ArticleScientific reports2026
The anti-interleukin-6 antibody ALD518-P18 mitigates murine kidney ischemia-reperfusion injury.
Article in Scientific reports, 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
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin-6 (IL-6) is a key pleiotropic cytokine implicated in kidney injury; however, the therapeutic potential of IL-6 blockade against acute ischemia-reperfusion injury (IRI) remains uncertain, with previous murine studies yielding conflicting results. This study investigated the protective effects of the high-affinity chimeric anti-IL-6 monoclonal antibody, cALD518-P18, in a non-transplant mouse model of warm renal IRI (22 min ischemia, 24 h reperfusion). Male C57BL/6 mice received a single 40 mg/kg dose of cALD518-P18 or an isotype control, administered either intraperitoneally 30 min before ischemia or intravenously immediately after ischemia. At 24 h, control mice exhibited significant kidney dysfunction (serum creatinine, urea), injury, and inflammation, consistent with elevated pro-inflammatory IL-6 trans-signalling (soluble IL-6R (sIL-6R) and tubular STAT3 phosphorylation (pSTAT3)). Treatment with cALD518-P18, in both regimens, significantly protected the kidneys from IRI, demonstrating improved renal function and reduced tissue damage. The antibody attenuated inflammation, endothelial activation and pSTAT3 signalling, significantly downregulating gene expression of the acute tubular stress marker NGAL. These findings confirm the pathogenic role of IL-6 and highlight its early blockade with cALD518-P18 as a promising therapeutic strategy to improve outcomes in acute kidney injury and transplantation.
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.