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estradiol +levonorgestrel (Fem7 Plus / HRT, Merck)

✓ Approved

Merck KGaA · ESR1 · Small Molecule

What is estradiol +levonorgestrel?

estradiol +levonorgestrel is a small molecule developed by Merck KGaA. It is approved for therapeutic indications via topical or transdermal.

Drug Profile

Brand NamesFem7 Plus, HRT, Merck
CompanyMerck KGaA
Drug ClassSmall Molecule
Molecular TargetESR1, PGR
RouteTopical, Transdermal
StatusApproved
Sources: ClinicalTrials.gov, Merck KGaA

Mechanism of Action

Molecular Targets

estradiol +levonorgestrel 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.

Therapeutic Indications

estradiol +levonorgestrel is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Surgical and medical proceduresHormone replacement therapy✓ Approved

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Yeshitela Biruk B, Abegaz Woldaregay Erku WE, Alemu Fekadu F, Mengesha Mesfin M et al.

Antiretroviral therapy (ART) has revolutionized the management of HIV/AIDS, yet the emergence of drug resistance mutations remains a significant concern. This study aimed to characterize drug resistance mutations among patients failing first-line antiretroviral treatment in Ethiopia. A total of 52 HIV-infected patients who experienced first-line ART failure were recruited between March 2020 - March 2021 from selected hospitals of Amhara and Oromiya regions. The viral load was measured by Abbott Real-Time HIV-1 automated extraction and detection m2000 system platform (Abbott Molecular Inc., Des Plaines, IL, USA). The partial pol gene region of HIV-1 was amplified and sequenced using an in-house HIV - 1 drug resistance assay. The Stanford HIVDB v9.0 algorithm, and the Calibrated Population Resistance (CPR) Tool and the IAS-USA mutation lists were used to identify mutations conferring resistance. A total of 52 HIV-positive individuals met the study's inclusion criteria. Genotypic analysis revealed a diverse spectrum of resistance mutations, with the prevalence of potential drug resistance (PDR) reaching 46.2% (24/52) for nucleoside reverse transcriptase inhibitors (NRTIs), 69.2% (36/52) for non-nucleoside reverse transcriptase inhibitors (NNRTIs), and 32.7% (17/52) for protease inhibitors (PIs). The most commonly identified mutations associated with high-level drug resistance included M184V/I, K103N/S, V82I and K20R. This study reveals a significant burden of drug resistance mutations among Ethiopian HIV patients on ART, reinforcing the urgent need for continuous surveillance to inform and strengthen treatment protocols. Targeted interventions-such as pre-treatment resistance testing and individualized regimen optimization-are essential to stem the transmission of resistant HIV strains and safeguard the sustainability of Ethiopia's ART programs.

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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.

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Vankemmel Romain R, Chaib Sofiane S, Malléa-Hivert Marine M, Merlen Emilie E et al.

Cross-reactivity with high molecular-weight (MW) macroprolactin in prolactin (PRL) immunoassays has been the subject of numerous studies. In contrast, little data are available regarding Big-PRL, a 50-60 kDa PRL isoform. The immunoreactivity of Big-PRL was evaluated on five platforms (Alinity (Abbott), DxI 800 (Beckman Coulter), Liaison XL (DiaSorin), Kryptor compact plus (Thermo Scientific), and iSYS (IDS Immunodiagnostic Systems)) using 10 serum samples characterized by gel filtration chromatography (GFC) and containing between 17 and 80 % of Big-PRL. The spread of the results as a function of Big-PRL percentage was determined. Bland Altman bias between assays was calculated using a panel of GFC-characterised sera containing macroprolactin (n=46) or monomeric PRL (n=45). The Big-PRL samples were obtained from nonpregnant women, seven of whom had galactorrhea or oligospaniomenorrhea. All assays recognized Big-PRL in undiluted serum but to a variable extent. The spread of total PRL values correlated positively with Big-PRL percentage (r=0.954, p<0.0001). In samples containing >70 % Big-PRL, the methods ranked in the same order of recognition as that observed with macroprolactin-rich samples. Big-PRL was strongly detected by Alinity and iSYS whereas Kryptor and DxI were less sensitive to Big-PRL, as observed with macroprolactin. Consequently, the risk of false diagnosis of hyperprolactinemia tended to be lower with these two last assays. All five immunoassay platforms recognize the Big-PRL component in serum but to a variable extent. A high proportion of Big-PRL, combined with the use of a highly cross-reactive assay, may cause a false diagnosis of hyperprolactinemia.

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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.

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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.

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