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A Method to Study the C924T Polymorphism of the Thromboxane A2 Receptor Gene
Published on: April 1, 2019
Genetic CYP2C19 polymorphism dependent non-responders to clopidogrel therapy--does structural design, dosing and
1Suramus Biopharm, Integrated Drug Development, J.P. Nagar I phase, Bangalore 560 025, India.
Abstract:
Recent evidences suggest that genetic CYP2C19 polymorphism plays a role in the development of treatment resistance for clopidogrel's antiplatelet therapy. This short communication puts forward some strategies that could be potentially used to overcome the genetic polymorphism associated hurdles. While there is some established evidence for an induction strategy and design of chemical structure, the proposed dosing input strategy is speculative in nature. Such thought process and novel explorations are important for delivering medicines in genetically and ethnically diverse populations.
Insights
Genetic CYP2C19 polymorphism can cause clopidogrel resistance. This study explores strategies, including induction and chemical design, to overcome these genetic hurdles for diverse patient populations.
Area of Science:
- Pharmacogenomics
- Drug Metabolism
- Cardiovascular Therapeutics
Background:
- Clopidogrel is a widely used antiplatelet medication.
- CYP2C19 genetic variations are linked to clopidogrel treatment resistance.
- This resistance impacts therapeutic efficacy in certain patient groups.
Purpose of the Study:
- To propose strategies for overcoming CYP2C19-related clopidogrel resistance.
- To address challenges in delivering effective antiplatelet therapy in diverse populations.
Main Methods:
- Review of existing evidence on CYP2C19 polymorphism and clopidogrel response.
- Exploration of potential therapeutic strategies: induction, chemical structure modification, and dosing adjustments.
Main Results:
- Established evidence supports induction strategies and chemical structure design to mitigate polymorphism effects.
- A speculative dosing input strategy is proposed as a potential avenue for further research.
Conclusions:
- Novel approaches are crucial for personalized antiplatelet therapy.
- Addressing genetic variations like CYP2C19 polymorphism is key for equitable and effective medicine delivery.
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