fulvestrant

Factors affecting the efficacy of fulvestrant monotherapy in second-line therapy include prior treatments, treatment duration, and genetic mutations. Given that the efficacy of fulvestrant was short-lived in the second or subsequent lines, participating in clinical trials is a vital option until a novel alternative treatment choice becomes available.

P=N/A, N=2615, Completed, Novartis Pharmaceuticals | Active, not recruiting --> Completed

And compared with fulvestrant, QDE-003-W exhibited more favorable pharmacokinetic (PK) characteristics. No significant adverse side effects were observed under the administration protocol, which indicates that the tested mice had excellent tolerance to both the administration method and the dosage. Such favorable PK characteristics and safety features further enhance the prospects of QDE-003-W as a viable candidate for subsequent preclinical and clinical development.

P2, N=60, Recruiting, University of Washington | Trial completion date: Jun 2026 --> Jun 2028 | Trial primary completion date: Mar 2025 --> Mar 2027

Given the tumor's limited sensitivity to chemotherapy, she was treated with neoadjuvant endocrine therapy (ET) using fulvestrant, palbociclib, and leuprolide. This case supports the potential role of endocrine-based targeted therapy in managing pediatric LGSOC, offering a viable alternative for patients with limited treatment options. Further research is needed to optimize treatment strategies and improve survival outcomes in this rare population.

The in vitro model system was used to test the plasticizer Bisphenol A (BPA), a known endocrine disruptor (EDs) with estrogen-like action, aga inst 17β-Estradiol (E2), the endogenous nuclear estrogen receptor (nERs) ligand, and the anti-estrogenic drug Fulvestrant (FUL)...Through the use of these in vitro model systems - 2D and especially 3D, the latter of which allow better emulation of complex physiological and pathological processes occurring in vivo, the effects caused by EDs on nERs pathways can be detected and studied under various conditions. This approach performs as a preliminary screening tool to identify estrogenic substances, offering the potential to reduce reliance on in vivo experiments and contributing to improved environmental and health risk assessments.

P=N/A, N=1443, Active, not recruiting, Pfizer | Recruiting --> Active, not recruiting | Trial completion date: Mar 2029 --> Mar 2039

Endocrine resistant breast cancer cells undergo a metabolic shift toward increased triglyceride storage and PUFAs with high degrees of desaturation. While TVB-2640 reduced lipid storage in most conditions, it had limited effects on the growth of endocrine resistant breast cancer cells. Targeting specific lipid metabolic dependencies, particularly pathways that produce PUFAs, represents a potential therapeutic strategy in endocrine resistant breast cancer.

P1, N=265, Active, not recruiting, Relay Therapeutics, Inc. | Trial completion date: Jul 2024 --> May 2025 | Trial primary completion date: Jun 2024 --> Mar 2025

P3, N=405, Active, not recruiting, ETOP IBCSG Partners Foundation | Recruiting --> Active, not recruiting | Trial completion date: Nov 2027 --> Jan 2029 | Trial primary completion date: Jan 2025 --> Jan 2026

P3, N=209, Active, not recruiting, Novartis Pharmaceuticals | Recruiting --> Active, not recruiting

P2, N=220, Active, not recruiting, Dana-Farber Cancer Institute | Trial completion date: Dec 2024 --> Jun 2025

The phase 2 NA-PHER2 trial (NCT02530424) investigated chemo-free preoperative HER2 blockade (trastuzumab + pertuzumab) and CDK4/6 inhibition (palbociclib) with or without endocrine therapy (fulvestrant) in HER2+ER+ breast cancer. The LowLow group exhibited a Luminal A phenotype by the end of treatment. This study expands our understanding of drivers and dynamics of HER2+ER+ tumour response, towards treatment tailoring.

P=N/A, N=36, Recruiting, Fudan University

P1, N=54, Active, not recruiting, Abramson Cancer Center at Penn Medicine | Trial completion date: Dec 2024 --> Aug 2025 | Trial primary completion date: Dec 2024 --> Aug 2025

P1/2, N=75, Not yet recruiting, Chia Tai Tianqing Pharmaceutical Group Co., Ltd.

P2, N=18, Active, not recruiting, Duke University | Trial completion date: Dec 2024 --> Dec 2025 | Trial primary completion date: Dec 2024 --> Dec 2025

P2, N=50, Active, not recruiting, Dana-Farber Cancer Institute | Trial completion date: Dec 2024 --> Dec 2025

Ribociclib with spartalizumab and fulvestrant showed limited efficacy and elevated hepatotoxicity, precluding further development. Correlative analyses revealed treatment-induced immunological effects, and genomic alterations associated with PFS.

P1/2, N=54, Recruiting, Memorial Sloan Kettering Cancer Center

P3, N=27, Active, not recruiting, Spanish Breast Cancer Research Group | Trial completion date: Nov 2024 --> Jun 2025 | Trial primary completion date: Nov 2024 --> Jun 2025

P2, N=60, Active, not recruiting, Carrick Therapeutics Limited | Trial completion date: Jun 2025 --> Dec 2025 | Trial primary completion date: Dec 2024 --> Jun 2025

P1, N=6, Terminated, Tvardi Therapeutics, Incorporated | Phase classification: P1/2 --> P1 | Completed --> Terminated; The study was terminated prior to Phase 2 due to slow accrual.

