ArticleBiomaterials research2025
The Peptide-Drug Conjugate M1pep-Tasquinimod Ameliorates Acute Pancreatitis via Selectively Clearing M1-like Macrophages.
Article in Biomaterials research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Targeted inhibition of M2 macrophages polarization via a PDC attenuates chronic pancreatitis through the PPARα pathway.iScience · 2026Article
- Peptides in the Diagnosis and Treatment of Pancreatic Cancer and Other Pancreatic Diseases from Basic Research to Clinical Translation.Drug design, development and therapy · 2026Review
- Spatiotemporal Heterogeneity of Macrophages in Acute Pancreatitis: From Inflammatory Initiators to Repair Coordinators and Targeted Therapeutics.Mediators of inflammation · 2026Review
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Authors and funding
11 authors.
Funding
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Abstract
M1-like macrophages dominate local and systemic inflammatory response progression in acute pancreatitis (AP). The development of strategies to target pro-inflammatory M1-like macrophages in conjunction with primary pathophysiology-specific pharmacological therapy presents a challenge in the management of AP. Peptide-drug conjugates (PDCs), which are emerging second-generation conjugate drugs, have quickly become a new favorite in the field of targeted drug delivery due to their superior drug bioavailability, affinity, and stability. Tasquinimod (Tasq) is a specific inhibitor of S100A9 that is expressed mainly in M1-like macrophages during AP. Drug repositioning revealed that Tasq improved AP in a dose-dependent manner, but drug toxicity occurred at doses of 30 mg/kg. Therefore, we selected 2 specific M1-like macrophage-binding peptides (M1peps) by phage display technology and developed a novel PDC, M1pep-Tasq, by connecting M1peps to activated Tasq with a cleavable linker. Based on a mouse model of AP constructed by retrograde injection of sodium taurine cholate into the bile pancreatic duct and an M1-like macrophage polarization model induced by lipopolysaccharide + interferon-γ stimulation, we confirmed that M1pep-Tasq reduces the drug toxicity of Tasq and improves its efficacy by enhancing the targeting of Tasq to damaged organs in vivo and to M1-like macrophages in vitro. Furthermore, M1pep-Tasq effectively improves AP by inhibiting M1-like macrophage polarization by suppressing the S100A9-TLR4-MAPK pathway. Overall, we have developed a novel PDC, M1pep-Tasq, with promising applications in clinical settings to treat a range of inflammatory disorders by increasing the efficacy and reducing the toxicity of Tasq.
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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 OpenQuestion graph.