DPP3 Biomarker-Guided Anti-ADM Antibody Therapy for Shock
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Solution Overview
Problem
Current methods for therapy guidance and monitoring in patients with shock lack effective biomarkers for determining the appropriate use of anti-ADM antibodies or fragments, leading to suboptimal treatment strategies.
Innovation Solution
Determining the level of dipeptidyl peptidase 3 (DPP3) in bodily fluids to guide the administration of anti-adrenomedullin (ADM) antibodies or fragments, with specific binding to the N-terminal part of ADM, to tailor therapy based on pre-determined thresholds.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Reliability
If current therapy guidance methods are used in patients with shock, then treatment can be provided, but the treatment strategy is suboptimal due to lack of effective biomarkers
Solution Approach 1:
The patent applies preliminary action by measuring DPP3 levels in bodily fluids before initiating anti-ADM antibody treatment. This allows the therapy strategy to be predetermined based on biomarker status, ensuring that only patients with elevated DPP3 levels receive the treatment, thereby optimizing treatment effectiveness and avoiding unnecessary interventions in patients who would not benefit.
2Reliability
If DPP3 level determination is implemented to guide anti-ADM antibody treatment, then therapy stratification and treatment efficacy are improved, but the complexity of the diagnostic process increases
Solution Approach 1:
The patent applies segmentation by dividing patients into distinct therapeutic groups based on their DPP3 biomarker status. Patients are segmented into those with elevated DPP3 levels who require anti-ADM antibody treatment and those with normal levels who do not require this specific therapy. This segmentation simplifies the overall treatment decision-making process by creating clear, binary classification criteria.
3Reliability
If anti-ADM antibody treatment is administered based on DPP3 levels, then patient outcomes are improved and mortality risk is reduced, but the treatment can only be targeted to specific patient groups
Solution Approach 1:
The patent applies local quality by tailoring the treatment approach to the specific characteristics of different patient groups. Instead of a uniform treatment strategy for all shock patients, the therapy is locally optimized: patients with elevated DPP3 levels receive anti-ADM antibody treatment while those with normal levels receive alternative or no such treatment. This localized approach maximizes therapeutic benefit for the specific subgroup that requires it.
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
This approach enables targeted therapy stratification and monitoring, improving patient outcomes by identifying patients who would benefit from anti-ADM treatment based on DPP3 levels, thereby enhancing treatment efficacy and reducing mortality risk in shock conditions.
Implementation Method 1
DPP3 is known to hydrolyze dipeptides from the N-terminus of its substrates, including angiotensin II, III and IV; Leu- and Met-enkephalin; endomorphin 1 and 2
Implementation Method 2
administering an anti-adrenomedullin (ADM) antibody or anti-ADM antibody fragment or anti-ADM non-Ig scaffold to said patient, wherein said patient is treated with said anti-adrenomedullin (ADM) antibody or anti-ADM antibody fragment or anti-ADM non-Ig scaffold if said determined level of DPP3 is below a pre-determined threshold
Data Source
AI summary
The present application is directed to to a method for therapy guidance and/ or therapy monitoring and/ or therapy stratification in a patient with shock and/or in a patient running into shock. In particular, the method comprises providing a sample from said patient, determining a level of DPP3 in said sample, and wherein the level of DPP3 in said sample is indicative of whether a treatment with an anti-ADM antibody or anti-ADM antibody fragment or anti-ADM non-Ig scaffold is required. In a preferred embodiment of the invention, the method comprises additionally determining in a sample from said patient a level of ADM-NH2.