Pharmacogenomics is the study of the role of
the genome in drug response.
-Pharmacogenomics is the study how an
individual genetic inheritance affected the body response to the drug.
-Pharmacogenomics aims to develop rational drug
with respect to patients genotype to ensure maximum efficiency with minimal
adverse effect.
-Taking into account the variability in the
drug response from person to person, pharma-cogenesis ends at one drug for each
individual [one drug for a group of persons with similar properties i.e.
identical agent]
-Therefore, a better effect of the drug will be
achieve preventing the adverse drug reaction.
Traditional drug designing ends at one for all
approaches and the does depend on majority an age factor i.e low dose for young
once and high dose for adults.
-But such problem can be illuminated by one
person is equal to one drug approaches.
Four Steps in Pharmacokinetics [ADME]
1.
Absorption.
2.
Distribution.
3.
Metabolism.
4.
Excretion.
SNP: - Single Nucleotide Polymorphism.
Enzyme present in liver [at the side of metabolism]
e.g. Cytochrome, P450, TPMT, VKORC
In case of active drug: -
1.
Enzyme
activity high, drug dose is high.
2.
Enzyme
activity high, drug dose is low.
In case of inactive
drug.
3.
Enzyme
activity high, drug dose is low.
4.
Enzyme
activity low, drug dose is high.
- All the drugs we inject are metabolism by our
body.
- some drugs get activated after metabolism and
some remain active
before metabolism.
- This metabolism is carried out by special
enzyme, which are generally present in liver cells.
e.g. Cytochrome P450
- This enzyme are expressed whenever they are
required for the expression are not identical in every individual.
-Each gene sequence varies approximately
nucleotide 100-300 bases. This is called as single, nucleotide polymorphism
[SNP]
- Because the genes are different in their
sequence the enzyme produced by expression of this gene also very in their
activity from person to person.
- Therefore, the role of metabolism of a drug
in each individual may differ
e.g. In case of drug which get inactivated
after metabolism may show different response in different individual having
different enzyme different individual having different enzyme activities.
1.
In
person having highly active enzyme the drug will be metabolised very fast and excreted
from the body may not rich which is required to excretes its therapeutic
effect.
2.
In
case of person having less enzyme activity the drug will be metabolise slowly, therefore
it may remain in active from for a long period in the body.
3.
The
person with very slow metabolic rate may show toxic effect of that drug [e.g.
in case of cytotoxic drug used in cancer therapy]
Benefit of Pharmacogenomics: -
1.
Production
of powerful medicine; -
2.
Accuracy
of therapy will be increased.
3.
The
undesirable side effect will be minimized and the patient will be prescribed
drug based on their genotypes.
Disadvantages: -
1.
It
is not possible to study genotype of each individual.
2.
One
drug one-person approach is very costly.
3.
It
is not yet in use.
REFERENCE: -
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(November 2003). "Pharmacogenetics: potential for individualized drug
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LJ, Phillimore HE (2009). "Clinical use
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6. ^ Shin J, Kayser SR, Langaee TY (April 2009).
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8. ^ Becquemont L (June 2009). "Pharmacogenomics of adverse
drug reactions: practical applications and
perspectives". Pharmacogenomics. 10 (6):
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9. ^ Hauser AS,
Chavali S, Masuho I, Jahn LJ, Martemyanov KA, Gloriam DE, Babu MM (January
2018). "Pharmacogenomics
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10.
^ "Guidance for
Industry Pharmacogenomic Data Submissions" (PDF). U.S. Food and Drug Administration. March 2005.
Retrieved 2008-08-27.
11.
^ Squassina A, Manchia M, Manolopoulos VG, Artac M, Lappa-Manakou
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12.
^ Jump up to:a b c Huser V,
Cimino JJ (2013). "Providing pharmacogenomics clinical decision support
using whole genome sequencing data as input". AMIA Joint Summits on
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13.
^ Jump up to:a b Pirmohamed
M (2001). "Pharmacogenetics
and pharmacogenomics". Br J Clin Pharmacol. 52 (4):
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14.
^ Jump up to:a b Prasad K
(2009). "Role of
regulatory agencies in translating pharmacogenetics to the clinics". Clin Cases
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15.
^ Evans DA, Clarke CA (1961).
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16.
^ Kalow W (2006). "Pharmacogenetics and pharmacogenomics:
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