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tamoxifen (tamoxifen, Douglas)

✓ Approved

Douglas Pharmaceuticals Limited · ESR1 · 小分子

什么是 tamoxifen？

tamoxifen 是一种小分子，由Douglas Pharmaceuticals 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tamoxifen, Douglas
公司Douglas Pharmaceuticals Limited
药物类别小分子
分子靶点ESR1
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, Douglas Pharmaceuticals Limited

作用机制

分子靶点

tamoxifen 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

tamoxifen 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
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Breast cancer✓ Approved

相关研究文献

PubMedGraefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie2026-07-27

Structural and microvascular retinal changes in tamoxifen users assessed by optical coherence tomography and OCT angiography.

Kilic Songul S, Ozturk Mine M, Ağın Abdullah A, Onder Feyza F

To investigate subclinical retinal structural, microvascular, and outer retinal reflectivity changes in women receiving tamoxifen therapy for at least 12 months without clinically apparent retinopathy. A total of 48 eyes from 48 women who had been receiving tamoxifen therapy for at least 12 months and 52 eyes from 52 age-matched healthy female controls were included in the study. Only the right eye of each participant was analyzed to avoid inter-eye correlation. All participants underwent comprehensive ophthalmic examination, swept-source optical coherence tomography (OCT), OCT angiography (OCTA), and quantitative outer retinal reflectivity analysis using ImageJ. Retinal thickness, choroidal thickness, and OCTA-derived vessel density parameters were compared between groups. Absolute and RPE-normalized reflectivity values of the retinal pigment epithelium (RPE), ellipsoid zone (EZ), and external limiting membrane (ELM) were quantified using standardized vertical line-profile analysis. The mean age was 45.9 ± 5.4 years in the tamoxifen group and 46.6 ± 4.7 years in the control group. Retinal thickness parameters, choroidal thickness, and OCTA-derived vessel density metrics of the superficial and deep capillary plexuses and choriocapillaris were comparable between tamoxifen users and controls (all p > 0.05). Mean and central RPE reflectivity were significantly higher in the tamoxifen group than in controls (RPEav, p = 0.037; RPEc, p = 0.003), whereas EZ and ELM reflectivity values and all RPE-normalized relative reflectivity indices did not differ significantly between groups. A localized increase in outer retinal vessel density was observed in the superior sector in tamoxifen users, without corresponding widespread microvascular alterations. No significant correlations were found between duration of tamoxifen exposure and OCT, OCTA, or reflectivity parameters. Tamoxifen therapy for at least 12 months is associated with selective increases in RPE reflectivity despite preserved retinal structure and microvasculature. Quantitative reflectivity analysis may serve as a sensitive, noninvasive marker for early, subclinical retinal stress preceding clinically apparent tamoxifen retinopathy.

PMID 42507182
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PubMedDentistry journal2026-07-27

Estradiol Enhances Alveolar Bone Resorption by Promoting Osteoclast Differentiation in Experimental Periodontitis.

Yasuda Keisuke K, Matsuda Shinji S, Memida Takumi T, Yoshimoto Tetsuya T et al.

Background/Objectives: Estrogen is a key female hormone; however, its role in periodontitis remains poorly understood. This study investigated the effects of 17β-estradiol (E2) on experimental periodontitis using an ovariectomy (OVX) model with E2 administration. Methods: Female mice aged 8-10 weeks underwent OVX, followed by induction of ligature-induced periodontitis, and subsequent quantification of alveolar bone resorption. Additional groups received an aromatase inhibitor or E2 supplementation after OVX, with subsequent induction of periodontitis and evaluation of bone resorption. Histological analysis assessed multinucleated giant cells and tartrate-resistant acid phosphatase-positive osteoclasts on the bone surface. Gingival tissue was analyzed for gene expression related to osteoclastogenesis. The effect of E2 on osteoclast differentiation from bone marrow cells was also examined. Results: OVX significantly reduced serum E2 levels and decreased alveolar bone resorption. Aromatase inhibitor administration similarly reduced bone loss. Histological evaluation revealed a reduced number of resorbing osteoclasts in OVX mice, whereas E2 supplementation increased osteoclast numbers. No significant changes in inflammatory cytokine or receptor activator of nuclear factor-kappa B ligand (RANKL) expression were observed. E2 promoted osteoclast differentiation in vitro, and treatment with E2 prior to RANKL stimulation further increased the number of osteoclasts. This effect was suppressed by an estrogen receptor antagonist. Moreover, E2 enhanced the expression of osteoclast differentiation-associated genes in the presence of RANKL, an effect abolished by tamoxifen. Conclusions: E2 increased alveolar bone resorption in experimental periodontitis, likely by promoting osteoclast differentiation, independent of inflammatory cytokine or RANKL gene expression.

