Compound Disrupts Dupuytren's Myofibroblast Activity
A small-molecule CREBBP/EP300 inhibitor suppresses fibrosis-linked gene expression in cultured Dupuytren cells.
Updated on Nov. 1, 2026 in Biotech
Researchers report that SGC-CBP30, a small-molecule inhibitor of the CREBBP/EP300 bromodomain, suppressed collagen VI expression and reduced proliferation in Dupuytren myofibroblasts in vitro. The compound also altered cell morphology and showed dose-dependent viability declines without immediate acute cytotoxicity.
Why it matters
Dupuytren's disease involves fibrotic thickening of connective tissue in the hand, and current treatments do not target the underlying myofibroblast activity. The findings point to epigenetic regulators as a possible avenue for future antifibrotic approaches, though results remain at the cell-culture stage.
The study measured changes in cultured myofibroblasts, with reduced ACTA2 and COL1A1 mRNA expression observed within 24 hours and actin filament disassembly within 48 hours of treatment. Whether these laboratory results would hold in animal models or human tissue remains unknown.
The details
Using cultured myofibroblasts derived from Dupuytren tissue, the researchers treated cells with SGC-CBP30 and tracked gene expression, cell growth, and cell structure. The compound suppressed transcripts for ACTA2, COL1A1, and several collagen VI genes, while contractile actin filaments broke down over two days. The mechanism involves blocking the CREBBP/EP300 bromodomain from binding acetylated histones, which prevents assembly of coactivators at pro-fibrotic gene promoters.
Field Context
Targeting CREBBP and EP300 bromodomains has emerged as an epigenetic strategy in several disease areas, and SGC-CBP30 is a widely used chemical probe in that research. This study applies the probe to Dupuytren's disease, extending its use from oncology-focused work into fibrosis.
At this stage the findings do not change current Dupuytren's treatment options or daily hand care. Patients and clinicians would need animal and clinical studies before any therapy based on this mechanism could reach practice.
The takeaway
Laboratory results on a fibrosis-linked epigenetic target are an early step, and readers should watch for follow-up animal and human studies before drawing conclusions about treatment.
Further reading
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Source note: This article includes information reported by Alwasat-ye.
