estradiol (Vagifem)
✓ ApprovedNovo Nordisk A/S · ESR1 · 小分子
什么是 estradiol?
estradiol 是一种小分子,由Novo Nordisk A/S研发。该药已获批,用于治疗相关适应症,给药途径:Intravaginal。
药物档案
| 商品名 | Vagifem |
| 公司 | Novo Nordisk A/S |
| 药物类别 | 小分子 |
| 分子靶点 | ESR1 |
| 给药途径 | Intravaginal |
| 状态 | Approved |
作用机制
分子靶点
estradiol 作用于 1 个分子靶点:
| ESR1 | estrogen receptor 1 (ER, ESR) |
治疗适应症
estradiol 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 |
|---|---|---|
| Reproductive system and breast disorders | Atrophic vulvovaginitis | ✓ Approved |
相关研究文献
Vaginal cuff dehiscence and bowel evisceration as a late-onset complication of vaginal vault prolapse: a case report.
Schröder Carolin C, Egger Eva K EK, Pantenburg Jakob Friedemann JF, Dohmen Jonas J et al.
Vaginal cuff dehiscence (and evisceration, VCDE) after hysterectomy is a rare, but potentially serious complication. Current medical literature describes the most critical risk factors for VCDE after hysterectomy as surgical technique, use of thermal energy, early mechanical stress (especially sexual intercourse), infection, smoking, and obesity. There is currently no evidence regarding a potential association between VCDE and anti-HER2 therapy. We report a late-onset VCDE in a patient receiving combined antihormonal and anti-HER2 therapy, and discuss the hypothesis-generating question of a potential association, as well as the bowel-preserving surgical management. We report the case of an 81-year-old White woman with hormone receptor-positive breast cancer receiving antihormonal therapy with anti-HER2 treatment and recurrent vaginal vault prolapse who presented with acute vaginal evisceration of the small bowel. She had undergone a vaginal hysterectomy for pelvic organ prolapse 3 years earlier. Emergency surgical management was performed via laparotomy with repositioning of the small bowel, vaginal cuff closure, and concomitant sacrocolpopexy. One week later, re-laparotomy was required due to an open abdomen associated with paralytic small bowel ileus; bowel resection was not necessary. The last follow-up was carried out 21 months postoperatively. The patient was asymptomatic and showed no evidence of recurrent prolapse. This case highlights a rare late-onset VCDE in a patient receiving combined antihormonal and anti-HER2 therapy, a clinical context not previously described. While causality cannot be established, this report raises the hypothesis of a potential association between targeted therapy and impaired tissue integrity.
Is Vaginal Estrogen Treatment Associated with Risk of Thrombosis in Postmenopausal Women? A Scoping Review.
Juul Sofie L SL, Glavind-Kristensen Marianne M, Bor Pinar P, Bor Mustafa Vakur MV
Although the thromboembolic risk associated with oral estrogen is recognized, the risk profile of vaginal estrogen treatment remains inconclusive. This scoping review aims to explore available evidence on the association between vaginal estrogen treatment in postmenopausal women and the risk of thrombosis. We conducted a systematic search of PubMed and Embase, investigating vaginal estrogen treatment and thrombosis, for all records up to May 21, 2025. The process was performed according to the Preferred Reporting Items for Systematic Reviews and Meta-Analysis Extension for Scoping Reviews (PRISMA-ScR) and a preregistered protocol (osf.io/hgecd). We excluded systemic estrogen treatments, contraception, fertility treatments, gender-affirming therapies, and hormone treatments other than estrogen. Eligible study designs included clinical trials, randomized controlled trials, observational, case-control, and cohort studies. The search identified 866 articles, whereof 8 were eligible. Manual searching through citations and references yielded 3 additional studies, resulting in 11 included articles, all observational. One study reported a reduced risk of recurrent myocardial infarction (MI) following discontinuation of vaginal estrogen treatment (adjusted hazard ratio [aHR]: 0.54; 95% confidence interval [CI]: [0.34-0.86]). Remaining studies found no thrombosis risk in vaginal estrogen users. For venous thromboembolism (n = 6), effect estimates ranged from null to reduced risk (aHRs: 0.68 [0.36-1.28], to 1.06 [0.58-1.93]), similar for MI (n = 5; aHRs: 0.52 [0.31-0.85] to 0.83 [0.77-0.89]) and stroke (n = 6, aHRs: 0.68 [0.62-0.70] to 0.96 [0.93-0.99]). This scoping review, including studies of generally moderate to high methodological quality, indicates no increased risk of thrombosis associated with vaginal estrogen use in postmenopausal women. Further prospective, high-quality clinical trials, including high-risk populations and women with prior thrombosis, are warranted.
