ArticleCancer cell international2025
A1, an innovative fluorinated CXCR4 inhibitor, redefines the therapeutic landscape in colorectal cancer.
Article in Cancer cell international, 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.
- The role of deubiquitinase USP33 in colorectal cancer tumorigenesis and its potential as a therapeutic target predictor.Discover oncology · 2026Review
- The CXCL12-CXCR4 axis in colorectal cancer: immune regulation, metastatic progression, and therapeutic implications.Frontiers in immunology · 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
10 authors.
Funding
Abstract
backgroundColorectal cancer (CRC) is a globally prevalent malignancy, primarily affecting the colon and rectum, characterized by uncontrolled cellular changes in the intestinal wall lining. Recent evidence underlines the significant role of the CXCL12/CXCR4 axis in the development of CRC, suggesting that inhibiting this pathway could be a promising therapeutic approach. This study focuses on investigating the potential of N, N''-thiocarbonylbis (N'-(3,4-dimethyl phenyl)-2,2,2-trifluoroacetimidamide) (A1), a novel fluorinated CXCR4 inhibitor, through a comprehensive analysis encompassing in silico, in vitro, and in vivo studies.
methodsThe molecular dynamic simulation method was employed to compute A1 binding affinity and energy for the CXCR4 receptor compared to AMD3100. In vitro experiments utilized the CT-26 mouse CRC cell line to compare the inhibitory effects of A1 and AMD3100 on tumor cell proliferation and migration. Following the development of the CRC animal model in BALB/c mice, immune system responses within the tumor microenvironment (TME) were evaluated. Flow cytometry and real-time PCR (RT-PCR) were used to measure the effects of AMD3100 and A1 on regulatory T-cell (Treg) infiltration and the expression of CXCR4, vascular endothelial growth factor (VEGF), fibroblast growth factors (FGF), interleukin-10 (IL-10), and tumor growth factor-beta (TGF-β) genes in tumor tissue. Additionally, enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry (IHC) techniques were employed to assess VEGF, IL-10, and TGF-β tissue levels at the protein level.
resultsMolecular dynamic simulation studies with molecular mechanics Poisson-Boltsman surface area (MM-PBSA) analysis revealed that A1 exhibits significantly lower binding energy for the CXCR4 receptor than AMD3100. A1 effectively inhibited the proliferation of CT-26 cells, significantly reduced tumor cell migration, attenuated Treg infiltration, and suppressed IL-10 and TGF-β expression at both mRNA and protein levels in vivo. Notably, A1 outperformed AMD3100 in reducing tumor size and increasing survival rate in treated animals, with minimal side effects.
conclusionThese findings emphasize the potential of A1 as a favorable anti-tumor small molecule in CRC. Further validation through rigorous preclinical and clinical studies may position A1 as a promising alternative to AMD3100 in human cancers.
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.