LAG-3 Protein MHC II Binding for Luminal B Breast Cancer
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Solution Overview
Problem
Current cancer treatments, particularly those targeting PD-1 and CTLA-4 immune checkpoints, fail to effectively respond in many patients, and there is a need for improved therapies, especially for cancers with poor prognosis and specific patient populations such as those with low monocyte counts or Luminal B breast cancer.
Innovation Solution
The use of a LAG-3 protein or derivative that binds to MHC class II molecules to activate antigen-presenting cells, enhancing the immune response in cancer treatment, including for patients with low monocyte counts, Luminal B breast cancer, and those who have not responded to CDK4/6 inhibitors or taxane chemotherapy.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Reliability
If PD-1 and CTLA-4 immune checkpoint inhibitors are used as standard of care therapies, then the immune system is blocked from down-regulation, but many patients still fail to respond to these treatments
Solution Approach 1:
The patent combines LAG-3 protein (an APC activator that pushes the immune system) with PD-1 and CTLA-4 inhibitors (that block immune down-regulation) to create a multi-checkpoint therapy. This combination addresses treatment resistance by simultaneously activating antigen-presenting cells and blocking multiple inhibitory pathways, thereby improving response rates in patients who fail standard checkpoint inhibitors
Solution Approach 2:
The LAG-3 protein serves multiple functions: it activates antigen-presenting cells through MHC class II molecules, induces anti-cancer T cell responses, and works synergistically with other checkpoint inhibitors. This multi-functional approach enhances adaptability across different patient populations and cancer types, including those with poor prognosis
2Reliability
If LAG-3 inhibitors are used to block immune system down-regulation, then the immune response is enhanced, but there is a need for improved therapies especially for patients with poor prognosis
Solution Approach 1:
The LAG-3 protein activates antigen-presenting cells before tumor antigen exposure, priming the immune system in advance. By pre-activating APCs through MHC class II molecules, the patent ensures that when tumor antigens are presented, the immune system is already in an activated state, improving outcomes for patients with poor prognosis who need maximum immune activation
3Productivity
If APC activators are used to activate antigen-presenting cells via MHC II molecules, then CD4+ and CD8+ T cells are activated and proliferated, but there remains a need for improved cancer therapies leading to better outcomes
Solution Approach 1:
The LAG-3 protein acts as an intermediary that binds to MHC class II molecules on antigen-presenting cells, translating this interaction into powerful immune activation. By using LAG-3 as the mediating structure that connects APCs to the adaptive immune system, the patent achieves both high T cell proliferation and improved cancer treatment outcomes, addressing the contradiction between activation intensity and treatment efficacy
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 LAG-3 protein or derivative effectively activates the immune system, improving progression-free survival and overall survival in patients with low monocyte counts and those with Luminal B breast cancer, offering a treatment option for patients who have not responded to standard therapies.
Implementation Method 1
a LAG-3 protein, or a derivative thereof that is able to bind to MHC class II molecules
Data Source
AI summary
This invention relates to the use of a LAG-3 protein or a derivative thereof and optionally a chemotherapy agent for the treatment of cancer in a subject. The subject may have one or more of a low monocyte count, a Luminal B breast cancer, an age of less than about 85 years, has been previously treated with a CDK4/6 inhibitor, and has not previously undergone treatment with a taxane chemotherapy. Suitably, the cancer is a breast cancer, such as a hormone receptor positive breast cancer.