Clopidogrel is currently the most widely used anti-platelet aggregation drug for the treatment of acute coronary syndrome, atherosclerosis and other cardiovascular and cerebrovascular diseases. Clopidogrel is a prodrug that is metabolized by hepatic cytochrome P450 enzymes (mainly CYP2C19 enzymes) into active products to exert its drug effect. Different individuals have different responses to clopidogrel. About 40% of Asian patients develop clopidogrel resistance, mainly due to weak metabolism caused by CYP2C19 gene mutation. There are at least 36 alleles of CYP2C19, among which CYP2C19*2 and CYP2C19*3 account for more than 99% of the weak metabolic phenotypes in the Asian population, and CYP2C19*17 is the only genotype with ultra-fast activity found so far [1-3]. In 2010, the FDA issued a black box warning, clearly recommending that doctors conduct CYP2C19 genotyping tests on patients who will take clopidogrel and implement personalized medicine according to the patient's genotype.
Clinical studies have shown that individuals with poor metabolism caused by CYP2C19 gene mutations have an increased risk of thrombus re-formation, increased risk of cardiovascular and cerebrovascular events, and increased mortality [4].
Relationship between CYP2C19 genotype and clopidogrel metabolism [5]
Warfarin is the first-line drug for the prevention and treatment of thromboembolic diseases, but its drug response varies greatly among individuals, and the difference in the stable dose of warfarin between different individuals can reach more than 20 times, and the therapeutic window is narrow, so the dose is difficult to control, especially In the early stage of anticoagulant therapy with warfarin, it is very easy to cause serious bleeding complications. A large number of studies have shown that the pharmacokinetics and pharmacodynamics of warfarin are closely related to the genotypes of CYP2C9 and VKORC1 [6-7]. In 2010, the FDA added a starting dose selection table to the instructions for warfarin, suggesting that CYP2C9 and VKORC1 gene testing should be performed before medication.
Clinical studies have shown that: Using genotype and traditional methods to guide the dosage of warfarin, the hospitalization rate of bleeding or thrombosis in the former is significantly lower than that in the latter, and patients can benefit from genotype guided warfarin treatment [8]。
The genetic algorithm can significantly change the recommended dose of the clinical algorithm to make it closer to actual needs [9]
Triple quality control and double guarantee of anti-pollution system.
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Triple quality control and double guarantee of anti-pollution system.
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1. PCR machine
2. ABI Series Genetic Analyzer
[1] Simon T, etal. N Engl J Med. 2009 Jan 22;360(4):363-75.
[2] Hu LM, etal. Pharmacogenomics. 2012 Nov;13(14):1571-81.
[3] Sim SC,etal. Clin Pharmacol Ther. 2006 Jan;79(1):103-13.
[4] Jessica LM, et al. N Eng J Med. 2009;360:354-62.
[5] Wei W, et al. Chin J Med Genet. 2012;29(4):420-25.
[6] Rieder MJ, et al. N Engl J Med. 2005;352:2285-93.
[7] Manolopoulos VG, et al. Pharmacogenomics. 2010;11:493-6.
[8] H.L.Weinshilboum R.M.N et al., Engl J Med 2011; 364:1144-1153
[9] Klein TE, et al. N Engl J Med. 2009 Feb 19;360(8):753-64.
※This information is only for reference by relevant medical professionals.Please refer to the instruction manual for the use or precautions of the kit.
[ENG]CV.pdf:Reference:[ENG]CV.pdf
