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estrogens (Cenestin / Bijuva, Barr)

✓ Approved

Teva Pharmaceutical Industries Ltd. · ESR1

什么是 estrogens？

estrogens 是一种治疗药物，由Teva Pharmaceutical Industries Ltd.研发。该药已获批，用于治疗相关适应症，给药途径：Intravaginal、Oral (PO)。

药物档案

商品名Cenestin, Bijuva, Barr
公司Teva Pharmaceutical Industries Ltd.
分子靶点ESR1
给药途径Intravaginal, Oral (PO)
状态Approved
来源： ClinicalTrials.gov, Teva Pharmaceutical Industries Ltd.

作用机制

分子靶点

estrogens 作用于 1 个分子靶点：

ESR1estrogen receptor 1 (ER, ESR)
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

estrogens 针对 3 个适应症，涉及 2 个治疗领域。

治疗领域疾病/病症分期
Reproductive system and breast disordersAtrophic vulvovaginitis✓ Approved
Surgical and medical proceduresHormone replacement therapy✓ Approved
Reproductive system and breast disordersMenopausal symptoms✓ Approved

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Dengue virus-2 triggers Epstein-Barr virus replication in primary B cells by co-opting the IRE1-XBP1 signaling axis.

Deng Xiaomei X, Deng Rongping R, Guo Xiuyan X, Li Jialing J et al.

The intricate interplay between co-infecting viral pathogens within a host can significantly influence disease outcomes. Dengue virus (DENV), a globally prevalent arbovirus from the Flaviviridae family, and Epstein-Barr virus (EBV), a ubiquitous human herpesvirus, share extensive geographical overlap, yet their potential interactions remain largely uncharacterized. This study elucidates a novel molecular mechanism whereby DENV-2 infection triggers disruption of EBV latency. We systematically demonstrate that DENV-2 infection consistently induces EBV lytic gene expression and viral replication in diverse cellular contexts, including epithelial cell lines and, critically, in primary human B lymphocytes-the principal reservoir of latent EBV. Mechanistically, we establish that the substantial burden of DENV-2 protein synthesis and replication induces profound endoplasmic reticulum (ER) stress, activating the unfolded protein response (UPR). Through pharmacological inhibition and genetic knockdown, we dissect the three UPR branches and identify the IRE1-XBP1 signaling axis as the indispensable pathway for this phenomenon. DENV-2 infection promotes the endoribonuclease activity of IRE1, leading to the unconventional splicing of XBP1 mRNA into its transcriptionally active isoform, XBP1s. Depletion of IRE1 or XBP1 attenuated DENV-induced BZLF1 expression, whereas ectopic XBP1s expression increased BZLF1 transcription. Our findings delineate a precise virus-host-virus signaling model in which an acute RNA virus engages a cellular stress pathway to promote entry into the EBV lytic program and viral genome amplification. This provides a new paradigm for understanding the pathobiology of dengue fever and the complex dynamics of the human virome.IMPORTANCEThis research uncovers a previously unrecognized molecular dialog between two of the world's most common viral pathogens. By demonstrating that dengue virus infection can awaken dormant Epstein-Barr virus, this study provides a mechanistic basis for the long-suspected but poorly understood complications arising from viral co-infections. We pinpoint a specific cellular stress pathway, the IRE1-XBP1 axis of the unfolded protein response (UPR), as the critical molecular switch. This discovery is significant because it not only explains how an acute viral illness can trigger the reactivation of a latent, potentially oncogenic virus but also opens new avenues for therapeutic intervention. Understanding this intricate interplay could lead to novel strategies for managing severe dengue and other diseases where viral co-infection is a contributing factor to pathogenesis.

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Novel roles of the Epstein-Barr virus BRRF1 protein in post-transcriptional RNA regulation.

Campbell Ashley M AM, Shire Kathy K, Ho Talia T, Sinay Zora Z et al.

In lytic infection, Epstein-Barr virus (EBV) proteins manipulate cellular processes in multiple ways to facilitate virion production and overcome host antiviral responses. Here, we screened a library of EBV lytic proteins for those that manipulate or localize to cellular processing bodies (PBs), known to play important roles in RNA surveillance and miRNA-mediated translational control. One EBV protein, BRRF1, was identified that partially localized to PBs, and affinity purification-mass spectrometry experiments showed that it interacted with the CCR4-NOT complex-a known component of PBs with multiple roles in post-transcriptional mRNA regulation. The CNOT9 subunit of CCR4-NOT was sufficient to bind BRRF1, and its downregulation diminished BRRF1 interaction with the CNOT1 scaffold protein, indicating its importance in mediating the CCR4-NOT interaction with BRRF1. A BRRF1 double-point mutant was generated that failed to bind CNOT9 or interact with CCR4-NOT and was used to assess the importance of the BRRF1-CCR4-NOT interaction. Luciferase reporter assays identified multiple roles for BRRF1 in post-transcriptional regulation, including polyadenylation-dependent destabilization effects and interference with miRNA function, the latter of which was dependent on BRRF1 binding to CCR4-NOT. In addition, mRNA sequencing experiments comparing cells with and without BRRF1 expression identified multiple transcripts affected by BRRF1, some of which were at least partly dependent on the BRRF1-CCR4-NOT interaction. These include Claudin 6, whose transcripts and protein were downregulated by BRRF1 expressed on its own, as well as in lytic infection. Thus, we have identified multiple roles for BRRF1 in post-transcriptional mRNA regulation, some of which involve interaction with CCR4-NOT. To efficiently generate virions, Epstein-Barr virus (EBV) must manipulate cellular processes to optimize the environment and overcome host antiviral defenses. Through unbiased screening methods, we have identified an EBV protein (BRRF1) that localizes to cellular bodies, which play key roles in mRNA regulation, and that interacts with a cellular complex with multiple critical roles in post-transcriptional mRNA regulation. As expected from these interactions, we found that BRRF1 has multiple previously unknown roles in disrupting mRNA levels and translation. Interestingly, one of the transcripts targeted by BRRF1 is Claudin 6, which has multiple roles in cancers, leading to increased cell proliferation and invasion. Our study provides additional insight into how EBV proteins manipulate cells to promote infection and affect oncogenesis.

