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ethinyl estradiol + norethindrone (WC3026 / Generess Fe)

✓ Approved

Actavis · ESR1 · Small Molecule

What is ethinyl estradiol + norethindrone?

ethinyl estradiol + norethindrone is a small molecule developed by Actavis. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesWC3026, Generess Fe
CompanyActavis
Drug ClassSmall Molecule
Molecular TargetESR1, PGR
RouteOral (PO)
StatusApproved

Mechanism of Action

Molecular Targets

ethinyl estradiol + norethindrone acts on 2 molecular targets:

ESR1estrogen receptor 1 (ER, ESR)
PGRprogesterone receptor (NR3C3, PR)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Related Research Articles

PubMedRSC advances2026-11-11

Upcycling recycled PET into a conductive electrode for a molecularly imprinted polymer based electrochemical sensor for 17β-estradiol detection.

Tahir Muhammad Faran MF, Yimyai Tiwa T, D'Haen Jan J, Thoelen Ronald R et al.

The upcycling of plastic waste into advanced materials has emerged as a promising strategy across various technologies, including the development of next-generation sensors. This sustainable approach promotes green technological development. In this work, we transformed recycled polyethylene terephthalate (rPET) into a functional conductive electrode substrate for a molecularly imprinted polymer (MIP) based electrochemical sensor for the detection of 17β-estradiol (E2). The latter also serves as a relevant model compound as a pollutant to study the sensor's applicability in complex matrices. The MIP-based sensor was fabricated by the electropolymerization of an o-phenylenediamine (o-PD) monomer in the presence of E2 template molecules and gold(iii) chloride trihydrate onto gold-coated rPET substrates. The physical properties of MIP films were characterized by scanning electron microscopy (SEM), atomic force microscopy, contact angle measurement, cyclic voltammetry, and electrochemical impedance spectroscopy. The binding of E2 molecules to the MIP surface hindered electron transfer of the redox probes, resulting in a concentration-dependent suppression of the electrochemical current measured by square wave voltammetry. The sensor showed high affinity for E2 molecules with a dissociation constant (K d) of 11.2 nM over a linear detection range of E2 concentrations (0.5-500 nM), and a limit of detection (LOD) of 0.18 and 0.41 nM in PBS and in wastewater samples without any complex pretreatment steps, respectively. This developed MIP-based sensor demonstrated the potential of alternative sensors for real-world environmental monitoring of trace endocrine disruptors, while successfully converting rPET into valuable technological products offers a practical roadmap to accelerate the development of sustainable and circular electronics.

PubMedAnalytical chemistry2026-11-11

Soft Wearable Aptamer Wristband Enables Real-Time Sweat Dual-Hormone Monitoring for Menstrual Cycle Tracking.

Liu Jiaqi J, Yang Yuyang Y, Dong Renfeng R, Xu Tailin T

Noninvasive and longitudinal monitoring of female reproductive hormones could provide valuable information on individualized endocrine dynamics across the menstrual cycle. Here, we developed an integrated wearable electrochemical platform for simultaneous monitoring of estradiol (E2) and progesterone (P4), together with sweat pH and ionic strength. Competitive-displacement aptamer sensing interfaces were constructed for dual-hormone detection, while a Tesla-valve microfluidic network supported passive sweat transport and sequential sample replacement. A flexible wireless electronic system provided multiplexed signal acquisition and wireless data transmission. To improve quantitative reliability under variable sweat conditions, pH-dependent calibration was incorporated into hormone analysis. The platform was evaluated in two volunteers over approximately one complete menstrual cycle, and the longitudinal E2 and P4 profiles obtained by the wearable sensors showed similar temporal trends to those obtained by paired sweat enzyme-linked immunosorbent assay (ELISA) measurements. pH compensation further improved the correlation between sensor and ELISA measurements of hormone concentrations. These results demonstrate the feasibility of integrating dual-hormone sensing, pH-dependent calibration, microfluidic sweat management, and wireless electronics into a wearable platform for longitudinal monitoring of reproductive hormone dynamics.

PubMedTranslational psychiatry2026-11-11

Disruption of the Non-classical ERα-PCYT1A-Phospholipid-NR5A2 Axis impairs kisspeptin signaling in hypothalamic KNDy neurons and drives postpartum depression.

Yang Juanjuan J, Shen Yifen Y, Zhang Jiayi J, Chen Xuan X et al.

