Elucidating the structure of poly dopamine

As a consequence of influence from non-genetic factors in the development of ADRs, the association between a specific genotype and an ADR will always be less than 100 %.Thus, there is a need for well-designed clinical trials to ascertain the extent of environmental influences on the ADRs for which a genetic basis has been implicated (Guzey and Spigset, 2004).In the more frequent heterozygous carriers (genotype *1/*3), the clearances were between 40 and 75 %.In these cases in which individual dosages are derived from clinical drug effects, such as for oral anticoagulants, the pharmacogenetics-based dose adjustments showed a good correlation with the genotype-specific empirically derived doses.Pharmacogenomics testing is laboratory testing which has the potential to determine how an individual’s genetic factors may affect the safety and effectiveness of that individual’s response to a specific medication.The goal of pharmacogenomics testing is to reduce the incidence of adverse medication reactions while improving an individual’s positive response to the medication.Additionally, some tests may help provide information on how well a specific treatment may work for an individual.Cytochrome P450 enzymes are a group of enzymes that account for approximately 75 percent of drug metabolism in the human body.

It is now clear that a significant portion of these ADRs as well as therapeutic failures are caused by genetic polymorphism and genetically based inter-individual differences in drug absorption, disposition, excretion or metabolism.Enzymes encoded by the P450 genes (eg, CYP2C9, CYP2C19, CYP2D6, CYP3A4, CYP3A5 etc.) are found primarily in the liver.The action of the P450 enzymes affects the blood levels of many drugs.This is in agreement with the observation of Pirmohamed and Park (2003) who stated that “ADRs are common and many are suggested to have a genetic predisposition.There has been intense research in the role of CYP enzyme gene polymorphisms in the cause of ADRs.Kirchheiner and Brockmoller (2005) stated that the genetic coding for the CYP enzyme 2C9 (CYP2C9) carries many inherited polymorphisms.Those coding for R144C (*2) and I359L (*3) amino acid substitutions have both significant functional effects and appreciable high population frequencies, and their in vivo consequences have been examined in humans in relation to drug metabolism -- pharmacokinetics, drug responses as well as outcomes of clinical trials in subjects with different CYP2C9 genotypes.Tentative estimates of how CYP2C9 genotyping might be applied to dose adjustments in clinical therapy were based on dose-related pharmacokinetic parameters such as clearance or trough drug concentrations.Mean clearances in homozygous carriers of the *3 allele were below 25 % of that of the wild type for S-warfarin, tolbutamide, glipizide, celecoxib, and fluvastatin.The Ampli Chip was cleared for marketing for CYP2D6 testing in December 2004, and for CYP2C19 testing in January 2005.The Ampli Chip is marketed for use in screening of patients who are to be treated with drugs metabolized by the CYP system that have a narrow therapeutic ratio with serious toxic effects.

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