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Pharmacogenomics
identifies responders and non responders to different treatments, casual genes and biomarkers to see who responds to treatment
Pharmacokinetics
deals with how the body processes the drug (ADME) (absorption distribution metabolism excretion)
Pharmacodynamics
Activity of the drug in the body
Warfarin
anticoagulant that inhibits vit k synthesis factors
(larger window for therapeutic effect)
variation in individual therapy requiring for a response
SNPS in metabolic and target proteins determining effective warfarin dose
CYP450 enzyme that found in many drugs, SNPS with this enzyme can alter metabolism and decrease dose
VKORC1 is the target that has many SNPS that be sensitive
Pharmacogenetic testing
Blood tests can be ordered via doctors to test metabolization
Biopsies of cancer tissue needed
DTC available for drugs
Molecular etiology of Cystic fibrosis
CTFR ABC transposon > anion channel conducts chloride and bicarbonate ions out of cell > mutations cause CFTR linked to development of CF
Cf therapeutics (f508 deletions)
functional channel misfolding resulting in degradation
treated with fold corrector
cf therapuetic (early stop codon)
needs to promote stop codon readthrough
Pharmacogenetic testing
blood tests can be ordered to see how metabolization works
Genotyping and breast cancer
The types of gene received can determine whether hormonal therapy would work
RNA based gene therapy
addresses diseases caused by mutation o target degradation of the non-functional copy of the gene. viral diseases by targeting viral RNA
cancer treatment, can target undruggable genes, doesn’t change the host genome
Antisense oligonucleotides therapy
results in less protein production using RNA interference (cleaving mRNA)