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Drug Database
ES

estrogen (Estratab / esterified estrogen / Menest)

✓ Approved

AbbVie, Inc. · ESR1

什么是 estrogen？

estrogen 是一种治疗药物，由AbbVie, Inc.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Estratab, esterified estrogen, Menest
公司AbbVie, Inc.
分子靶点ESR1
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, AbbVie, Inc.

作用机制

分子靶点

estrogen 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

estrogen 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
Surgical and medical proceduresHormone replacement therapy✓ Approved

相关研究文献

PubMedCells2026-10-26

Selective Estradiol Sensitivity in 12Z Human Endometriotic Epithelial Cell Line.

Banerjee Shohini S, Chopra Esha E, Smith Ian M IM, Stroka Kimberly M KM

Estradiol (E2) is a potent estrogen molecule that plays a crucial role in regulating numerous healthy and pathophysiological processes. To model estrogen-dependent cellular activities in vitro in a physiologically meaningful way, cells chosen for experimentation should exhibit sensitivity to E2. The 12Z human endometriotic epithelial cell line is gaining attention as a model for estrogen-dependent conditions, but its functional responsiveness to E2 has not been well characterized. For the passage range in the following study, we found that E2 does not statistically significantly influence 12Z proliferation, wound closure, or single-cell migration. However, 12Zs were selectively responsive to E2 in 3D migration models where the cells were physically confined. Upregulating ESR1, the primary mediator of estrogenic action, in the 12Zs did not enhance their functional E2 sensitivity. These results highlight the importance of verifying hormone responsiveness when using 12Z cells to model estrogen-dependent processes and conditions.

PMID 42929847
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PubMedFood & function2026-10-26

The remodeling of gut microbiota driven by changes in the living environment: a new perspective on the imbalance of the gut-bone axis in perimenopausal women.

Jin Jiayi J, Wang Xinyu X, Ma Jing J, Du Peng P et al.

The perimenopausal period represents a critical transition stage during which female bone health shifts from a relatively stable state to accelerated bone loss. The development and progression of osteoporosis during this stage are influenced not only by estrogen decline but also by the gut microbial ecological background shaped by long-term environmental factors. With changes in modern dietary patterns, lifestyles, and environmental exposure profiles, the human gut microbiota undergoes continuous remodeling, which may disrupt the gut-bone axis regulatory network by affecting estrogen metabolism, immune-inflammatory homeostasis, and microbiota-derived metabolite production, thereby contributing to impaired bone metabolism in perimenopausal women. This review focuses on the research framework of "changes in the living environment-gut microbiota remodeling-osteoporosis" and systematically summarizes the theoretical basis of gut microbiota-mediated regulation of bone homeostasis. Furthermore, the potential mechanisms by which gut-bone axis dysregulation contributes to the development of osteoporosis during the perimenopausal period are discussed, and future research directions involving multi-omics integration, artificial intelligence, and longitudinal cohort studies are highlighted. Accordingly, this review proposes a conceptual framework linking long-term changes in the living environment, gut microbiota remodeling, and altered bone metabolism. This framework provides a new perspective for understanding how an environmentally shaped microbial background may contribute to changes in bone health during the perimenopausal transition.

PMID 42929788
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PubMedInternational journal of fertility & sterility2026-10-26

Therapeutic Potential of Bone Marrow-Derived Mesenchymal Stem Cells in A Letrozole-Induced Rat Model of Polycystic Ovary Syndrome.

M Abou-El-Naga Amoura A, Younes Elarby Nada N, El-Dusoky Sara S, Fayad Eman E et al.

Polycystic ovary syndrome (PCOS) is a prevalent metabolic and reproductive disorder and one of the leading causes of infertility. Bone marrow-derived mesenchymal stem cells (BM-MSCs) possess anti-inflammatory properties and have shown potential in alleviating PCOS manifestations in experimental models. This study aimed to evaluate the therapeutic efficacy of transplanted BM-MSCs and BM-MSC-derived culture media in a letrozole (LTZ)- induced PCOS rat model. The experimental study was conducted on 50 female Sprague Dawley rats aged (4-6 weeks) and weighing (100-120 g), using a LTZ-induced PCOS model. Animals were randomly assigned to 4 groups, including control, PCOS, BM-MSC-treated, and BM-MSC culture media-treated groups. BM-MSCs were isolated from (bone marrow) and administered via (tail vain) at a dose of (1×106 BM-MSC). Blood samples were collected to measure hormonal and metabolic parameters (insulin, androgen, progesterone, estrogen, follicle-stimulating hormone (FSH), and luteinizing hormone (LH) using [enzyme-linked immunosorbent assay (ELISA) technique). Ovarian tissues were analyzed by for histopathological and immunohistochemical methods to assess [key markers, e.g., follicular development, tumor necrosis factor-alpha (TNF), and vascular endothelial growth factor (VEGF)]. The PCOS group exhibited hormonal imbalance, metabolic disturbance, and ovarian dysfunction. BMMSC treatment significantly reduced insulin (P=0.003) and androgen levels (P=0.040), while restoring progesterone (P=0.003), estrogen (P=0.007), FSH (P=0.009), and LH (P=0.001) to near-normal levels. BM-MSCs markedly improved both metabolic and reproductive parameters, effectively restoring fertility in the PCOS model. Treatment with BM-MSC-derived culture media produced partial improvement but did not fully reverse PCOS manifestations. BM-MSCs improved ovarian structure and function, ameliorating both metabolic and reproductive dysfunction in the PCOS rat model. BM-MSC transplantation yielded the most favorable outcomes, whereas BM-MSCderived culture media alone provided incomplete therapeutic benefits.

