A method for inhibiting UHRF1 in colorectal cancer

Value Proposition

• Reversal of colorectal cancer-specific DNA hypermethylation
• mRNA-based strategy for UHRF1 inhibition
• A lipid nanoparticle-based delivery platform

Unmet Need

1 out of 24 people will develop colorectal cancer. Current technologies do not maximize the bodies’ native ability to suppress tumors. Existing therapies lack specificity and cause significant collateral damage to normal cells. Epigenetic therapy can regulate gene expression by targeting the epigenome, without editing the genomic code. The development of epigenetic therapies is challenging because of the need for precise targeting, the risk of off-target effects, potential resistance, and the complex interplay between genetics and epigenetics across the population and cancer expression.

Technology Description

Researchers at Johns Hopkins have developed a small peptide that mimics the natural inhibitor of UHRF1. It has been reported that overexpression of UHRF1 promotes down regulation of tumor suppressor genes without activating viral defense genes and the interferon pathway, contributing to carcinogenesis. Delivery of this peptide to cancer cells via a lipid nanoparticle impairs colorectal cancer tumorigenicity.

Stage of Development

• In vitro and in vivo testing completed
• Data available on request

Publications:

• Bai, W., Xu, J., Gu, W. et al. Defining ortholog-specific UHRF1 inhibition by STELLA for cancer therapy. Nat Commun 16, 474 (2025).
• WO 2025/064873