Patent 8084210 Issued on December 27, 2011. Estimated Expiration Date: November 19, 2030. Estimated Expiration Date is calculated based on simple USPTO term provisions. It does not account for terminal disclaimers, term adjustments, failure to pay maintenance fees, or other factors which might affect the term of a patent.
The present invention provides methods for predicting or determining a subject's response to an antiplatelet agent, and methods for determining a subject's suitability to a treatment regime or intervention for a disease associated with platelet aggregation, using analysis of genetic polymorphisms. The present invention also relates to the use of genetic polymorphisms in assessing a subject's response to an antiplatelet agent. Nucleotide probes and primers, kits, and microarrays suitable for such assessment are also provided.
Other References
Simon et al., “Genetic Determinants of Response to Clopidogrel and Cardiovascular Events,” N Eng J Med., 2009, 360:363-375.
Mega et al., “Cytochrome P-450 Polymorphisms and Response to Clopidogrel,” N Eng J Med., 2009, 360:354-362.
Helsby, N. A., “Pheno- or Genotype for the CYP2C19 Drug Metabolism Polymorphism: the Influence of Disease,” Proc. West. Pharmacol. Soc., 2008, 51:5-10.
Freedman et al., “Clopidogrel, Genetics, and Drug Responsiveness,” N Eng. J. Med., 2009, 360:411-413.
Desta et al., “Rapid Identification of Hepatic Cytochrome P450 2C19 Activity Using a Novel and Noninvasive [13C] Pantoprazole Breath Test,” J Pharmacol. Exp. Thera., 2009, 329:297-305.
Demorais et al., “Identification of a New Genetic Defect Responsible for the Polymorphism of (s)-Mephenytoin Metabolism in Japanese,” Molecular Pharmacology, 1994, 46:594-598.
Sim et al., “A common novel CYP2C19 gene variant causes ultrarapid drug metabolism relevant for the drug response to proton pump inhibitors and antidepressants,” 2006, Clinical Pharmacology & Therapeutics (2006) 79, 103-113.
Rudberg et al., “Impact of the ultrarapid CYP2C19*17 allele on serum concentration of escitalopram in psychiatric patients,” Clin Pharmacol Ther. Feb. 2008;83(2):322-7. Epub Jul. 11, 2007.
Payne et al. “Increased Active Metabolite Formation Explains the Greater Platelet Inhibition With Prasugrel Compared to High-dose Clopidogrel,” Journal of Cardiovascular Pharmacology:Nov. 2007—vol. 50—Issue 5—pp. 555-562.
Kurzawski et al., “Effect of CYP2C19*17 gene variant on Helicobacter pylori eradication in peptic ulcer patients.” Eur J Clin Pharmacol. Oct. 2006;62(10):877-80. Epub Aug. 16, 2006.
Ingelman-Sundberg et al., “Polymorphic human cytochrome P450 enzymes: an opportunity for individualized drug treatment,” Trends Pharmacol Sci. Aug. 1999;20(8):342-9.
Ingelman-Sundberg et al., “Influence of cytochrome P450 polymorphisms on drug therapies: pharmacogenetic, pharmacoepigenetic and clinical aspects,” Pharmacol Ther. Dec. 2007;116(3):496-526. Epub Oct. 9, 2007.
Ingelman-Sundberg et al., “Human drug metabolising cytochrome P450 enzymes: properties and polymorphisms,” Naunyn Schmiedebergs Arch Pharmacol. Jan. 2004;369(1):89-104. Epub Oct. 22, 2003.
Hulot et al., “Cytochrome P450 2C19 loss-of-function polymorphism is a major determinant of clopidogrel responsiveness in healthy subjects,” Blood 108:2244-2247, Oct. 2006.
Hahnenberger, et al., “Use of oligonucleotide array hybridization for genotyping CYP2D6 and CYP2C19,” 1997, Clinical Pharmacology and Therapeutics, 61(2):165.
Goldstein & Blaisdell. “Genetic tests which identify the principal defects in CYP2C19 responsible for the polymorphism in mephenytoin metabolism.” Methods Enzymol. 1996;272:210-8.
Geisler et al. “CYP2C19 and nongenetic factors predict poor responsiveness to clopidogrel loading dose after coronary stent implantation.” Pharmacogenomics. Sep. 2008;9(9):1251-9.
Fontana et al., “Influence of CYP2C19 and CYP3A4 gene polymorphisms on clopidogrel responsiveness in healthy subjects,” J Thromb Haemost. Oct. 2007;5(10):2153-5. Epub Aug. 3, 2007.
Fontana et al., “Biological effect of increased maintenance dose of clopidogrel in cardiovascular outpatients and influence of the cytochrome P450 2C19*2 allele on clopidogrel responsiveness,” Thromb Res. 2008;121(4):463-8. Epub Aug. 2, 2007.
Farid et al., “Cytochrome P450 3A inhibition by ketoconazole affects prasugrel and clopidogrel pharmacokinetics and pharmacodynamics differently.” Clin Pharm Ther., 2007, 81:735-741.
Evans & Johnson, Annual Review of Genomics and Human Genetics 2 (2001), 9-39.
Daniel & Edeki. “Genetic polymorphism of S-mephenytoin 4′-hydroxylation.” Psychopharmacol Bull. 1996;32 (2):219-30.
Chen et al., “Inhibition of ADP-Induced Platelet Aggregation by Clopidorgrel is Related to CYP2C19 Genetic Polymorphisms,” Clin. and Exp. Pharma. and Physiol., 2008, 35:904-908.
Brockimöller & Tzvetkov, “Pharmacogenetics: data, concepts and tools to improve drug discovery and drug treatment,” Eur J Clin Pharmacol. Feb. 2008;64(2):133-57. Epub Jan. 26, 2008.
Brandt et al., “Common polymorphisms of CYP2C19 and CYP2C9 affect the pharmacokinetic and pharmacodynamic response to clopidogrel but not prasugrel,” Journal of Thrombosis and Haemostasis (2007) vol. 5, Issue 12, pp. 2429-2436.
Abell & Liu. “Abstract 272: In vitro Platelet Aggregation as a Biosensor for Clopidogrel Active Metabolite Formation,” Circulation. 2006;114:II—27.
Dahlman, I et al. Nature Genetics 30:149-150 (Feb. 2002).
Trenk, D. et al. Circulation 118(18):Suppl 2:S814-S815 (Oct. 2008).
Sibbing, D. et al. Circulation 121:512-518 (Feb. 2010; published online Jan. 18, 2010).
November 19, 2030. Estimated Expiration Date is calculated based on simple USPTO term provisions. It does not account for terminal disclaimers, term adjustments, failure to pay maintenance fees, or other factors which might affect the term of a patent.