Postpartum depression (PPD) is a common neuroendocrine disorder associated with the rapid decline in estrogen levels following childbirth. However, the precise molecular mechanisms through which estrogen withdrawal disrupts hypothalamic signaling, particularly in key reproductive neurons, remain poorly understood. To investigate this, we developed an in vitro PPD-like model using primary embryonic hypothalamic Kisspeptin/Neurokinin B/Dynorphin (KNDy) neurons subjected to estradiol (E2) exposure and subsequent withdrawal. Multi-omics analyses, including proteomics, lipidomics, and transcriptomics, were integrated with functional studies. We discovered that the transcription factor NR5A2 is critical for initiating Kisspeptin rebound after short-term E2 withdrawal by directly binding to the Kiss1 promoter. However, under prolonged withdrawal conditions, this recovery fails. This failure is driven by a disruption in neuronal phospholipid metabolism, characterized by the downregulation of the rate-limiting enzyme PCYT1A and a consequent reduction in specific phosphatidylcholines, PC(32:1) and LPC(24:0), which we identified as crucial stabilizers of NR5A2 activity. Further mechanistic analysis revealed that prolonged E2 withdrawal impairs non-classical Estrogen Receptor α (ncERα) signaling, which upstream regulates PCYT1A expression. Reactivating this ncERα pathway restored phospholipid synthesis and NR5A2-mediated Kisspeptin expression. The entire ncERα-PCYT1A-phospholipid-NR5A2-Kiss1 axis was validated in an in vivo rat model of PPD, where direct intracerebroventricular administration of phospholipids successfully alleviated depressive-like behaviors. Our study defines a novel signaling cascade that links estrogen dynamics with neuronal lipid metabolism to control postpartum neuroendocrine recovery, offering fresh mechanistic and therapeutic insights into PPD.

PubMedAMB Express2026-11-11

HSD17B8 axis modulates Pseudomonas aeruginosa-associated lung inflammatory injury in bronchiectasis.

Zheng Shaochu S, Bao Chongxi C, Tang Jinling J, Hong Kangkang K et al.

Non-cystic fibrosis bronchiectasis (NCFB) is characterized by persistent Pseudomonas aeruginosa (P. aeruginosa) colonization and uncontrolled pulmonary inflammation, while the underlying metabolic regulatory mechanism remains poorly understood. This study aimed to explore the potential analyze correlations of the HSD17B8 metabolic axis in lung inflammatory injury related to P. aeruginosa in NCFB. Transcriptome sequencing was performed on peripheral blood and tissue samples from NCFB patients and healthy controls to screen differentially expressed genes. Two-sample Mendelian randomization integrated with protein quantitative trait locus data was applied to evaluate the potential association between candidate genes and NCFB susceptibility. The expression of HSD17B8 in clinical samples was further validated by RT-qPCR. Meanwhile, a rat model of P. aeruginosa-infected pulmonary inflammation was established to investigate the influences of estrone intervention on lung pathology, pro-inflammatory cytokines (IL1β, IL6), and steroid metabolite homeostasis. A total of 249 overlapping differentially expressed genes were identified. Mendelian randomization analysis indicated that downregulated HSD17B8 expression was nominally correlated with elevated NCFB risk (OR 0.76, 95% CI 0.60-0.95, P = 0.0159). Clinically, HSD17B8 was significantly decreased in NCFB patients and correlated with higher E-FACED severity scores. In the P. aeruginosa-related rat model, reduced HSD17B8 expression disturbed estradiol/estrone balance, increased IL1β and IL6 levels, and aggravated lung pathological lesions. Exogenous estrone was correlated with dose-dependent alleviation of inflammatory lesions via inhibiting inflammatory response and restoring metabolic homeostasis. Collectively, HSD17B8 is potentially involved in the progression of P. aeruginosa-associated NCFB. Altered HSD17B8 expression is associated with disturbed steroid balance and aggravated inflammatory responses related to microbial infection. Targeting HSD17B8 and its downstream steroid metabolites may offer a promising metabolic intervention strategy for P. aeruginosa-associated infectious bronchiectasis.

PubMedMedicine2026-11-11

Comprehensive identification of lactate metabolism-related genes in recurrent spontaneous abortion: An observational study integrating bioinformatics and experimental validation.

Tang Daili D, Chen Lin L, Zheng Huiling H, Huang Zhi Z et al.

Recurrent spontaneous abortion (RSA) is a complex multifactorial disease. Lactate metabolism (LM) has been implicated in RSA pathogenesis, but the underlying molecular mechanisms remain unclear. This observational study aimed to identify key LM-related genes (LM-RGs) in RSA and explore their potential regulatory mechanisms and therapeutic targets. The study combined bioinformatics analysis with experimental validation. The training dataset GSE26787 and validation dataset GSE165004 were obtained from the Gene Expression Omnibus database. Differentially expressed genes were identified using the limma package. Candidate LM-RGs were obtained by intersecting differentially expressed genes with 262 LM-RGs from the Gene Set Enrichment Analysis database. Hub genes were identified through protein-protein interaction network analysis using the CytoHubba plugin (National Cheng Kung University). Key genes were further screened using Boruta and random forest machine learning algorithms, followed by expression validation in both Gene Expression Omnibus datasets. Reverse transcription-quantitative polymerase chain reaction was performed on 10 RSA and 10 control endometrial samples to validate key gene expression. Gene set enrichment analysis and gene set variation analysis were conducted to explore functional pathways. Regulatory networks involving microRNAs, long noncoding RNAs, and transcription factors were constructed, and potential therapeutic drugs were predicted using the Drug Signatures Database. CALR (upregulated) and PIEZO1 (downregulated) were identified as key genes in RSA and were functionally linked to pathways such as cytokine signaling. Furthermore, we delineated a regulatory network governing these genes, implicating the long noncoding RNA X-inactive specific transcript and shared transcription factors, including MYC proto-oncogene, bHLH transcription factor and vitamin D receptor. We propose several candidate drugs, including estradiol, predicted to target both CALR and PIEZO1. This study identifies CALR and PIEZO1 as key LM-RGs in RSA, with significant dysregulation confirmed in clinical samples. These genes are involved in cytokine signaling pathways and are regulated by complex molecular networks. The identification of common targeting drugs provides a foundation for developing novel therapeutic strategies for RSA. Further studies are warranted to validate these findings and explore their clinical applications.