PMID 42505728
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PubMedCureus2026-07-25

Synchronous HER2-Positive Breast and Gastric Cancers: A Dual Diagnostic Challenge With a Single Treatment Possibility.

Morka Jeremi J, Biernat Paula P, Czerwinska Anna A, Cybulska Klaudia K et al.

Synchronous primary malignancies are rare and represent a significant diagnostic and therapeutic challenge, particularly when both tumors share a targetable molecular alteration. We present a case of synchronous human epidermal growth factor receptor 2 (HER2)-positive breast and gastric cancers treated using a common HER2-directed strategy. A 77-year-old female was admitted with a right breast lesion classified as Breast Imaging Reporting and Data System (BI-RADS) 5. A core needle biopsy was performed, which confirmed a grade 2 invasive ductal carcinoma. The results showed positivity for estrogen receptor and progesterone receptor, a HER2 immunohistochemical score of 2+, and a Ki-67 index of 15%. Chromogenic in situ hybridization (CISH) confirmed HER2 amplification, establishing a luminal B/HER2-positive subtype (cT4b cN0 cM0). The patient was started on a course of tamoxifen treatment. During the course of treatment, there was a progression of dysphagia and rapid weight loss, which prompted further investigation. A CT scan revealed thickening of the gastric cardia. Following the failure of gastroscopies due to esophageal stenosis, exploratory laparoscopy was performed. The histopathological examination revealed that the gastric cardia tumor was grade 1 tubular adenocarcinoma, with HER2 overexpression (immunohistochemistry (IHC) 3+), proficient mismatch repair (pMMR)/microsatellite stability (MSS) status, and no hormone receptor expression. Due to the unresectable nature of the disease, the patient received a combination of palliative mFOLFOX6 (leucovorin calcium (folinic acid), fluorouracil, and oxaliplatin) and trastuzumab, in addition to ongoing endocrine therapy. Following four cycles, imaging showed disease stabilization, with decreased cancer antigen 19-9 (CA 19-9) and carcinoembryonic antigen (CEA) levels, and evidence of local tumor regression. Despite an initial positive response, the patient subsequently experienced disease progression and clinical deterioration after three months. The overall survival rate was 11.25 months. This case demonstrates the importance of comprehensive molecular diagnostics and the potential of HER2-targeted therapy as a unified treatment approach for synchronous HER2-positive malignancies.

PMID 42500763
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PubMedACS omega2026-07-24

pH-Responsive Tamoxifen-Loaded Poly(ε-caprolactone)/Poly(vinylpyrrolidone)/Poly(ethylene oxide) Fibers for Treatment of Breast Cancer: Investigation of Controlled Drug Release Properties.

Selçuk Pekdemir Sibel S, Doğan Ulu Öznur Ö, Ulu Ahmet A, Pekdemir Mustafa Ersin ME et al.

Herein, this study reports the production of fiber mats obtained by electrospinning, produced by mixing tamoxifen (TAM) drug with polycaprolactone (PCL), polyvinylpyrrolidone (PVP), and poly-(ethylene oxide) (PEO), with the aim of eliminating cancer cells through controlled drug release. The fabricated fiber mats were thoroughly characterized by several analytical techniques. FTIR analysis indicated strong intermolecular interactions between polymer molecules of the fiber. XRD analysis revealed that fibers are semicrystalline in nature. Scanning electron microscopy verified the uniform nanofibers with bead-free morphology and the average fiber diameter ranged from 346 to 418 nm with drug loading. An increase in tensile strength (TS) and elongation at break (EAB) values of the fibers was observed after drug loading. TS and EAB was obtained up to 0.35 MPa and 88.69%, which are desired for the application. The release of TAM from the fabricated fibers strongly depended on pH value and the drug was fully released in 100 h at pH 5.5. Moreover, Higuchi, Hixson-Crowell, and Korsmeyer-Peppas kinetics confirmed the controlled release of the drug from the fiber mats via diffusion. After 24, 48, and 72 h, the cell viability rates in L929 cells were determined to be 69.7%, 88.5%, and 63.7%, respectively, while cell viability rates were calculated as 69.9%, 68.9%, and 57.7%, respectively, in MCF-7 cells. Additionally, acridine orange (AO)/ethidium bromide (EB) staining was used to detect apoptosis, and fluorescent staining images revealed apoptotic effects. Taken together, these findings suggested that the produced fiber mats could be a promising candidate for controlled TAM release in breast cancer treatment.

