Genetic diagnosis for QT prolongation related adverse drug...

Chemistry: molecular biology and microbiology – Measuring or testing process involving enzymes or... – Involving nucleic acid

Reexamination Certificate

Rate now

  [ 0.00 ] – not rated yet Voters 0   Comments 0

Details

C536S023200, C536S023500, C536S023100, C536S024310

Reexamination Certificate

active

10257573

ABSTRACT:
The specification is directed to a method of diagnosing whether a subject is predisposed to an adverse reaction to one or more pharmaceutical agents which may induce a prolonged QT interval or acquired LQTS in that individual. The diagnosis is genetic analysis of at least two polymorphisms or mutations which the individual may have, which are associated with an increased risk for prolonged QT intervals or Torsades de Pointes (TdP). Genetic screening for determining the predisposition of prolonged QT intervals induced by a pharmaceutical agent is performed by identifying genetic polymorphisms or mutations located in at least two classes of genes, wherein the genes are (1) LQT genes, (2) altered sensitivity genes (e.g., MiRP1) or (3) increased exposure genes (e.g., MDR genes or P450 cytochrome genes). The specification is also directed to compositions and kits for determining such predispositions to adverse drug reactions.

REFERENCES:
patent: WO 99/13106 (1999-03-01), None
patent: WO 00/06199 (2000-02-01), None
patent: WO 00/06772 (2000-02-01), None
Ingelman-Sundberg, “Polymorphic human cytochrome P450 enzymes: an opportunity for individualized drug treatment”, Trends in Pharmaceutical Sciences, 199, vol. 20, p. 342-349.
Abbott et al., “MiRP1 forms IKr potassium channels with HERG and Is associated with cardiac arrythmia”, Cell, vol. 97, 1999, p. 175-187.
Drolet et al., “Block of the rapid component of the delayed rectifier potassium current by the prokinetic agent cisapride underlies drug-related lengthening of the QT interval”, Circulation, 1998, vol. 97, p. 204-210.
Weyerbrock et al., “Rate-independent effects of the new class III antiarrhythmic agent ambasilide on transmembrane action potentials in human ventricular endomyocardium”, Journal of Cardiovascular Pharmacology, 1997, vol. 30, p. 571-575.
Viskin, “Long QT syndromes and torsade de pointes”, The Lancet, 1999, vol. 354, p. 1625-1633.
Larsen et al., “Recessive Romano-Ward syndrome associated with compound heterozygosity for two mutations in the KVLQT1 gene”, European Journal of Human Genetics, 1999, vol. 7, p.724-728.
Itoh et al., Genomic organization and mutational analysis of KVLQT1, a gene responsible for familial long QT syndrome, Human Genetics, Sep. 1998, vol. 103, No. 3, p. 290-295.
Donger et al., KVLQT1 C-terminal missence mutation causes a forme fruste long QT-syndrome, Circulation, Nov. 4, 1997, vol. 96, No. 9, p. 2778-2781.
Schulze-Bahr, E., et al., “Molecular genetics of arrhythmias—a new paradigm,” 2000, Z. Kardiol., 89 Suppl 4:IV1. pp. 12-15.
Hahnenberger K., et al., “Use of oligonucleotide array hybridization for genotyping CYP2D6 and CYP2C19,” 1997, Clinical Pharmacology and Therapeutics, 61(2):165.
Wang, Q., et al., “Cardiac sodium channel mutations in patients with long QT syndrome, an inherited cardiac arrhythmia,” 1995, Hum. Mol. Genet., 4(9):1603-7.
Gintant GA., “Azimilide causes reverse rate-dependent block while reducing both components of delayed-rectifier current in canine ventricular myocytes,” 1998, J. Cardiovasc. Pharmacol., 31(6):945-53.
Selnick H.G., et al., “Class III antiarrhythmic activity in vivo by selective blockade of the slowly activating cardiac delayed rectifier potassium current IKs by (R)-2-(2,4-trifluoromethyl)-N-[2-oxo-5-phenyl-1-(2,2,2-trifluoroethyl)- 2, 3-dihydro-1H-benzo[e][1,4]diazepin-3-yl]acetamide,” 1997, J. Med. Chem., 40(24):3865-8.
