Gal3:TIM-3 Inhibitor Blocks Immune Checkpoint Interaction
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Solution Overview
Problem
Current treatments for cancer are ineffective due to the immune system's inability to recognize and target cancer cells, as tumors exploit immune checkpoint mechanisms to evade destruction.
Innovation Solution
Developing a Gal3:TIM-3 inhibitor that interferes with the interaction between galectin-3 (Gal3) and T-cell immunoglobulin and mucin-domain containing-3 (TIM-3), thereby activating immune responses and targeting cancer cells.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Reliability
If the immune system is allowed to respond endogenously to cancer, then immune response is observed, but the response is ineffective and tumors evade immune destruction
Solution Approach 1:
The patent introduces TIM-3 inhibitors as intermediary substances that block the interaction between TIM-3 receptors on T-cells and their ligands (Gal9, CEACAM1) on tumor cells. This intermediary agent prevents the suppressive signal transmission, thereby enhancing immune response effectiveness without requiring complete redesign of the immune system
Solution Approach 2:
The patent applies preliminary anti-action by administering TIM-3 inhibitors before tumors can fully suppress the immune response. The inhibitor pre-empts the suppressive mechanism by blocking the TIM-3 ligand-receptor interaction, preventing tumor-induced immune evasion before it can take effect
2Object-generated harmful factors
If immune checkpoints are utilized by tumors to suppress immune response, then tumor evasion is achieved, but immune destruction capability is reduced
Solution Approach 1:
The patent inverts the normal immune checkpoint function by using TIM-3 inhibitors to block the suppressive pathway. Instead of allowing the checkpoint mechanism to suppress immune response (as tumors exploit), the inhibitor reverses this effect by preventing ligand binding, thereby converting the checkpoint from a suppressive to an activating influence on immune destruction capability
3Object-generated harmful factors
If TIM-3 ligands (Gal9, CEACAM1) are present on tumor cells, then immune suppression is enhanced, but T-cell activation is inhibited
Solution Approach 1:
The patent extracts or removes the suppressive effect by using TIM-3 inhibitors to specifically bind and neutralize the TIM-3 ligands (Gal9, CEACAM1) on tumor cells. This extraction of the suppressive interaction allows T-cell activation to proceed without the inhibitory influence of the TIM-3 pathway
Solution Approach 2:
The patent converts the harmful TIM-3 ligand presence into a benefit by using the ligand-inhibitor complex as a target for therapeutic intervention. The very presence of TIM-3 ligands that cause suppression becomes the basis for developing specific inhibitors that, when administered, transform the suppressive pathway into an activated immune response
Applied Scientific Principles
This section explains which scientific principles are used to turn an abstract innovation direction into a practical engineering solution.
Function Achieved in This Case
The Gal3:TIM-3 inhibitor effectively activates immune responses, leading to a decrease in cancer load by enhancing T-cell activation and overcoming immune suppression mechanisms employed by tumors.
Implementation Method 1
a Gal3:TIM-3 inhibitor that interferes with the interaction between the Gal3 and TIM-3
Data Source
AI summary
Provided herein are methods of activating immune response and/or treating cancer in a patient comprising administering to the patient a Gal3:TIM-3 inhibitor that interferes with the interaction between Gal3 and TIM-3, where said inhibitor is administered in an amount sufficient to activate immune response. Also provided are a humanized anti-Gal3 antibodies that can block the interaction between Gal3 and TIM3 and methods of using the anti-Gal3 antibody to treat cancer. Methods for determining if a patient's cancer is suitable for treatment with a Gal3:TIM-3 inhibitor and methods for selecting compounds that can block interaction between Gal3 and TIM-3, activating immune response and/or treating cancer are also provided.