Drug Database
ES

estrogen (Estratab / esterified estrogen / Menest)

✓ Approved

AbbVie, Inc. · ESR1

What is estrogen?

estrogen is a therapeutic agent developed by AbbVie, Inc.. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesEstratab, esterified estrogen, Menest
CompanyAbbVie, Inc.
Molecular TargetESR1
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, AbbVie, Inc.

Mechanism of Action

Molecular Targets

estrogen acts on 1 molecular target:

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

Therapeutic Indications

estrogen is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Surgical and medical proceduresHormone replacement therapy✓ Approved

Related Research Articles

PubMedFrontiers in oncology2026-10-22

Integrated CDK4/6 inhibitor resistance and primary-metastatic discordance in hormone receptor-positive/HER2-negative metastatic breast cancer: a translational framework focused on invasive ductal carcinoma with gastric metastasis.

Cheng Minyi M, Wang Dongqing D, Lin Yingyi Y, Wu Cangui C et al.

CDK4/6 inhibitors have reshaped treatment for hormone receptor-positive (HR+)/HER2-negative metastatic breast cancer, but resistance frequently emerges and may interact with metastatic phenotypic evolution. We developed an integrated resistance-discordance framework and explored its clinical interpretability in invasive ductal carcinoma (IDC) with gastric metastasis. Public MSK-INK4 (cBioPortal study ID: breast_ink4_msk_2021) and MBCproject (brca_mbcproject_wagle_2017) cohorts were curated for HR+/HER2-negative disease. A five-module CDK4/6 inhibitor resistance score (0-5) was constructed from predefined mutation and copy-number events. In MBCproject RNA-seq samples, single-sample gene-set enrichment analysis quantified proliferation and estrogen-response activity. Discordance burden was defined as z(proliferation score) minus z(ER score), using primary tumors as the reference. Three institutional IDC gastric-metastasis cases were projected onto the framework for interpretability but not inferential testing. Seventy HR+/HER2-negative MBCproject samples and 1116 deduplicated MSK-INK4 metastatic samples were analyzed. MBCproject metastases had higher resistance scores than primary tumors (P = 0.001), whereas metastatic scores were similar between MBCproject and MSK-INK4 (P = 0.202). Metastases showed higher proliferation activity (P = 0.014) and a trend toward lower ER activity (P = 0.071). The high-resistance/high-discordance quadrant was enriched for PI3K-axis events (OR = 16.52; P = 0.034), chromatin-remodeling loss-of-function events (OR = 12.47; P = 0.001), and cell-cycle/RB-axis events (OR = 9.03; P = 0.001). Among the three IDC gastric-metastasis cases, two available gastric NGS profiles mapped to predefined resistance modules, and the case with increased gastric Ki-67 showed the strongest IHC-adapted discordance and projected toward the high-resistance/high-discordance phenotype. Coupling resistance-associated genomic events with metastatic phenotype discordance may provide a clinically interpretable lens for HR+/HER2-negative metastatic breast cancer and for rare IDC gastric-metastasis presentations.

PMID 42903090
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PubMedBMB reports2026-10-21

8-Chloro-cyclic AMP mediates growth inhibition of breast cancer cells via regulation of Yin-Yang 1 and estrogen receptor α levels.

Cho Young Jun YJ, Choi Ki Young KY, Byeon Soo-Min SM, Kim Soyeon S et al.

As a derivative of cyclic AMP (cAMP), 8-Chloro-cyclic AMP (8-Cl-cAMP) is shown to induce growth inhibition, apoptosis, and differentiation in different cancer cells by activating AMP-activated protein kinase (AMPK) and p38 mitogen-activated protein kinase (p38 MAPK). The p38 MAPK is known as a downstream mediator of 8-Cl-cAMP and binds to a multifunctional transcription factor Yin-Yang 1 (YY1). Although cytotoxic effects of 8-Cl-cAMP on cancer cells have been studied over several decades, molecular details or interplays by which they allow selective cytotoxicity to certain cancer cells remain unclear. Here, we further examined how YY1 expression could be affected by 8-Cl-cAMP treatment to understand the mechanism involved in cytotoxic effects of 8-Cl-cAMP on breast cancer cells. Treatment with 8-Cl-cAMP significantly decreased YY1 levels. Such decrease was reversed by co-treatment with ABT702, an adenosine kinase inhibitor. Moreover, pre-treatment with Compound C, an AMPK inhibitor, restored 8-Cl-cAMP-mediated decrease of YY1 expression, whereas SB203580 (a p38 MAPK inhibitor) did not. Meanwhile, siRNA against YY1 caused phosphorylation of p38 MAPK but not of AMPK, resulting in cell growth inhibition and cell death, as did 8-Cl-cAMP. These in vitro results suggest that 8-Cl- cAMP-mediated cytotoxicity might involve downregulations of YY1, which functions downstream of AMPK and upstream of p38 MAPK, and of ERα levels, supporting AMPK-YY1-p38 MAPK signaling axis in response to 8-Cl-cAMP. This study also indicates that 8-Cl-cAMP may have therapeutic potential against breast cancers expressing YY1 and ERα.

