ArticleDiscover oncology2025
F-α-DDB-derivative, a novel synthetic of bifendate, plus epirubicin improves antitumor efficacy against triple negative breast cancer without additional cardiotoxicity.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Article
- Ferroptosis in Doxorubicin-Induced Cardiotoxicity: From Molecular Mechanisms to Therapeutic Strategies and Clinical Management Paradigms.Reviews in cardiovascular medicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Triple negative breast cancer (TNBC) refers to a molecular subtype of breast cancers (BC) with high rate of distant metastases and poor prognosis. Epirubicin (EPI) is widely used for the therapy of TNBC but it's limited in clinical use due to cardiotoxicity and chemotherapy resistance. We previously identified F-α-DDB-derivative, a novel synthetic of bifendate, as a potential agent to improve the therapeutic efficacy of TNBC in combination with EPI since F-α-DDB-derivative inhibited MDA-MB-468, but not as much as EPI. In this study, we investigated the antitumor activity of F-α-DDB-derivative in combination with EPI against TNBC in vitro and in vivo and whether co-treatment would induce additional cardiotoxicity. In human TNBC MDA-MB-468 cells, application of F-α-DDB-derivative (11.5, 23.0, 46.0 μg/ml) in combination with EPI (1.5, 3.0, 6.0 μg/ml) exhibited great inhibition on cell viability and cell proliferation. Additionally, F-α-DDB-derivative (5.75, 11.5, 23.0, 46.0 μg/ml) interacted with EPI (0.75, 1.5, 3.0, 6.0 μg/ml) synergistically to induce apoptosis in MDA-MB-468 cells. This suggests that F-α-DDB-derivative may be more sensitive to apoptotic pathways. Furthermore, we revealed that co-administration of EPI and F-α-DDB-derivative (ip, once every other day for 14 days) significantly increased the therapeutic efficacy of EPI (2.0 mg/kg) or F-α-DDB-derivative (20.0 mg/kg) in mice harboring MDA-MB-468 cell xenografts without additional cardiotoxicity compared to that in EPI monotherapy group. These results implicate that co-treatment of EPI and F-α-DDB-derivative may be a potential therapeutic approach for the treatment of TNBC.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.