PMID 42929028
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PubMedFrontiers in molecular biosciences2026-10-26

Copper complexes in the triple-negative breast cancer landscape: advances and opportunities.

Lima Paula Marynella Alves Pereira PMAP, de Matos André Carlos Pereira ACP, Guimarães Gabriela da Silva GDS, Barbosa Laryssa Aparecida Sales LAS et al.

Triple-negative breast cancer (TNBC) is a subset of mammary tumors with heterogeneous biology, lacking estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2 (HER2). Patients generally exhibit an aggressive course, less favorable disease-specific outcomes, and a higher propensity for early recurrence, with chemotherapy remaining the primary systemic treatment eligible for all patients. In this sense, efforts are urgent to identify new effective compounds, aiming to increase disease-free and overall survival. Copper complexes have emerged as promising in oncology by regulating redox balance and modulating hallmarks such as proliferation, apoptosis, epithelial-mesenchymal transition, and angiogenesis. Furthermore, complexes containing copper tend to have low adverse effects. In TNBC, copper compounds may represent at least one component of a multi-action management strategy, being potentially effective against these tumors. The focus of this review is to provide information on TNBC biology and the role of copper in its signaling pathways, addressing the current copper complexes that have been explored to improve treatment.

PMID 42928858
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PubMedFASEB journal : official publication of the Federation of American Societies for Experimental Biology2026-10-26

Persistent Pelvic Adhesions and Fibrotic Remodeling Following Ectopic Lesion Ablation in a Mouse Model of Endometriosis.

Yun Sohyeon S, So Kyeong A KA, Jeong Eunhee M EM, Hoover Marissa G MG et al.

Endometriosis is a chronic, estrogen-dependent inflammatory disorder characterized by ectopic endometrial-like lesions, fibrosis, and persistent pelvic pain. Although ectopic lesions are important contributors to pain, symptom severity often correlates poorly with lesion burden, suggesting lesion-independent mechanisms. Here, we investigated the contribution of ectopic lesion-derived cells to persistent pelvic adhesions, fibrotic remodeling, and endometriosis-associated behavioral alterations using a mouse model. A syngeneic model combined with inducible diphtheria toxin receptor (iDTR)-mediated cell ablation was used to selectively eliminate donor-derived progesterone receptor-expressing ectopic cells. Endometriosis was induced by transplantation of uterine tissue from Pgrcre/+Rosa26iDTR/mTmG donor mice into recipients, followed by diphtheria toxin-mediated lesion ablation. Lesion burden, pelvic adhesions, and fibrotic remodeling were assessed by imaging, histology, and molecular analyses, while behavioral outcomes were evaluated using non-evoked assays. Selective ablation eliminated detectable GFP-positive ectopic lesions. Histological and molecular analyses demonstrated significantly reduced collagen deposition and α-SMA-positive fibrotic remodeling within adhesion-associated tissues relative to established ectopic lesions, although these measures remained elevated above sham controls. However, despite lesion ablation, no statistically significant differences were detected between DT- and vehicle-treated mice in nesting or marble-burying performance, although the modest cohort size may have limited detection of partial behavioral effects. These findings indicate that, although fibrosis in adhesion-associated tissues was reduced relative to established ectopic lesions, residual fibrotic remodeling persisted above sham levels, whereas behavioral outcomes showed variable responses without a significant, uniform reversal, highlighting the potential importance of targeting fibrotic and adhesive remodeling in addition to ectopic lesions.

PMID 42929462
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PubMedCurrent oncology (Toronto, Ont.)2026-10-26

Targeted Hotspot Mutation Analysis of KRAS, TP53, and PTEN in Endometrial Cancer Revealed by Next-Generation Sequencing.

Hussain Salar Saadi SS, Amin Zahra Abdulqader ZA

Endometrial cancer (EC) is a heterogeneous malignancy characterized by diverse molecular and clinicopathological features. This study investigated somatic mutations in three hotspot-region genes commonly implicated in EC pathogenesis (KRAS, TP53, PTEN) and their associations with clinical characteristics and biomarkers, rather than comprehensive genomic profiling. Targeted next-generation sequencing (NGS) was used to analyze hotspot regions of KRAS (exons 2 and 4), TP53 (exons 4 and 7), and PTEN (exon 2), while mutation parameters, including mutant allele frequency (MAF), allelic depth, and variant frequency, were assessed alongside clinicopathological data. Pathogenic KRAS missense mutations (p.G12D and p.A146V), TP53 missense (p.G245C) and stop-gain (p.W91*) variants, and a pathogenic PTEN mutation (p.D52Y) were identified, with MAF values ranging from 36.2% to 77.1%. One patient also exhibited microsatellite instability-high (MSI-H) status. Serum CA125 concentrations were significantly higher in serous carcinoma than in endometrioid carcinoma and non-malignant cases, suggesting potential prognostic rather than diagnostic value. This suggests an association between CA125 levels and histological subtype rather than diagnostic or prognostic value, as this study did not evaluate survival, recurrence, or longitudinal outcomes. The detected mutations highlight disruptions in estrogen signaling, DNA damage response, and PI3K/AKT pathway regulation, illustrating the diversity of alterations detectable within these three hotspot regions in EC. These findings provide insight into the mutational status of KRAS, TP53, and PTEN hotspot regions in endometrial cancer and support the potential use of identified genetic alterations as biomarkers for precision medicine and targeted therapeutic strategies, while indicating that CA125's clinical utility in EC, whether diagnostic or prognostic, remains to be established through outcome-based studies. This also reinforces CA125's limited diagnostic but possible prognostic role in EC management.

PMID 42930168
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