Schulze-Bahr, E., et al., “The LQT syndromes—current status of molecular mechanisms,” 1999, Z. Kardiol., 88(4):245-54.
Wei Jian et al., “KCNE1 polymorphism confers risk of drug-induced long QT syndrome by altering kinetic properties of IKs potassium channels,” Nov. 2, 1999, Circulation, 100(18 Suppl.):I.495; & 72ndScientific Sessions of the American Heart Association; Atlanta, Georgia, USA; Nov. 7-10, 1999.
Wei Jian et al., “KCNE2 (Mirp1) mutations in acquired long QT syndrome,” Nov. 2, 1999, Circulation, 100(18 Suppl.): I.495; & 72ndScientific Sessions of the American Heart Association; Atlanta, Georgia, USA; Nov. 7-10, 1999.
Donger, C., et al., “KVLQT1 C-terminal missense mutation causes a forme fruste long-QT syndrome,” 1997, Circulation, 96(9):2778-81.
Cavero, I., et al., “Drugs that prolong QT interval as an unwanted effect: assessing their likelihood of inducing hazardous cardiac dysrhythmias,” 2000, Expert Opin. Pharmacother., 1(5):947-73.
Sesti, F., et al., “A common polymorphism associated with antibiotic-induced cardiac arrhythmia,” 2000, Proc. Natl. Acad. Sci. U. S. A., 97(19):10613-8.
Busch., A.E., “Inhibition of I-Ks in guinea pig cardiac myocytes and guinea pig I-sK channels by the chromanol 293b”, 1996, Pflugers Archiv. European Journal of Physiology,.432(6):1094-1096.
Mohler, Peter J., et al., “Ankyrin-B mutation causes type 4 long-QT cardiac arrhythmia and sudden cardiac death,” Feb. 6, 2003, Nature, (London), 421(6923):634-639.
European Search Report dated Aug. 9, 2004 in PCT/US0112087.
Benson et al., “Missense Mutation in the Pore Region ofHERGCauses Familial Long QT Syndrome,” Circulation 93: 1791-5 (1996).
Chen et al., “Internal Duplication and Homology with Bacterial Transport Proteins in themdrl(P-Glycoprotein) Gene from Multidrug-Resistant Human Cells,” Cell 47: 381 (1986).
Donger et al., “KVLQT1 C-Terminal Missense Mutation Causes a Forme Fruste Long-QT Syndrome,” Circulation 96: 2778-81 (1997).
Keating and Sanguinetti, “Molecular and Cellular Mechanisms of Cardiac Arrhythmias,” Cell 104: 569 (2001).
Neyroud et al., “Heterozygous mutation in the pore of potassium channel geneKvLQT1causes an apparently normal phenotype in long QT syndrome,” Eur J Hum Genet 6: 129-33 (1998).
Russell et al., “KVLQT1 mutations in three families with familial or sporadic long QT syndrome,” Hum. Molec Genet 5: 1319-24 (1996).
Schulze-Bahr et al., “KCNE1mutations cause Jervell and Lange-Nielsen syndrome,” Nature Genet 17: 267-8 (1997).
Wang, “Cardiac sodium channel mutations in patients with long QT syndrome, an inherited cardiac arrhythmia,” Hum Molec Genet 4: 1603-7 (1995).
Wang et al., “Positional cloning of a novel potassium channel gene:KVLQT1mutations cause cardiac arrhythmias,” Nature Genet 12: 17-23 (1996).
Wang et al., “Genetics, molecular mechanisms and management of long QT syndrome,” Ann Med 30: 58 (1998).

LandOfFree

Say what you really think

Search LandOfFree.com for the USA inventors and patents. Rate them and share your experience with other people.

Rating

Genetic diagnosis for QT prolongation related adverse drug... does not yet have a rating. At this time, there are no reviews or comments for this patent.

If you have personal experience with Genetic diagnosis for QT prolongation related adverse drug..., we encourage you to share that experience with our LandOfFree.com community. Your opinion is very important and Genetic diagnosis for QT prolongation related adverse drug... will most certainly appreciate the feedback.

Rate now

     

Profile ID: LFUS-PAI-O-3883609

  Search
All data on this website is collected from public sources. Our data reflects the most accurate information available at the time of publication.