ArticleBMC cancer2025
Preclinical studies of the falnidamol as a highly potent and specific active ABCB1 transporter inhibitor.
Article in BMC cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
backgroundABCB1 overexpression is a key factor in causing multidrug resistance (MDR). As a result, it is crucial to discover effective medications against ABCB1 to overcome MDR. Falnidamol, a tyrosine kinase inhibitor (TKI) targeting the epidermal growth factor receptor (EGFR), is currently in phase 1 clinical trials for the treatment of solid tumors. In this work, we assessed whether falnidamol could act as an inhibitor of ABCB1 to reverse ABCB1-mediated MDR.
methodsThe reversal effect of falnidamol on MDR was assessed by MTT, colony formation, 3D microsphere, and xenograft model assays. The protein expression or cellular localization was tested by western blot and immunofluorescence analysis. The intracellular doxorubicin accumulation and efflux were assessed by flow cytometry. The ATPase activity of ABCB1 was detected by a microplate reader. The interaction between falnidamol and ABCB1 was evaluated by docking analysis and cellular thermal shift assay.
resultsOur data showed that falnidamol specifically reversed ABCB1-mediated MDR but not ABCG2-mediated MDR in vitro and in vivo. Mechanistic studies suggested falnidamol had no effect on ABCB1 expression or cellular localization, nor on the AKT or ERK pathways. Further studies found that falnidamol reduced ABCB1's efflux function, resulting in enhanced intracellular agent accumulation and thus overcoming MDR. ATPase assay showed that falnidamol suppressed the ABCB1 ATPase activity. Furthermore, docking analysis and cellular thermal shift assay indicated that falnidamol bound directly to the drug-binding site of ABCB1 transporter.
conclusionThe present study proves that falnidamol acts as a highly potent and specific active ABCB1 transporter inhibitor, and can reverse ABCB1-mediated MDR, implying that combining falnidamol with ABCB1 substrate chemotherapeutic agents has the potential to overcome ABCB1-mediated MDR.
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.