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tamoxifen (tamoxifen, Douglas)

✓ Approved

Douglas Pharmaceuticals Limited · ESR1 · Small Molecule

What is tamoxifen?

tamoxifen is a small molecule developed by Douglas Pharmaceuticals Limited. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand Namestamoxifen, Douglas
CompanyDouglas Pharmaceuticals Limited
Drug ClassSmall Molecule
Molecular TargetESR1
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Douglas Pharmaceuticals Limited

Mechanism of Action

Molecular Targets

tamoxifen acts on 1 molecular target:

ESR1estrogen receptor 1 (ER, ESR)
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Therapeutic Indications

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

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

Related Research Articles

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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PubMedNPJ breast cancer2026-07-21

The WinPro trial: window-of-opportunity study of endocrine therapy with micronised progesterone in ER-positive breast cancer.

Haggstrom Lucy L, Middleton Kate K, Parker Andrew A, Segara Davendra D et al.

Progesterone can inhibit tumoural proliferation in oestrogen receptor positive (ER+) breast cancer. The WinPro trial (Australian New Zealand Trials Clinical Trials Registry number: ACTRN12618000928213, date of registration 01/06/2018) was a randomised, multi-centre, phase 2, window-of-opportunity trial evaluating micronised progesterone (MP) in post-menopausal women with early-stage, ER+, progesterone receptor (PR) positive, HER2- breast cancer. Patients were randomised to letrozole, letrozole and MP, or tamoxifen and MP for 14 days preoperatively. The primary endpoint was the percent proportional reduction in Ki67 ('Ki67 suppression') between the two letrozole groups in the per protocol population. From February 2018 to June 2024, 244 patients were enrolled. 189 patients completed per protocol: letrozole (n = 66, 34.9%), letrozole + MP (n = 64, 33.9%), and tamoxifen + MP (n = 59, 31.2%). There was no difference in Ki67 suppression between letrozole (88.2%) versus letrozole + MP (89.2%) (p = 0.39). Ki67 suppression appeared lower with tamoxifen + MP (61.5%). Hot flushes appeared less frequent with letrozole + MP (13.3%) versus letrozole (22.4%) or tamoxifen + MP (20.5%).

PMID 42477003
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PubMedNPJ breast cancer2026-07-21

Novel (Z)-endoxifen-related new chemical entities exhibit potent anti-cancer activity in ERα+ breast cancer.

Batoon Lena L, Muthyala Rajeev S RS, Wang Xiyin X, Rodman Esther E et al.

Approximately 80% of breast cancers express estrogen receptor alpha (ERα), yet ERα-positive disease remains associated with high recurrence and late relapse. (Z)-Endoxifen (ENDX), the most abundant active metabolite of tamoxifen, is a potent, orally bioavailable, selective estrogen receptor modulator currently in development for breast health indications. During its synthesis, structurally related compounds are generated as byproducts termed here as new chemical entities (NCEs): AT416E, AT416Z, AT402E, AT402Z, and AT300, which have not been previously studied. We evaluated these NCEs alongside ENDX using multiple ERα-positive breast cancer cell lines, including models harboring clinically relevant ESR1 mutations. Activity was assessed using 2D and 3D proliferation, apoptosis, cell cycle profiling, migration, invasion, ERα transcriptional activity, RNA sequencing and synergy with abemaciclib. Several NCEs exhibited potent anti-estrogenic and anti-cancer effects. In various settings, these compounds matched or exceeded ENDX's activity, highlighting their therapeutic promise. RNA sequencing analysis revealed both shared and compound-specific transcriptional programs. Some NCEs also combined favorably with abemaciclib, producing additive to synergistic effects comparable to or greater than ENDX. Together, our findings support further investigation of select NCEs for ERα-positive breast cancer, particularly for tumors with ESR1 activating mutations and as potential second- or third-line options for recurrent disease.

PMID 42476993
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