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Elimination of tumors and their metastasis by a thermally responsive silica nanoparticle decorated with an anti-PD-L1 antibody fragment.

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Metastasis and recurrence remain the leading causes of cancer-related mortality; however, existing therapies offer limited protection against systemic tumor spread following primary treatment. Here, we report a dual-function nanoplatform, anti-programmed cell death protein-ligand 1 PD-L1 antigen-binding fragment (Fab)-conjugated thermally responsive silica (α-TRS) nanoparticles, rationally designed to achieve complete ablation of primary tumors through photothermal therapy (PTT) while simultaneously priming systemic antitumor immunity to suppress distant metastasis. Indocyanine green (ICG) was encapsulated within mesoporous silica nanoparticles with high efficiency (91.2%), and the Fab of an anti-PD-L1 antibody was site-specifically conjugated to the nanoparticle surface via NTA-Ni2+/His-tag chemistry. With 808 nm near-infrared (NIR) laser irradiation, α-TRS generated sufficient heat (∼50 °C) to induce ablative tumor cell death in vitro and achieved complete remission of 4T1 breast tumors and CT-26 colon tumors in vivo following intratumoral injection. Critically, mice cured of primary tumors by α-TRS-mediated PTT were fully protected against subsequent intravenous rechallenge with lung-metastatic 4T1 and CT-26 cells, whereas mice treated with PTT alone (TRS without Fab) showed only partial protection. This abscopal-like protection was mechanistically linked to the robust activation of tumor antigen-specific CD4+ and CD8+ T cells, including enhanced production of interferon (IFN)-γ, tumor necrosis factor (TNF)-α, perforin, and granzyme B in response to tumor antigens. These findings suggest that ablative PTT combined with local PD-L1 checkpoint blockade can convert a localized thermal intervention into durable systemic immunity, offering a promising proof-of-concept strategy for simultaneously treating primary tumors and preventing metastatic recurrence.

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Mechanistic Insights into Palladium-Catalyzed 1,4-Hydrofunctionalization of 1,3-Enynes through a Coordination-Induced Orbital Polarization Framework.

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Palladium-catalyzed 1,4-hydrofunctionalization of 1,3-enynes provides a powerful and atom-economical approach to multisubstituted allenes. Despite extensive synthetic developments, the fundamental origin of activation mode selection and regioselectivity in these transformations remains elusive. Herein, we propose a coordination-induced orbital polarization (CIOP) framework that describes how established metal-substrate orbital interactions associated within different Pd coordination environments generate distinct site-dependent redistributions of frontier-orbital character across the conjugated enyne π-system. These electronic responses provide a common basis for rationalizing activation mode selection and regioselectivity. The applicability of the CIOP framework was examined through density functional theory investigations of Pd-catalyzed hydroboration, hydroamination, and hydrosilylation. Across all three reaction classes, the calculated orbital polarization patterns were consistent with the experimentally observed activation pathways and site selectivities. These findings support CIOP as a unified interpretative framework for relating metal coordination, enyne electronic structure, and catalytic divergence across the Pd-catalyzed hydrofunctionalization reactions examined in this study.

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Exciton diffusion length (LD) is a key parameter determining the power conversion efficiency of organic solar cells (OSCs), yet its fast and accurate calculation is computationally challenging due to thin-film structural disorder and the long-range nature of excitonic coupling. Herein, we introduce a coarse-grained Coulomb matrix (CG-CM) descriptor that enables rapid and accurate prediction of excitonic couplings. By mapping molecular conjugated backbones onto a fixed number of beads, our descriptor eliminates the dimensionality dependence on the number of atoms, allowing the machine learning model to generalize across molecules with different sizes and chemical structures. The model achieves high accuracy with a coefficient of determination (R2) exceeding 0.92 across diverse nonfullerene acceptor systems, including Y-type and ITIC-type materials. We further demonstrate the model's reliability in capturing excitonic coupling fluctuations, predicting LD in disordered thin films, and reproducing LD anisotropy in crystalline systems. This work provides a powerful and efficient tool for high-throughput screening of high-performance organic photovoltaic materials.

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Developing organic photodetectors (OPDs) that can detect in deep shortwave infrared (deep-SWIR) region (1.2-1.6 μm) is technologically important. Yet, the performance of the state-of-the-art deep-SWIR OPDs remains substantially limited. Herein, we report a selenium-integrated quinoidal small molecular acceptor, SeBz-4Cl, enabling highly sensitive deep-SWIR photodetection. Selenium incorporation enhances quinoidal character along the conjugated backbone of the molecules, thus expanding absorption approaching 1.5 μm. Moreover, SeBz-4Cl with strengthened intermolecular interactions led to an ideal film morphology, which reduced Urbach energy and favored charge dynamics. Under -1 V voltage bias, the SeBz-4Cl-based OPD achieved a low dark current density of 2.97 × 10-7 A cm-2 and an external quantum efficiency (EQE) of 7.8% at 1310 nm, together with a high specific detectivity (D*) exceeding 1011 Jones across 500-1400 nm, representing advanced deep-SWIR OPD performance. Furthermore, an optical communication system and a flexible imager under 1.2 μm illumination were demonstrated, highlighting potential of these deep-SWIR OPDs for information electronics and next generation optoelectronic applications in future.

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