Defining functional puberty in female C57BL/6J mice using endocrine, cytological and morphological markers.
Chester Mélanie M, Wyckens Noalig N, Airaud Eloïse E, Corre Raphaël R et al.
Puberty marks the transition to reproductive competence and is driven by activation of the hypothalamo/pituitary/gonadal axis, culminating in first ovulation in females. In mice, puberty onset is commonly inferred from vaginal opening and estrous cyclicity, but the precise timing of first ovulation remains unclear. Here, we aimed to define reliable parameters of functional puberty in female C57BL/6J mice by integrating external, endocrine, and morphological measures. Vaginal opening and daily vaginal cytology were combined with daily serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) measurements and ovarian histology using the Pubertal Ovarian Maturation Score (Pub-Score), which estimates ovulation based on follicular development and corpus luteum morphology. Notably, we observed substantial inter-individual variability in puberty-related events, and no link between estrous cytology and first ovulation. Pub-Score analysis indicated that first ovulation occurred between 36 and 54 days postnatal, with a mean around 44 days, with no correlation with vaginal cytology. LH surges were detected in some of the females that had ovulated and showed limited temporal correspondence with vaginal cytology or Pub-Score estimates. Together, these findings demonstrate that puberty in female mice is a gradual, asynchronous process and that external or cytological markers alone are insufficient to define functional reproductive maturity.
Genome-scale metabolic modelling identifies vaginal microbiome members as potential probiotics.
Glass Emma M EM, Kolling Glynis L GL, Papin Jason A JA
Probiotic supplements are marketed for diverse health benefits, yet species inclusion often lacks functional rationale. Our survey of 352 over-the-counter probiotic products available in the USA revealed 36 unique microbial species. However, there is no clear link between species inclusion and the intended health benefit. Here, to address this gap, we developed HaPaPro, a collection of 1,012 genome-scale metabolic models spanning pathogenic, probiotic and host-associated bacteria, constructed from publicly available genome sequences. Flux balance analysis revealed that probiotic species fail to capture the metabolic diversity of host-associated microbes. Focusing on vaginal health, we computationally identified vaginal microbes with metabolic profiles overlapping Gardnerella vaginalis. In vitro spent media assays using 11 vaginal isolates showed variable inhibition of G. vaginalis, primarily driven by D-lactic acid production, which was also produced by non-Lactobacillus species. These findings highlight the need for function-based probiotic design and demonstrate a scalable framework integrating metabolic modelling with experimental validation.
Timing of carbetocin administration in vaginal deliveries: a double-blind, randomized controlled trial.
Yıldız Pınar P, Keles Esra E, Yıldız Gazi G, Kırlangıç Mehmet Mete MM et al.
This study aimed to compare the efficacy of administering carbetocin before versus after placental delivery in preventing PPH in low-risk vaginal deliveries. The randomized controlled trial was conducted at Kartal City Hospital, Istanbul, Turkey. A total of 160 primiparous women with uncomplicated pregnancies who underwent vaginal delivery were enrolled. Participants were randomly assigned to receive 100 mcg of carbetocin either before or after placental delivery. The primary outcome was the incidence of PPH. Secondary outcomes included the need for additional uterotonics, manual removal of the placenta with consequent antibiotic administration, blood transfusions, maternal adverse events, and changes in hemoglobin levels at baseline and 24 h postpartum. The incidence of PPH was significantly lower in the carbetocin-before group than in the carbetocin-after group (p=0.015). The carbetocin-before group had a significantly lower mean hemoglobin drop compared to the carbetocin-after group (p<0.001). The need for additional uterotonics was significantly higher in the carbetocin-after group (p<0.001). Manual placenta removal and the need for antibiotics were more frequent in the carbetocin-before group (p=0.017). No significant differences in adverse maternal events were observed between the groups. Administering carbetocin before placental delivery significantly reduces the incidence of PPH, blood loss, and the need for additional uterotonics. However, the increased rate of manual placenta removal necessitates individualized risk-benefit assessment; pre-placental administration may be most advantageous in women at elevated risk for PPH, in whom the hemorrhagic benefit outweighs the risks associated with manual extraction.
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