Please wait while the transcript is being prepared...
Hello. I'm Jill Kolesar.
Today we're going to talk about the second part of the lecture,
which is the pharmacodynamics of anticancer agents.
So, let's move on to pharmacodynamics,
which is what the drug does to the body.
So, in pharmacodynamics we draw a different type of
curve and this is concentration versus effect curve.
So, in this diagram,
you can see concentration is going to be on the x-axis,
so that's concentration in plasma,
and then we look at effect and that's going to be on the y-axis.
So, what you can see from this slide that way to the very left of the diagram,
where the concentration is low,
you'll have little effect,
and then what we like to see with drugs,
so this is kind of an ideal concentration versus
effect slide that we have a linear relationship between concentration effect.
So, you can see that in a more linear part of the curve and then typically,
you reach a plateau effect where even as concentration goes higher,
you don't get a higher effect.
So, this is a typical diagram for drug-receptor interactions.
Drugs typically act by binding to receptors and they may activate or inactivate it.
It's also a mechanism of action for anticancer agents.
What we're really looking for here is our dose response relationships.
So, let's look at some of our anticancer drugs and how they work.
So, the mechanism of action,
one of the main things we have are DNA synthesis inhibitors.
So, we have purines which are the adenine and guanine and
we have pyrimidines which are the cytosines and thymines.
So, in the Purine family we have Pentostatin which inhibits adenosine deaminase,
6-MP, which inhibits purine ring biosynthesis
and methotrexate which inhibits purine ring biosynthesis as well.
So, essentially what these drugs are doing,
is they're preventing the synthesis of the building blocks of DNA,
so therefore, the DNA cannot be synthesized because you run out of starting materials.