ArticleInflammopharmacology2026
Repurposing amlexanox as a topical anti-inflammatory and antioxidant intervention for diabetic foot ulcers: insights from in-silico and in-vivo studies.
Article in Inflammopharmacology, 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDiabetic foot ulcers (DFUs), a debilitating manifestation of diabetes mellitus, involve persistent inflammation, oxidative stress, and impaired wound healing, largely driven by NF-κB overactivation. Amlexanox (ALX), a synthetic anti-inflammatory and antioxidant agent, was evaluated for its therapeutic potential in DFUs.
methodsIn-silico molecular docking and pharmacokinetic studies were conducted to predict ALX's interactions with major DFU targets and to assess its topical suitability. STZ-induced diabetic rats with full-thickness foot ulcers (5 mm) received topical ALX (2.5% and 5%) or silver sulfadiazine ointments for 14 days. Wound closure, antioxidant enzymes, oxidative stress markers, connective tissue markers, pro-inflammatory markers and NF-κB expression were assessed in the wound tissue.
resultsALX demonstrated strong binding to the pathological targets (NF-κB, MMP-9, MPO, and COX-2) and displayed a favourable PK profile. Moreover, ALX topical treatment did not normalise diabetic metabolic alterations, but it dose-dependently promoted wound healing. Indeed, ALX 5% significantly accelerated wound closure (p < 0.0001) and led to marked suppression of NF-κB and MMP-9 expression (p < 0.0001). It also enhanced the levels of connective tissue markers, including hexosamine (p < 0.001), hydroxyproline, and hexuronic acid (p < 0.0001). Robust anti-inflammatory effects were also observed, as ALX reduced IL-1β, IL-6, TNF-α levels and COX-2 activity (p < 0.0001). Furthermore, ALX 5% diminished oxidative stress by lowering LPO, PCO, and MPO levels (p < 0.0001), and restoring GSH levels and SOD and CAT (p < 0.001) activities indicating its anti-oxidant properties.
conclusionTaken together, the present work highlights the mechanisms associated with ALX mediated wound healing in diabetic rats thereby demonstrating its potential as a promising strategy for DFU management.
Indexed as
Identifiers
41318858What 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.