PD-l1-targeting protac peptide, protac nanoparticles comprising same, and composition for cancer prevention or treatment containing same as active component

The PD-L1 targeting PROTAC peptide nanoparticles address absorption and bioavailability issues by forming self-assembled nanoparticles that degrade cancer cell targets and inhibit regeneration, enhancing therapeutic efficacy in cancer treatment.

WO2026127735A1 Publication Date: 2026-06-18EWHA UNIV IND COLLABORATION FOUND
0 Cites 0 Cited by

Patent Information

Authority / Receiving Office
WO · WO
Patent Type
Applications
Current Assignee / Owner
EWHA UNIV IND COLLABORATION FOUND
Filing Date
2025-10-28
Publication Date
2026-06-18

AI Technical Summary

⚠Technical Problem

Existing PROTACs face issues with low absorption and bioavailability, insufficient tumor targeting, and significant side effects due to insolubility and instability, limiting their therapeutic efficacy in cancer immunotherapy.

⚗Method used

A PD-L1 targeting PROTAC peptide with a cancer-targeting peptide, a phenylalanine linker, and an E3 enzyme ligand, forming nanoparticles through self-assembly, which selectively degrade target proteins in cancer cells via two pathways and inhibit regeneration, enhancing therapeutic efficacy.

🎯Benefits of technology

The PROTAC nanoparticles demonstrate specific selectivity for cancer targets, effectively degrading proteins on cancer cell surfaces and blocking immunosuppressive signals, thereby inducing apoptosis and improving cancer treatment precision and efficacy.

✦ Generated by Eureka AI based on patent content.

Smart Images

  • Figure 1
    Figure 1
  • Figure 2
    Figure 2
  • Figure 3
    Figure 3
Patent Text Reader

Abstract

The present invention relates to a PD-L1-targeting PROTAC peptide, PROTAC nanoparticles comprising same, and a composition for cancer prevention or treatment containing same as an active ingredient, wherein in cancer tissues, the PD-L1 receptor is subjected to a direct lysosomal degradation pathway and a PROTAC-mediated degradation pathway, thereby not only inducing PD-L1 protein degradation but also fundamentally blocking PD-L1 protein regeneration, thus inhibiting the transmission of immunosuppressive signals in the interaction between cancer cells and T cells to activate immune responses, so that the effect of inducing the death of cancer cells can be continuously and effectively achieved.
Need to check novelty before this filing date? Find Prior Art