BMS 123 · Common Core (Tronc commun)Section 6.3 · Dose–response, interactions and variability
Section 25 of 27
Reading dose–response curves
Compare full and partial agonists on one plot, and tell competitive from non-competitive antagonism by the way the curve moves.
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“Go deeper” is optional. It adds mechanism and extra detail for when you are ready — nothing you need for the checks is hidden there.
Why this matters
Two drugs can look similar in a formulary and behave very differently on a graph. The shape of the curve tells you whether a drug can reach the full effect, whether a blocker can be overcome by giving more agonist, and whether a loss of effect is a matter of dose or a matter of lost receptors. These are not academic distinctions: they decide whether increasing the dose is rational or useless, and whether the effect of a treatment can be rescued at all.
What you need to know first
You need Units 5.5 and 6.1: the definitions of agonist, antagonist, Emax and EC50. The words surmountable and dextral are explained here, so no extra vocabulary is assumed.
Words to know (5)
Full agonist
A drug that combines with its receptor and produces the maximal response obtainable in that tissue. A full agonist reaches the top of the graph even at relatively low concentrations.
Partial agonist
A drug that binds and activates the receptor but produces a sub-maximal response at any concentration. A partial agonist flattens below the full agonist whatever dose is given.
Competitive antagonist
A drug that binds reversibly at the same site as the agonist and competes with it, so its block can be overcome by more agonist. The agonist curve shifts right but keeps the same maximum height.
Non-competitive antagonist
A drug that binds irreversibly or away from the agonist site and reduces the maximum effect, so the block cannot be overcome. The agonist curve shifts right and its ceiling falls.
Dextral shift
A movement of the curve to the right, meaning a larger concentration of agonist is needed for the same effect. Adding an antagonist without changing its amount shifts the agonist curve to the right.
One idea at a timeIdea 1 / 4
In one sentence On one plot, how far left a curve lies tells you potency, and how high its plateau reaches tells you efficacy.
Position and height answer two different questions
When several agonists are drawn on the same plot, read the graph in two passes. First look at the plateaus: curves A and B share the same Emax, so they are equally efficacious, while C sits below them at every dose and is therefore less efficacious. Then look at the horizontal positions: A reaches that shared Emax at a lower concentration than B, so A is more potent than B, and both A and B are more potent than C because C’s curve lies to the right of theirs. A and B are full agonists, since they can produce the maximal response, and C is a partial agonist. Two passes are needed because the graph encodes two independent properties, and a comparison that mentions only one of them is incomplete.
For example
If A reaches its plateau at 5 units and B at 50 units while both plateaus are equal, then A is about ten times more potent than B and neither is more effective. B can still be used, but a larger dose is needed.
Pause and check yourself
Two curves share the same plateau but one lies far to the left. What is the difference between the two drugs?
Show the answer
Their efficacy is the same because the plateaus are equal; the drug on the left is more potent because a smaller concentration reaches that plateau. Only the dose needed differs.
Read detailed explanations
Why a rightward shift is not the whole story
The textbook picture of competitive antagonism is a clean parallel shift, and it rests on assumptions that are worth stating. The shift is parallel only if the agonist and the antagonist compete reversibly for one homogeneous population of receptors and if the antagonist reaches equilibrium with them. When those conditions hold, the size of the shift depends on the antagonist concentration and on its affinity: doubling the antagonist concentration roughly doubles the agonist concentration needed for the same effect. This relationship is used experimentally to estimate antagonist affinity, and it is the reason a competitive antagonist can be titrated — the clinician can choose how much blockade to produce. Several practical complications follow. If the antagonist dissociates slowly, the block deepens over time and the curve measured at ten minutes is not the one measured at an hour. If the drug is a mixed agonist–antagonist, part of the rightward shift is accompanied by a partial activation, so the apparent maximum may drop even though no receptor was destroyed. If the tissue has receptor reserve, a substantial fraction of receptors can be blocked before the maximum effect falls, so the curve may look purely competitive until the reserve is exhausted and the plateau then collapses. Finally, an antagonist that acts at an allosteric site may change the agonist’s affinity without competing at the same pocket; the shift is competitive in appearance but the mechanism is different, and the distinction matters when choosing a rescue strategy.
