Bispecific CD3-PDL1 T-Cell Engager Against PD1 Immune Suppression

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Solution Overview

Problem

Existing bi-specific T-cell engagers fail to effectively reduce immune suppression in cancer patients, limiting their therapeutic efficacy as they do not simultaneously activate T-cells, induce cytotoxicity, and kill tumor cells despite the presence of immune suppression mediated by PD1.

Innovation Solution

A bispecific T-cell engager recombinant protein that binds to CD3 on T-cells and PDL1 on tumor cells, activating T-cells and redirecting them to tumor cells while neutralizing PD1-mediated suppression, comprising specific amino acid sequences and linkers for effective binding.

Engineering Contradictions & Design Principles

VSEngineering Contradiction Analysis

1Productivity

If existing bi-specific T-cell engagers are used to activate T-cells and kill tumor cells, then tumor cell cytotoxicity is improved, but immune suppression mediated by PD1 is not reduced

Engineering Contradiction:
Improvetumor cell killing efficiencyVSAvoidtherapeutic efficacy under immune suppression
Core Design Contradiction:
ProductivityVSReliability

Solution Approach 1:

The patent merges two distinct functions into a single bi-specific T-cell engager molecule: (1) T-cell activation through CD3 binding, and (2) PD1-mediated immune suppression neutralization through PDL1 binding. This unified approach allows the single molecule to simultaneously enhance T-cell cytotoxicity while counteracting immune suppression, resolving the contradiction between tumor cell killing efficiency and therapeutic reliability under immune suppression conditions.

Inventive Principle:
Principle #5Merging (Combining)

Solution Approach 2:

The bi-specific T-cell engager exhibits multi-functionality by performing three critical roles simultaneously: (a) activating T-cells via CD3 engagement, (b) redirecting T-cells to tumor cells through PDL1 binding, and (c) neutralizing PD1-mediated immune suppression. This universal design enables the single agent to address multiple barriers to effective cancer immunotherapy, thereby improving both productivity and reliability under immune suppression.

Inventive Principle:
Principle #6Universality (Multi-functionality)

2Productivity

If a bi-specific T-cell engager binds to CD3 and PDL1 simultaneously, then T-cell activation and tumor targeting are improved, but the complexity of the protein structure increases

Engineering Contradiction:
ImproveT-cell activation and tumor targeting efficiencyVSAvoidprotein structure complexity
Core Design Contradiction:
ProductivityVSDevice complexity

Solution Approach 1:

The bi-specific T-cell engager is constructed by segmenting two separate antibody variable regions (anti-CD3 and anti-PDL1) and linking them through a flexible peptide linker. This segmentation allows each functional domain to maintain its independent binding capability while being integrated into a single polypeptide chain, thereby achieving dual functionality without excessive structural complexity.

Inventive Principle:
Principle #1Segmentation

Solution Approach 2:

The protein structure employs a composite design combining antibody variable regions from different specificities (CD3-binding and PDL1-binding domains) into a single fusion protein. This composite structure leverages the proven binding capabilities of separate antibody fragments while integrating them through standardized linker sequences, balancing functional complexity with structural manageability.

Inventive Principle:
Principle #40Composite materials

3Reliability

If existing immunotherapy strategies are used, then some clinical efficacy is achieved, but robust levels of antibody and T-cell responses are not established due to tumor immune evasion

Engineering Contradiction:
Improveclinical efficacyVSAvoidrobustness of immune response
Core Design Contradiction:
ReliabilityVSProductivity

Solution Approach 1:

The bi-specific T-cell engager applies preliminary anti-action by proactively neutralizing PD1-mediated immune suppression before it can inhibit T-cell responses. By incorporating PDL1-binding capability directly into the T-cell engager structure, the molecule preemptively blocks the immunosuppressive pathway, preventing tumor cells from evading immune attack and thereby establishing robust and sustained immune responses.

Inventive Principle:
Principle #9Preliminary anti-action

Solution Approach 2:

The invention converts the harmful immunosuppressive interaction between PD1 and PDL1 into a beneficial therapeutic mechanism. By designing the bi-specific engager to bind PDL1, the molecule harnesses the tumor cell's own PDL1 expression (which normally mediates immune evasion) as a targeting handle to recruit and activate T-cells directly at the tumor site, transforming the immune suppression mechanism into a tool for enhanced tumor targeting and killing.

Inventive Principle:
Principle #22Blessing in disguise (Convert harm into benefit)

Data Source

PatentEP3390454B1A recombinant bi-specific polypeptide for coordinately activating tumor-reactive t-cells and neutralizing immune suppression
Publication Date: 2026.02.04 UNIV OF MARYLAND BALTIMORE COUNTY
  • EP3390454B1 patent drawingFigure 1A~1C
  • EP3390454B1 patent drawingFigure 2A~2C
  • EP3390454B1 patent drawingFigure 3

AI summary

The present invention relates generally to the field of generating fusion proteins to be used in cancer therapy, and more specifically, a bispecific T-Cell engager recombinant polypeptide comprising an antibody, fragment thereof, or single chain variable fragment that binds to CD3 of a T-cell antigen receptor and an antibody, fragment thereof, or single chain variable fragment that binds to Programmed Death Ligand 1 (PDL1) on a cancerous tumor cell to counteract the immune tolerance of cancer cells.