CD39–CD73 Enzyme Combination to Restore ATP–Adenosine Balance
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Solution Overview
Problem
Current treatments for rheumatoid arthritis, such as methotrexate and biological therapies, have significant side effects and limited efficacy, necessitating the development of new approaches that can effectively manage inflammatory disorders without these drawbacks.
Innovation Solution
A combination of a source of CD39 and a source of CD73, which convert ATP to ADP and AMP, respectively, to restore the ATP:adenosine balance at the site of inflammation, utilizing CD39 proteins and nucleic acid molecules with specific sequence identities and enzymatic activities.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Reliability
If current treatments such as methotrexate and biological therapies are used for rheumatoid arthritis, then inflammatory symptoms can be suppressed, but significant side effects and limited efficacy occur
Solution Approach 1:
The patent extracts and targets specific enzymes (CD39 and CD73) involved in the ATP:adenosine metabolic pathway that are directly responsible for inflammatory regulation. By isolating and inhibiting these specific enzymatic targets rather than using broad-spectrum immunosuppressants, the treatment achieves anti-inflammatory effects while minimizing off-target side effects.
Solution Approach 2:
The invention changes the therapeutic parameter from general immunosuppression to specific enzymatic inhibition in the purine metabolism pathway. By targeting CD39 and CD73 enzymes that control the conversion of ATP to adenosine, the treatment modifies the biochemical parameters of inflammation directly, improving efficacy while reducing systemic side effects associated with conventional therapies.
2Duration of action of stationary object
If conventional therapies are administered repeatedly to manage rheumatoid arthritis, then disease progression can be controlled, but treatment frequency and cumulative side effects increase
Solution Approach 1:
The patent employs preliminary action by targeting the root metabolic pathway (ATP:adenosine balance) that drives inflammation, rather than treating symptoms repeatedly. By establishing correct enzymatic function at CD39 and CD73, the treatment creates a sustained therapeutic effect that reduces the need for frequent dosing and repetitive interventions.
3Object-affected harmful factors
If broad-spectrum immunosuppressants are used to treat inflammatory disorders, then inflammation can be suppressed, but specificity and selectivity of treatment are reduced
Solution Approach 1:
The patent applies local quality by targeting specific enzymes (CD39 and CD73) within the purine metabolism pathway that are locally responsible for inflammatory regulation. This localized enzymatic targeting provides high treatment specificity, affecting only the inflammatory pathway while preserving other immune functions, unlike broad-spectrum immunosuppressants.
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 combination of CD39 and CD73 sources exhibits a synergistic effect on improving the ATP:adenosine balance, providing a therapeutic benefit for inflammatory disorders like rheumatoid arthritis, potentially reducing the need for repetitive therapies and minimizing side effects.
Implementation Method 1
the source of a CD39 has at least 95% sequence identity with any one of SEQ ID NO: 1, 5, 9 and 11 and having nucleoside triphosphate diphosphohydrolase activity, and wherein the source of a CD39 is able to convert adenosine triphosphate (ATP) to adenosine diphosphate (ADP) and adenosine monophosphate (AMP)
Implementation Method 2
the source of a CD73 has at least 95% sequence identity with any one of SEQ ID NO: 3, 7, 13 and 15 and having ecto-nucleotidase activity, and wherein the source of a CD73 is able to convert AMP to adenosine
Data Source
Figure 1~2b
Figure 2a
Figure 2c
AI summary
The invention provides a combination of a source of a CD39 and of a source of a CD73.