Abstract
“One size fits all” is an erroneous paradigm in drug delivery, due to side effects/adverse effects and variability observed in drug response. The variability is a result of geneotypic variations (variability in genomic constitution) which is studied in the branch of science called Pharmacogenomics. The variability in drug response is studied by multigene analysis or profiling of whole-genome single nucleotide polymorphism (SNP) and is recorded in terms of the pharmacokinetic (absorption, distribution, metabolism and elimination) and pharmacodynamic (drug-receptor interaction, immune response, etc.) response of the drug. Therefore, a foray into this research area can provide valuable information for designing of drug therapies, identifying disease etiology, therapeutic targets and biomarkers for application in treatment and diagnosis of diseases. Lately, with the integration of pharmacogenomics and nanotechnology, a new facade for the diagnosis and treatment of diseases has opened up, and the prescription pattern of drugs has moved to pharmacotyping (individualized dose and dosage-form adjusted therapy) using nanoplatforms like nanobioconjugates, nanotheranostics, etc.
Highlights
By the end of 1950s, pharmacogenetics had become a more established approach for the treatment of diseases
The history of pharmacogenetics can be traced back to 510 B.C. when Pythagoras recognized the dangers of ingesting fava beans that resulted in fatal reaction in some individuals, and later on the reaction was attributed to the deficiency of G6PD in those individuals [3]
Other studies which further supported the science of pharmacogenetics include occurrence of unusual reactions to drugs on the basis of biochemical individuality studied by JBS Haldane, inborn variation in individuals for phenylthiocarbamide, atropine esterase activity in rabbits and occurrence of hemolytic disease in American soldiers of only African descent upon administration of the drug primaquine [3, 4]
Summary
By the end of 1950s, pharmacogenetics had become a more established approach for the treatment of diseases. A major fraction of the population lacks either of CYP2D6 or CYP2C19 because of the presence of inactivating genetic polymorphisms [1, 5]. Mere appearance of these inactive forms of variant alleles brings about the absence of activity affecting the metabolism of certain drugs metabolized by these enzymes. The gene VKORC1, encodes for Vitamin K epoxide reductase to which warfarin and other coumarin anticoagulants bind and has shown to exhibit extensive genetic polymorphism affecting drug response. This enzyme regulates regeneration of reduced vitamin K during the blood coagulation process [9]. Indication of variation in drug metabolism and drug targets, pharmacogenetics helps to discover adverse drug reactions due to exaggerated drug response, interaction with an inappropriate target or an inappropriate immune response to the drug [1]
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