PMID 42495357
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PubMedAngewandte Chemie (International ed. in English)2026-07-23

A Self-Reinforcing LipoTIDE Nanoplatform That Overcomes Lipid-Buffering Ferroptosis Resistance for Enhanced Cancer Therapy.

Guan Guoqiang G, Hu Xi X, Zhou Mengjie M, Li Wenlong W et al.

Lipid metabolic rewiring is a hallmark of malignancy, allowing tumor cells to sequester fatty acids within lipid droplets (LDs) as a protective reservoir that quenches reactive oxygen species (ROS)-driven lipid peroxidation and thereby evades ferroptosis. Although lipophagy selectively degrades LDs to release free fatty acids (FFAs) and remodel lipid homeostasis, leveraging this process to overcome lipid-buffering ferroptosis resistance remains largely unexplored. Here, we report LipoTIDE (Lipophagy-Tuning Induced Death Enhancer), a self-reinforcing nanoplatform that primes lipophagy-primed ferroptosis by coupling precise lipophagy activation with catalytic ROS generation to dismantle LDs-mediated metabolic defenses in tumors. LipoTIDE co-delivers ultrasmall Pt3Co nanoalloys and tamoxifen within a pH-responsive amphiphilic polymer, enabling tumor-targeted disassembly and localized therapeutic amplification. Triggered by the tumor acidity, LipoTIDE releases Pt3Co nanoalloys for multiple catalytic activities and tamoxifen for initiating lipophagy and decreasing pH value, establishing a self-reinforcing loop that sustains lipophagy and ferroptosis. Additionally, FFAs from lipophagy, together with the Pt3Co nanoalloys, resensitize resistant cancer cells to Pt3Co-catalyzed ROS, thereby amplifying ferroptosis. Consequently, LipoTIDE precisely disrupts lipid homeostasis, triggers robust ferroptotic tumor suppression, and exhibits minimal systemic toxicity. These findings establish lipophagy-primed ferroptosis as a generalizable and actionable strategy for dismantling lipid-buffering defenses of tumors.

PMID 42490743
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PubMedKidney international2026-07-23

Biallelic pathogenic variants in EXOSC3 mediate renal thrombotic microangiopathy of the kidney.

Walsh Patrick R PR, Basu Uttiya U, Barakat Tahsin Stefan TS, Beck Bodo B BB et al.

Thrombotic microangiopathy (TMA) is characterized by the classical triad of microangiopathic hemolytic anemia, thrombocytopenia and acute kidney injury. Complement inhibition with eculizumab is highly efficacious in TMA secondary to complement dysregulation. However, there are a growing number of eculizumab nonresponsive TMAs reported. Recently a syndromic form of TMA due to recessive variants in RNA exosome components (EXOSC3, EXOSC5) has been identified. The underlying pathogenesis remains unclear. We identified 34 children across Europe with pontocerebellar hypoplasia 1b (PCH1b) due to EXOSC3 rare variants and reviewed their clinical history for signs of TMA. To further examine the pathogenesis, a tamoxifen-inducible whole body Exosc3 conditional knockout mouse model (Exosc3KO) was used. Thirteen (eight male, five female) cases of EXOSC3-TMA were identified. In the United Kingdom the incidence of EXOSC3-TMA was 0.004/million/year. Three children received long-term eculizumab therapy, one child failed to respond and two relapsed on treatment. Exosc3KO demonstrated cell cycle arrest and apoptosis resulting in death in a median of eight days with sequelae noted in actively dividing cells in the bone marrow and large intestine. In this timeframe no kidney pathology was identified. EXOSC3-TMA is a severe, early-onset, C5 inhibitor resistant TMA. EXOSC3-TMA should be considered in eculizumab resistant pediatric TMA, particularly in the context of neurodevelopmental disease.

PMID 42486191
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