PMID 42902568
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PubMedFrontiers in endocrinology2026-10-20

Integrated pituitary adaptations to the low estrogen state.

Miles Tiffany K TK, Odle Angela K AK, Herdman Ashley K AK, Clark Lillian G LG et al.

Estrogen's broad trophic effects on anterior pituitary function are not fully understood. The compound 4-vinyl cyclohexene diepoxide (VCD) induces early ovarian failure and reduced E2 production, which may differentially affect anterior pituitary cells. We recently identified transcriptomic changes in pituitary gonadotropes at the single-cell level in females treated with VCD for 20 days, which were acyclic, with low serum estradiol (E2) levels and 8-12-fold increases in gonadotropins 138 days later. We tested vehicle-control and VCD-treated female mice in metabolic cages and assayed serum hormone levels by EIA, and pituitary cell transcripts by qRT-PCR and single-cell RNA-seq. VCD-treated mice showed normal metabolic health. Compared with controls, VCD-treated females exhibited a 5-fold elevation in serum pituitary thyroid-stimulating hormone (TSH) levels and near-normal thyroid hormone levels. Pituitary Tshb mRNA levels were reduced, and pituitary Gh, Prl, and Pomc mRNA levels were unchanged. Serum growth hormone (GH) levels were higher in VCD-treated mice than in controls 62 days after the start of treatment (perimenopause) and then reduced to control levels after 118-138 days. Ingenuity Pathway Analyses (IPA) of upregulated differentially expressed gene (DEG) transcripts predicted activation of G protein-mediated signaling pathways in one scRNA-seq somatotrope subcluster and in the thyrotrope and lactotrope clusters. In contrast, downregulated DEGs in corticotropes and the remaining two somatotrope clusters predicted downregulation of critical signaling pathways. The unchanged pituitary Gh, Prl, and Pomc mRNA levels correlated with unchanged serum levels. The interim rise in serum GH 62 days after treatment agrees with reports of perimenopausal responses due to estrogen spikes. Reduced pituitary Tshb correlates with the recently reported reduced expression in gonadotropes. IPA analysis of upregulated DEGs in thyrotrope clusters predicted the activation of canonical signaling pathways that support elevated serum TSH levels. The near-normal thyroid hormone levels suggest subclinical hypothyroidism in menopausal women. Downregulated DEGs in corticotropes and in two somatotrope subclusters predicted compromised stress and metabolic responses. Finally, reduced multihormone gene expression suggested compromised plasticity in a low-estrogen environment. These different responses to a sustained low-estrogen state, such as that seen in menopause, reflect the diversity of estrogen's trophic actions.

PMID 42898303
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PubMedExpert opinion on drug metabolism & toxicology2026-10-20

Vepdegestrant (ARV-471): pharmacokinetics, drug metabolism and clinical translation of an oral ERα-targeting PROTAC.

Rana Nidhi N, Patel Ashish A

Vepdegestrant (VEPPANU) is an orally administered proteolysis-targeting chimera (PROTAC) that targets estrogen receptor-α (ERα), a main transcription regulator of estrogen receptor-positive (ER+)/human epidermal growth factor receptor 2-negative (HER2-) breast cancer. The molecule consists of a lasofoxifene-based ER-binding part and a rigid, nitrogen-containing linker with a glutarimide-based CRBN (cereblon)-binding part related to lenalidomide. Preclinical studies show extensive degradation of both wild-type and mutant ERα, while clinical pharmacology studies demonstrate clinically relevant oral exposure despite the molecule's beyond-Rule-of-5 (bRo5) physicochemical properties. The review integrates the absorption, distribution, metabolism and excretion of vepdegestrant with its event-driven pharmacology, CYP3A4-, P-glycoprotein- and BCRP (Breast Cancer Resistance Protein)-mediated drug-drug interactions, and the translational implications of oral PROTAC design. The literature was identified through a search of Scopus from database inception through 31 August 2026, supplemented by screening of relevant reference lists and appropriate regulatory and clinical-trial information. Vepdegestrant is a paradigm shift in the field of targeted protein degradation in endocrine oncology, yet its huge molecular size, metabolic problems, drug-drug interactions, development of resistance and persistent toxicological profile are all relevant matters of concern.