Although objective response rates were modest in this mixed cohort of heavily pretreated patients, ribociclib combined with letrozole or fulvestrant has shown robust PFS and OS in real-world practice. AEs related treatment discontinuation rate is higher than that reported in clinical trials with stringent inclusion criteria.

P3, N=230, Recruiting, Hoffmann-La Roche | Trial completion date: Jan 2028 --> Dec 2032

P2, N=14, Active, not recruiting, Ohio State University Comprehensive Cancer Center | Recruiting --> Active, not recruiting | N=37 --> 14 | Trial completion date: Dec 2024 --> Jul 2025 | Trial primary completion date: Dec 2023 --> Jul 2025

P2, N=95, Active, not recruiting, National Cancer Institute (NCI) | Recruiting --> Active, not recruiting

P1, N=92, Recruiting, BeiGene | Not yet recruiting --> Recruiting

The functional role of RET was assessed by siRNA-mediated RET silencing and targeted inhibition with the FDA/EMA-approved RET-selective inhibitor selpercatinib in resistant breast cancer cells and patient-derived organoids (PDOs)...We show that RET is upregulated in ER+ breast cancer cell lines resistant to combined CDK4/6i and fulvestrant compared to isogenic cells resistant to fulvestrant alone...We further observed a shorter median survival to combined CDK4/6i and endocrine therapy in patients with RET-positive compared to RET-negative tumors, but this difference did not reach statistical significance. Our findings show that RET is overexpressed in ER+ metastatic breast cancer resistant to combined CDK4/6i and endocrine therapy, rendering RET inhibition a promising therapeutic approach for patients who experience disease progression on combined CDK4/6i and endocrine therapy.

Although this regimen exhibits high rates of response and disease control in both HR+ and HR- cohorts, some patients could have intrinsic or develop acquired resistance to trastuzumab and/or pertuzumab. Here, we achieved a near-complete response in HR+ HER2-amplified and overexpressing metastatic BC twice through molecular tumor board (MTB) initially, with trastuzumab deruxtecan (T-DXd) when HER2 IHC was positive, and, then, with neratinib plus fulvestrant plus paclitaxel when IHC was negative...Furthermore, we demonstrated that triplet combination could induce a remarkable response in the T-DXd-refractory setting, which could be explored in future clinical trials in HR+ and HER2-activated (by RNA or protein overexpression, amplification, and mutation) patients. Our case also highlights the importance of the MTBs to dynamically and reactively manage the course of disease and treatment on a per-patient basis.

This study provided novel diagnostic biomarkers, therapeutic targets, and potential drugs for LUAD.

P1, N=19, Completed, Georgetown University | Active, not recruiting --> Completed | Trial completion date: Nov 2025 --> Jan 2025

P1, N=337, Recruiting, Pfizer | Phase classification: P1/2 --> P1

Treatment of BMECs with various inhibitors (fulvestrant, mifepristone, and pimozide) decreased LF gene transcript and LF protein levels. Our data indicate that E2 and hydrocortisone regulate LF protein synthesis through the ER and GR signaling pathways. These results provide new information about the regulation of the synthesis of functional proteins in milk.

P1, N=186, Recruiting, Pfizer | Trial completion date: Nov 2026 --> Mar 2027 | Trial primary completion date: May 2025 --> Aug 2025

SDSS relieves bone cancer pain by inhibiting osteoclast activity, providing a potential new drug option for cancer pain patients.

Estrogen receptor (ER)-positive breast cancer accounts for a substantial proportion of breast cancer cases and is typically managed using ER inhibitors, such as tamoxifen and fulvestrant. Interestingly, AXL knockdown did not enhance the sensitivity to 4-OHT or affect S6K1 signaling in either MCF7 or MCF7-TR cells, suggesting that the sensitizing effect of bemcentinib through S6K1 inhibition may be independent of AXL expression. Our findings suggest that bemcentinib treatment, particularly in combination therapy, could be a promising strategy for improving treatment efficacy and overcoming tamoxifen resistance in ER-positive breast cancer.

P1, N=15, Recruiting, H. Lee Moffitt Cancer Center and Research Institute | Initiation date: Apr 2024 --> Aug 2024

In this real-world cohort, we observed a wide variety of different treatment sequences applied in daily clinical practice, some of which were in discordance with the current guidelines. Fear that patients may never get around to treatment with CDK4/6i if a patient did not start with a CDK4/6i was not supported by our study results.

P2, N=66, Terminated, Breast Cancer Trials | Recruiting --> Terminated

P2, N=47, Active, not recruiting, City of Hope Medical Center | Trial completion date: Dec 2024 --> Mar 2026 | Trial primary completion date: Dec 2024 --> Mar 2026

P1, N=890, Recruiting, Relay Therapeutics, Inc. | N=400 --> 890