Efficacy, potency and the language of agonist classification
Everyday language blurs three properties that pharmacology keeps apart, and separating them makes the graphs easier to reason with. Affinity is the ability of the drug to bind the receptor; it determines how much drug is needed and therefore appears as horizontal position. Intrinsic activity, or efficacy, is the ability of the bound drug to activate the receptor and produce a response; it determines the height of the plateau. Potency, the dose required for a given effect, is a practical consequence of both, and it is the property a prescriber cares about when choosing a dose. With these three words, the classification becomes systematic. A full agonist has high affinity and full intrinsic activity, so its curve rises to the tissue maximum. A partial agonist has affinity but low intrinsic activity, so its curve plateaus below the maximum; as concentration rises it occupies more receptors but cannot activate them fully. A neutral antagonist has affinity and no intrinsic activity: alone it produces nothing, and in the presence of an agonist it lowers the agonist’s effect by occupying receptors. An inverse agonist has affinity and negative intrinsic activity: it reduces the receptor’s spontaneous signalling below its resting level, which is only visible in systems with constitutive activity. Mixed agonist–antagonists combine two of these roles at different receptor subtypes. Keep the vocabulary straight and a new curve becomes readable: ask what the plateau says about intrinsic activity and what the horizontal position says about affinity and dose.
Explore the diagram
Look at the whole drawing first. Then select one numbered part and connect it to the idea you just read.
Reading agonists and antagonists on one plot
Four curves for the same agonist under different conditions: a full agonist, a partial agonist, and the same agonist after a fixed dose of a competitive or a non-competitive antagonist.
New to diagrams? Read this first
Look at the whole drawing once without clicking anything. Ask yourself only: what kind of picture is this (a comparison, a route, a sequence, a table)?
Press Play, or use the arrows, to move through the numbered parts in order. The drawing stays still; only the highlight moves.
Click a number, or its name in the list below, to read what that part is and why it matters. Use “Hide labels” when you want to test your memory.
More controls
01 / 5Agonist alone
If the drawing is wider than this panel, scroll it sideways. Labels stay readable; the numbered explanations below show the same ideas.
Agonist alone
The dark curve is the control: the full agonist by itself. It reaches 100% of the maximal tissue response, so nothing can be added to its effect. Every other curve on this plot is the same agonist measured after something has been changed.
Schematic, not to scale. Curves are drawn for one agonist with one fixed antagonist concentration; changing that concentration moves the competitive curve further right, while a non-competitive block lowers the ceiling in proportion to the receptors removed.
Key points to remember
✓Read the plateau first for efficacy, then the horizontal position for potency; two independent properties need two readings.
✓A and B sharing an Emax are full agonists of different potency; C, below them at every dose, is a partial agonist.
✓A competitive antagonist shifts the curve right without changing slope or maximum, so the block is surmountable.
✓A non-competitive antagonist reduces slope and maximum and shifts the curve right; the block cannot be overcome by more agonist.
Go deeper
Worked example
Diagnosing a falling response from the graph. A patient who previously responded to an inhaled bronchodilator now responds less well. Two possible explanations are on the table: the patient has started another drug that competes with the bronchodilator at its receptor, or the second drug has irreversibly blocked part of the receptor population. You have a dose–response plot made before and after the second drug was started.
Look at the two plateaus. If the maximum reachable response is unchanged and the curve has only moved to the right, the antagonist is competitive: the same effect is still attainable with more agonist.
If the plateau has fallen and the curve has also moved right, the second drug has reduced the number of available receptors, which is the signature of non-competitive antagonism.
Check the slope as well as the maximum, because the notes describe both as reduced in non-competitive antagonism. A flatter curve with a lower ceiling is a stronger diagnosis than a lower ceiling alone.
Translate the graph into a decision. If the block is competitive, a higher dose of the bronchodilator or removal of the competing drug can restore the effect. If it is non-competitive, increasing the dose will not recover the lost maximum and the plan must change.
The graph answers the clinical question: an unchanged ceiling means the effect can be bought back with dose, while a lowered ceiling means the tissue has lost capacity. Reading the maximum before reading the position prevents the common error of chasing a lost effect with ever larger doses.
Common misconception
A frequent beginner error is to think that any antagonist can be overcome simply by giving more agonist. That is true only for competitive antagonism. When the antagonist binds irreversibly or reduces the number of available receptors, more agonist moves the curve but cannot raise the maximum, so the response stays capped.
Check your reasoning
You are shown two post-antagonist curves: one shifted right with an unchanged plateau, one shifted right with a lower plateau. Explain what each tells you and how the treatment plan differs.
Reveal an answer
The first is competitive block: the same maximum is still reachable, so more agonist or removal of the antagonist can restore the effect. The second is non-competitive block: receptors have been lost or irreversibly occupied, so no dose recovers the maximum and the plan must use a different drug or a different target.
Where this comes from
BMS 123 General Pharmacology II lecture notes, Part 2 — Principles of Pharmacodynamics · Unit 3.4.3, DRC for different types of agonists and antagonists: full and partial agonists, competitive and non-competitive antagonism
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About this course and its sources
Bilingual lessons organised from the supplied BMS 123 General Pharmacology II lecture notes (Principles of Pharmacokinetics and Principles of Pharmacodynamics). Diagrams are original educational schematics; pharmacology, nursing and French-language review are pending.