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i was looking into erdafitinib and the dose response is actually pretty interesting
the amount of erdafitinib in your blood obviously matters but the amount thats actually free matters too
AAG is one of the main proteins that binds to erdafitinib. since most of the drug is protein bound the amount of free drug can change depending on AAG levels and other factors
this is interesting because cancer patients can have higher AAG levels than healthy people. one study found the mean free fraction was around 0.51% in healthy people compared to 0.32% in cancer patients
so you cant just look at pharmacokinetic data from cancer patients and assume its gonna work exactly the same in a healthy person
the other thing i found interesting was the relationship between drug exposure and inhibition
i originally thought more drug = proportionally more inhibition but thats not necessarily how dose response works
basically
more drug = more exposure
but
more exposure doesnt always = the same increase in effect
a dose response curve can start flattening when you get closer to the upper end of the response
so doubling the exposure doesnt automatically mean youre gonna double the biological effect
also the specific numbers from theoretical calculations shouldnt be treated like actual human FGFR3 inhibition data. erdafitinib is a cancer drug and the clinical pharmacology data show dose proportional exposure across the studied 0.5–12 mg range
the main thing i found interesting is how much protein binding can affect the amount of free drug and how dose response isnt always as simple as looking at the mg
@Dearpleasehelpme what do u think abt it baby ive been working on it since I told u abt it in vc
the amount of erdafitinib in your blood obviously matters but the amount thats actually free matters too
AAG is one of the main proteins that binds to erdafitinib. since most of the drug is protein bound the amount of free drug can change depending on AAG levels and other factors
this is interesting because cancer patients can have higher AAG levels than healthy people. one study found the mean free fraction was around 0.51% in healthy people compared to 0.32% in cancer patients
so you cant just look at pharmacokinetic data from cancer patients and assume its gonna work exactly the same in a healthy person
the other thing i found interesting was the relationship between drug exposure and inhibition
i originally thought more drug = proportionally more inhibition but thats not necessarily how dose response works
basically
more drug = more exposure
but
more exposure doesnt always = the same increase in effect
a dose response curve can start flattening when you get closer to the upper end of the response
so doubling the exposure doesnt automatically mean youre gonna double the biological effect
also the specific numbers from theoretical calculations shouldnt be treated like actual human FGFR3 inhibition data. erdafitinib is a cancer drug and the clinical pharmacology data show dose proportional exposure across the studied 0.5–12 mg range
the main thing i found interesting is how much protein binding can affect the amount of free drug and how dose response isnt always as simple as looking at the mg