PubMedZhonghua nan ke xue = National journal of andrology2026-11-11

[Qianlie Shukang tablet ameliorates prostatic hyperplasia in rats: Mechanistic exploration integrating network pharmacology with experimental validation].

Liang Qiying Q, Wei Yanyun Y, Zhao Lijuan L, Sa Rina R et al.

Objective To evaluate the therapeutic efficacy of Qianlie Shukang (QLSK) tablet on benign prostatic hyperplasia (BPH) by establishing a rat model of BPH. Methods Forty SPF-grade male Sprague-Dawley (SD) rats were divided into six groups by random number table method: control (sham surgery, equal volume of CMC-Na solution), BPH model (equal volume of CMC-Na solution), positive control (finasteride 0.5 mg/kg), and QLSK low- (145.94 mg/kg), medium- (291.88 mg/kg), and high-dose (583.76 mg/kg) groups. Except for the control group which underwent sham surgery modeling (subcutaneous injection of peanut oil 0.5 mg/[kg·d] ), the BPH rat model was established in all other groups through castration surgery combined with testosterone propionate injection (0.5 mg/[kg·d], subcutaneously). All groups were intragastrically administered their respective drug solutions dissolved in carboxymethylcellulose sodium (CMC-Na) once daily. After 28 consecutive days of intervention, the rats were sacrificed for sample collection. The pathological changes in prostate tissue were observed using hematoxylin and eosin (HE) staining. Levels of inflammatory and oxidative stress factors in rat prostate tissue including tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), IL-8, IL-2, IL-1β, IL-10, prostaglandin E2 (PGE2), superoxide dismutase (SOD), and malondialdehyde (MDA) as well as levels of sex hormones and growth factors including dihydrotestosterone (DHT), testosterone (T), estradiol (E2), vascular endothelial growth factor (VEGF), transforming growth factor-β1 (TGF-β1) and immunoglobulin G (IgG) were measured by ELISA. Serum creatinine (CREA), urea (UREA), and glucose (GLU) levels were detected using an automatic biochemical analyzer. Network pharmacology technology was employed to screen for potential core targets of QLSK in treating BPH in rats (key molecules in pathways such as PI3K/AKT and NF-κB). The protein expression levels of Bax, PI3K, IL-1β, and TNF-α in rat prostate tissue were detected by immunohistochemistry (IHC). Results The increases of prostate wet weight and volume index in BPH rats were significantly inhibital by QLSK(P<0.05). Histopathological analysis demonstrated marked improvement in glandular epithelial hyperplasia and interstitial inflammatory infiltration, with no significant effects on renal function markers (CREA, UREA) or blood glucose levels (P>0.05). Medium- and high-dose QLSK groups exhibited decreased prostatic levels of pro-inflammatory factors (IL-8, IL-2, TGF-β1; P<0.05) and androgens (DHT, T; P<0.05), while elevating anti-inflammatory cytokines (IL-6, IL-10; P<0.01) and SOD activity (P<0.05). Based on TCMSP database and literature database, 35 active ingredients (ginsenoside Rb1, ginsenoside Rd, etc.) were screened and obtained, involving 44 core targets (PIK3CA, IL-1β, AKT1, TNF, etc.) and 72 KEGG pathways. The DAVID enrichment analysis showed that the PI3K-Akt and NF-κB signaling pathways (P<0.01) had a significant correlation. Immunohistochemical results showed that the expression of pro-apoptotic protein Bax was up-regulated (P<0.01) and the expression of PI3K and TNF-α was down-regulated (P<0.01) in prostate tissues after the intervention of QLSK, and the medium dose of QLSK could significantly reduce the expression level of IL-1β (P<0.01). Conclusion This study integrates experimental and bioinformatics approaches to reveal the "multi-component, multi-target, multi-pathway" therapeutic mode of QLSK against BPH. The anti-hyperplastic effects are mediated through dual inhibition of PI3K-Akt pathway activation and NF-κB-mediated inflammatory response. However, the in vivo validation of the key active ingredients and the mechanism of multi-target synergistic regulation still need to be further elucidated.

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