But great guess. The notion of ‘individual medicine’ and interpersonal variability in response to drugs is one of the main things looked at in Pharmacokinetics.
Some people are “poor metabolizers” of a drug, and so a normal dose regimen will lead to toxic accumulation as their liver doesn't clear it at the expected rate.
Others are “fast metabolizers” of a drug, and so a normal dose regimen will not accumulate to an efficacious dose - and they get little or no benefit from the therapy.
This is based upon genetic variability of CYP P450 enzymes expressed primarily in the liver.
Sometimes it is based upon genetic variability of the gene that codes for the protein the drug is supposed to act upon.
For example, if a small molecule drug is supposed to bind to a receptor and turn it “on” to stimulate a therapeutic response within the body - if there is high genetic variability in the gene that codes for that receptor - it might not bind in some people or it might bind and turn it “off”.
Luckily for me humans show a high level of genetic homology. We are all very similar in DNA despite the superficial differences that arose as a result of climactic differences over our worldwide distribution.
:)
Is it bad I understood everything you said, save the enzyme which I am unfamiliar with?
Cool beans. You must be excited with the recent
advancements. How much of the genotyping work is applicable to your field?