ArticleFrontiers in pharmacology2026
Gamma-glutamyl metformin inhibits renal cell carcinoma progression by activating AMPK signaling pathway.
Article in Frontiers in pharmacology, 2026. 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
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metformin is a promising candidate for the treatment of renal cell carcinoma (RCC), and elucidating its anti-tumor mechanisms is of great clinical significance. Overexpression of Gamma-glutamyl transpeptidase (GGT) in RCC tissues has been identified as a potential biomarker for renal cell tumors. Thus, there is an urgent need to develop a metformin prodrug that leverages the overexpression specificity of GGT in RCC tissues to achieve targeted release of metformin for RCC therapy. Herein, we innovatively report the development and the antitumor activity of gamma-Glutamyl Metformin (γE-Met), which exerts its effects by activating AMP-activated protein kinase (AMPK) signaling pathway. Compared with metformin, γE-Met specifically releases free metformin in renal cancer cells under the catalysis of GGT, thereby prolonging the retention time of metformin in tumor cells and more effectively inhibiting the growth and metastasis of renal cancer cells. Our experimental results demonstrate that GGT-responsive γE-Met can significantly enhance the therapeutic efficacy of metformin, rendering it a promising metformin prodrug with substantial clinical application prospects.
Indexed as
Identifiers
What Socratic 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 Socratic graph.