ArticleCancer medicine2026
Imeglimin Exerts Anti-Tumor Activity in Multiple Myeloma Through Affecting Energy Metabolism and Downregulating IL-16 Expression.
Article in Cancer medicine, 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
7 authors.
Funding
Abstract
backgroundImeglimin (IME) is a novel oral anti-diabetic agent with a similar chemical structure to metformin, which has shown broad-spectrum anti-tumor activity. However, the activity of imeglimin on tumor cells remains unclear. This study investigated the effects of IME on multiple myeloma (MM) cells and explored the underlying mechanisms.
methodsThe effects of IME on MM cell proliferation were evaluated in vitro using MM cell lines and in MM cell-derived xenograft (CDX) models. Seahorse metabolic analyses and RNA-Seq were performed in IME-treated and control MM cell lines. Single-cell transcriptomic data were further analyzed to assess the role of IL-16 in the bone marrow microenvironment.
resultsIME inhibited MM cell proliferation and tumor growth in MM cell-derived xenograft (CDX) models by inducing G1/G0 cell cycle arrest. IME suppressed oxidative phosphorylation and promoted glycolysis. IL-16 mRNA expression was downregulated, and multiple cytokine-cytokine receptor interaction pathways were altered following IME treatment. The anti-MM effect of IME was partly mediated by increased lactate production and decreased IL-16 expression. Single-cell transcriptomic data further demonstrated that IL-16 plays an important role in the bone marrow microenvironment of MM.
conclusionsThese findings suggest that IME may represent a novel approach for targeting IL-16 and energy metabolism in the treatment of MM.
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.