 So what would we do with these proteins? Well, there are things that are slightly more complex. There are, in principle, we could bind anything to them, right? But just binding is not really going to solve things for us. It's important, but they're not enough. The binding, we're typically going to talk about as affinity. Affinity, that's really just another word for the free energy of binding that we talked about in the molecular simulation lecture. But whereas in molecular simulation, we typically talk about this in delta G. We can do that here, too. But in terms of medicinal chemistry and understanding how good a compound is, we're frequently going to talk about concentration. I'll come back to that later, why it's so important. But we want drugs that have a high effect already at very low concentration. And this we can calculate from the equilibrium constant when it's binding. So a drug that is millimolar affinity, we're going to need, say, millimolar concentration of that. While something that is non-o- or picomolar affinity, that's going to be much more efficient drugs. We can get by with one millionth or one billionth of the concentration of that drug. And in most cases, that's going to be much more specific. So if you hear the concentration that it's a non-o-molar drug or something, we're really talking about affinity. Non-o-molar is going to correspond to a low free energy of binding. That is good. It's binding strong. But just binding is not enough. We also need this to do something. It needs to have effect or efficacy, as we call it. Actual output. Again, it's not going to help you to merely bind to a receptor that is related to blood pressure, right? If we want to reduce the blood pressure, what counts at the end of the day is that how much are we reducing the blood pressure? These frequently go hand in hand. Because again, if something isn't binding, it's not going to have an effect. But there are drugs that bind stronger, but they don't really have a particularly high effect. So ideally, we want things that bind specifically on everything, but it's even more important that they have a very high effect, high efficacy. What effect can that be? Well, I haven't told you, but there are multiple ones, in fact. So if we, in terms of effect, if I just call that response, and I put that on the y-axis here, there will be some sort of zero level here, right? Where nothing is happening. And then I'm going to say, N, this is the natural response. Say that if this is a receptor to a neurotransmitter, if I add the normal amount of neurotransmitter, this is how much I would expect to activate it. But if instead of the natural molecules, I try adding other things here. What can happen? Well, by far the easiest thing is if I add a small drug, and then I get the natural effect. If I get the natural effect, I'm going to call that this is a full agonist. We often don't say full. But an agonist is a molecule, a drug, that has the same effect as the natural response. It's not going to be my natural molecule. Hopefully this is a molecule that's smaller and easier to administer and everything. But a full agonist, I think, might just help the body to kickstart if, for whatever reason, there is not enough of the natural molecule. In many cases, we might not be quite as good as the natural full response. So then we might have to make do with a so-called partial agonist. And you can probably guess. That just means that we might just be activating it to 50%. But hey, 50% is sure better than nothing. Those are not the only things we can do, though. In many cases, we actually have the opposite problem in the body. That for whatever reason, a process has gone berserk. It's increasing my blood pressure too much. Or in the case of a virus, it's infecting myself. That is not a good process that I want to keep going. I would like to prevent a process from happening. I would like to inhibit it. And when we inhibit things, we usually say that we're adding a molecule, that it's an antagonist. Or strictly speaking, it should be a neutral antagonist. So antagonist is really just an anti-agonist. So this is a molecule. Think of this as putting a bit of gum in the doc. So normally we have a process here that activates the receptor. But an antagonist just stops this process from happening. Even if I'm adding my normal molecule or something, if this was an ion channel, suddenly the receptor is busy. It can't do its normal job. By far the most common type of molecule to inhibit a process. For a few ones, it's not common, but it can happen. Assuming that they have, say, ion channels in my nervous system. And these ion channels would normally have the effect of, say, responding positively to creating a nerve signal when something happens. And maybe, just maybe, I could find a drug that does the opposite. So now I'm not just shutting the process off. Now I'm literally doing the opposite of the process. So this is a so-called inverse antagonist. So an inverse antagonist does the opposite of the normal agonist process. Agonist, full normal process. Antagonist stops that process from happening. Inverse agonist, it explicitly goes in the opposite direction. So both these agonists create an effect while an antagonist merely stops the effect.