PMID 42900545
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PubMedOrganic & biomolecular chemistry2026-10-20

Regioselective copper-catalyzed domino synthesis of 7-iodobenzo[d]oxazoles as potential ERβ ligands.

Al-Jammal Walid K WK, Al-Zoubi Raed M RM, Al-Zoubi Sally R SR, Shkoor Mohanad M et al.

7-Halogenated benzoxazoles are a recurring motif in preclinical ligands for the estrogen receptor β (ERβ) and in other oxazole-based pharmacophores, yet selective and direct access to the 7-halo regiochemistry is not well served by classical condensation routes or by existing copper-catalyzed arylation methods. Here we report that 5-substituted 1,2,3-triiodobenzenes undergo a regioselective copper-catalyzed domino C-N/C-O arylation with primary amides to deliver 7-iodobenzoxazoles. Substrate-screening conditions implement the cascade as two in situ steps executed in a one-pot procedure. Across twenty substrate combinations explored under the two-stage protocol, yields reached up to 98% and the regiochemistry of the 7-iodo product was confirmed unambiguously by single-crystal X-ray diffraction of 7m. The reaction tolerates gram-scale execution (82% at 2.06 mmol). Using this methodology, human β-estrogen receptor 1 (7c) (AstraZeneca patent (WO2002051821)) is prepared in only one step with excellent regioselectivity and isolated yield. A subset of the 7-iodobenzoxazoles was evaluated in silico against the ERβ ligand-binding domain by convolutional-neural-network-guided and diffusion-based docking (GNINA and DiffDock), followed by 200 ns AMBER22 molecular dynamics and MM/GBSA free-energy calculations; 7g and 7e emerged as candidate scaffolds with MM/GBSA ΔGtotal values of -31.2 and -28.6 kcal mol-1, respectively, and reproducible binding poses centred on a conserved Met336 anchor.

PMID 42899827
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PubMedNutrition, metabolism, and cardiovascular diseases : NMCD2026-10-20

Metabolically healthy obesity in children and adolescents: A misleading label?

Davico Belén B, Martin Maximiliano M, Gaete Laura L, Lozano Chiappe Ezequiel E et al.

The concept of metabolically healthy obesity (MHO) remains debated, particularly in pediatric populations. Beyond traditional risk factors, evaluating high-density lipoprotein (HDL) functionality may provide further insight into cardiometabolic risk in this population. The aim of this study was to assess cardiometabolic alterations in pediatric MHO, including insulin sensitivity, lipid profile, inflammation, and atheroprotective properties of HDL. This cross-sectional study included 21 children and adolescents with MHO, 15 with metabolically unhealthy obesity (MUO) and 19 controls. Groups displayed no significant differences in age, sex, and Tanner stage. We measured anthropometrics, insulin resistance [HOMA-IR, QUICKI, non-esterified fatty acids (NEFA)], lipids, systemic and vascular [(lipoprotein-associated phospholipase A2 (Lp-PLA2) activity)] inflammation. HDL functionality was assessed by evaluating reverse cholesterol transport [cholesterol efflux capacity (CEC), lecithin:cholesterol acyltransferase (LCAT) and cholesteryl ester transfer protein (CETP) activities] and its antioxidant capacity (paraoxonase, arylesterase and inhibition of LDL oxidation). Both MHO and MUO groups exhibited multiple alterations compared to controls, including higher insulin, HOMA-IR, NEFA, LDL-C, and apo B, alongside lower QUICKI, HDL-C, and apo A-I (p < 0.05). Notably, Lp-PLA2 activity was elevated in both MHO and MUO. While HDL antioxidant capacity was preserved, the main steps of reverse cholesterol transport (CEC and LCAT) were significantly impaired in both groups with obesity. Children and adolescents with both MHO and MUO exhibit significant metabolic impairments compared with controls. Conventional criteria to define "metabolically healthy" may not capture the full spectrum of cardiometabolic abnormalities. Novel markers of cardiovascular risk could be incorporated into MHO definitions.

PMID 42901844
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