Gerardo G, Arriagada-Hernández Carlos C, Caamaño-Navarrete Felipe F, Correa-Araneda Francisco F et al.

This study examined the association between parental emotion regulation (ER) and family involvement in education (FIE), including the potential mediating role of psychological distress, operationalized through depressive, anxiety, and stress symptomatology (DASS), and the moderating role of caregiver gender, while accounting for sociodemographic variables. A cross-sectional study was conducted with a sample of n = 219 Chilean parents/caregivers. The Emotion Regulation Evaluation Scale (RE-MESACTS), the Depression, Anxiety and Stress Scale (DASS-21), and the Family Involvement in Education Scale (EPFE) were administered. A sequential observed-variable analytical strategy combining regression, mediation with non-parametric bootstrap (5000 resamples), moderation, covariate-adjusted models, and complementary sensitivity analyses was employed. ER was positively associated with FIE after accounting for DASS (β = 0.230, p = 0.004) and negatively associated with DASS (β = -0.410, p < 0.001). However, DASS was not significantly associated with FIE (β = -0.065, p = 0.365), and the indirect effect of ER on FIE through DASS was not statistically significant (B = 0.026, p = 0.374). A statistically significant ER × Gender interaction was observed (B = 0.739, p < 0.001). Simple-slope analyses showed a positive association among female caregivers (B = 0.345, p < 0.001) and a negative association among male caregivers (B = -0.394, p = 0.021). An exploratory complementary multigroup analysis showed that the ER → FIE path differed between gender groups, χ2(1) = 7.90, p = 0.005. Most sociodemographic covariates were not significantly associated with FIE; however, caregivers of students attending private fee-paying schools reported significantly higher FIE than those associated with public schools ( = 3.162, p = 0.045). Overall, ER was positively associated with educational involvement, whereas DASS did not statistically mediate the ER-FIE association. The observed ER × Gender interaction suggests a potential gender-dependent pattern; however, because the male subgroup was small (n = 38), the gender-specific estimates should be regarded as preliminary and require replication in larger and more gender-balanced samples. The findings highlight the relevance of parental emotion regulation for family involvement and provide a basis for further investigation of psychological and sociodemographic factors associated with educational involvement.

PMID 42938552
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PubMedAntioxidants (Basel, Switzerland)2026-10-27

Unusual Switch of Cell Death Mode by Docosahexaenoic Acid (DHA) via Enhancing Endoplasmic Reticulum Peroxidation Induced by Lipophilic Iron Complex.

Shao Bo B, Sheng Zhi-Guo ZG, Li Huan H, Jiang Shun-Li SL et al.

Although ferroptosis is a programmed iron-dependent cell death, many lipophilic iron complexes fail to induce ferroptosis through iron overload. The underlying mechanisms remain unclear. Here we found that a typical lipophilic iron complex 8-hydroxyquinoline (8HQ)-Fe(III) (1: 1, 10 μM), can efficiently induce cellular iron overload, lipid peroxidation, and finally cytotoxicity. However, the resulting cell death mode was not typical ferroptosis: it was not inhibited by the classic ferroptosis inhibitors and exhibited mitochondrial swelling rather than shrinkage. Mechanistic studies revealed that 8HQ-Fe(III) triggered both endoplasmic reticulum (ER) peroxidation and mitochondrial damage. The ER-targeted antioxidant (stobadine) inhibited lipid peroxidation but did not suppress cell death. In contrast, mitochondrial protectants effectively blocked 8HQ-Fe-induced cell death by mitigating mitochondrial damage. This indicates that mitochondrial damage plays an overwhelmingly dominant role in driving cell death. Strikingly, pre-incubation with docosahexaenoic acid (DHA) can strongly enrich the ER membrane and increase its peroxidation. As expected, both stobadine and the well-known ferroptosis inhibitor (Fer-1) suppressed 8HQ-Fe(III)-induced cell death via inhibition of ER peroxidation, while mitochondrial protectants failed to prevent cell death. Mitochondrial shrinkage was also observed. Thus, making ER peroxidation the dominant driver of cell death by DHA pretreatment will switch the cell death modality from non-ferroptosis to classical ferroptosis. This study revealed that the balance between ER peroxidation and mitochondrial damage dictated the type of iron-dependent cell death, and established DHA-primed 8HQ-Fe(III) as a novel, tunable strategy for efficiently inducing ferroptosis by deliberately shifting subcellular peroxidation dominance.

PMID 42939877
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