Potency vs efficacy: EC50, Emax and agonist types
Potency vs efficacy: potency is where a dose-response curve sits, efficacy is how high it reaches. Learn to read EC50 and Emax, and to tell full, partial and inverse agonists apart.
Chapters (9)
Distinguish potency (EC50) from efficacy (Emax) on dose-response curves and classify full, partial and inverse agonists.
The short version
- The EC50 sets potency: a lower EC50 means less drug is needed and the curve sits further left.
- The Emax sets efficacy: the largest effect the drug can produce, however much you give.
- Potency and efficacy are independent, so a drug can be potent but weak, or the reverse.
- A full agonist reaches the tissue maximum; a partial agonist plateaus below it.
- An inverse agonist pushes a constitutively active receptor's response below baseline; a plain antagonist leaves baseline alone.
Potency vs efficacy: why 1 mg can match 40 mg
Forty milligrams of furosemide and one milligram of bumetanide give roughly the same diuretic effect.[1][2] So is bumetanide the stronger drug? That depends on what you mean by stronger.
This lesson separates potency vs efficacy on a dose-response curve, then classifies full, partial and inverse agonists.
The dose-response curve
A drug binds a receptor, and the more drug you give, the more receptors are occupied, until all are taken.[3]
Plot log dose on the x axis and effect on the y axis, as a percentage of the maximum.[3][4] You get an S shape: flat at low doses, steep in the middle, and flat again once receptors are saturated.
EC50 and Emax: potency and efficacy
The concentration that gives half of the drug's own maximal effect is the EC50 (ED50 when the axis is dose rather than concentration), and it measures potency. A lower EC50 means less drug is needed: higher potency, with the curve further left.[3][4]
The plateau is the Emax, and it measures efficacy: the largest effect the drug can produce, however much you give.[3][4]
| Property | Read from | What it tells you |
|---|---|---|
| Potency | EC50 | Where the curve sits, left to right; lower EC50 means higher potency |
| Efficacy | Emax | How high the curve reaches; the ceiling effect |
Potency is where the curve sits, left to right. Efficacy is how high it reaches.
Worked example: three drugs on one receptor
Take three drugs acting on one receptor.
- Drug A: EC50 of 2 nM, and it reaches the full tissue maximum.
- Drug B: the same maximum, but an EC50 of 20 nM.
- Drug C: an EC50 of 2 nM, like A, but it tops out at half the maximum.
- B needs 20 nM for half effect; A needs 2 nM
- 20 / 2 = 10, so A is ten times more potent than B
- A and B have the same maximum, so the same efficacy
- C has A's EC50 (same potency) but half A's maximum (lower efficacy)
No dose of C reaches A's height. Potency and efficacy are independent, so a drug can be potent but weak, or the reverse.[4]
Back to the diuretics: by weight, bumetanide is about 40 times more potent than furosemide. That means a smaller dose, not by itself a bigger maximal effect.[1]
Full, partial and inverse agonists
Now the receptor's side. A full agonist can drive the tissue to its maximal response, as morphine is taught to do at the mu opioid receptor.[3][6][7]
A partial agonist cannot: even with every receptor occupied, it plateaus below the maximum, as buprenorphine does at the mu receptor. Drug C above is a partial agonist.[3][5][7]
Give a partial agonist with a full agonist and they compete for the same receptors, so the partial agonist acts as an antagonist, pulling the response toward its own lower ceiling, though enough full agonist can still win.[3][5]
An inverse agonist is different: some receptors are active even with no ligand. An inverse agonist stabilizes the inactive form, so the response falls below baseline, a negative efficacy. A plain antagonist just blocks, and leaves the baseline alone.[3][5]
| Type | Maximal response | Effect relative to baseline |
|---|---|---|
| Full agonist | Reaches the tissue maximum | Above baseline |
| Partial agonist | Plateaus below the maximum | Above baseline |
| Inverse agonist | Negative efficacy | Below baseline |
| Plain antagonist | None of its own (binds and blocks) | Baseline left alone |
Practice question
Original · USMLE styleA pharmacologist tests three new agonists at the same receptor in isolated tissue under identical conditions. The maximal response of the tissue is set at 100%. Drug K has an EC50 of 4 nM and produces a maximal response of 100%. Drug L has an EC50 of 0.5 nM and produces a maximal response of 35%. Drug M has an EC50 of 30 nM and produces a maximal response of 100%.
Common questions
What is the difference between potency and efficacy?
Potency is read from the EC50 and shows where the curve sits left to right. Efficacy is the Emax, how high the curve reaches.
What does a lower EC50 mean?
A lower EC50 means less drug is needed for half of its own maximal effect, so potency is higher and the curve sits further left.
Is a more potent drug always more efficacious?
No. Potency and efficacy are independent, so a drug can be potent but weak, or the reverse.
How does a partial agonist differ from a full agonist?
A full agonist can drive the tissue to its maximal response. A partial agonist plateaus below it even with every receptor occupied, and given with a full agonist it acts as an antagonist, though enough full agonist can still win.
What is an inverse agonist?
Some receptors are active even with no ligand. An inverse agonist stabilizes the inactive form, so the response falls below that baseline. A plain antagonist leaves the baseline alone.
Transcript
Read the full narration, by chapter686 words
0:00The hook: 40 mg vs 1 mg
Forty milligrams of furosemide, or one milligram of bumetanide: roughly the same diuretic effect. So is bumetanide the stronger drug? That depends on what you mean by stronger. Today: potency versus efficacy on a dose-response curve, and full, partial and inverse agonists.
0:20The dose-response curve
A drug binds a receptor, and the more drug you give, the more receptors are occupied, until all are taken. Plot log dose on the x axis and effect on the y axis, as a percentage of the maximum. You get an S shape: flat at low doses, steep in the middle, flat again once receptors are saturated.
0:40EC50 and Emax
The concentration that gives half of the drug's own maximal effect is the EC50, and it measures potency. A lower EC50 means less drug is needed: higher potency, the curve further left. The plateau is the E max, and it measures efficacy: the largest effect the drug can produce, however much you give. Potency is where the curve sits, left to right. Efficacy is how high it reaches.
1:08Three drugs on one receptor
Take three drugs on one receptor. Drug A has an EC50 of two nanomolar, and reaches the full tissue maximum. Drug B reaches the same maximum, but its EC50 is 20 nanomolar. B needs 10 times the concentration for half effect, so A is 10 times more potent, with the same efficacy. Drug C has an EC50 of two nanomolar, like A, but it tops out at half the maximum. Same potency as A, lower efficacy: no dose of C reaches A's height.
1:44Back to the diuretics
Back to the diuretics: by weight, bumetanide is about 40 times more potent than furosemide. That means a smaller dose, not by itself a bigger maximal effect.
1:56Full, partial and inverse agonists
Now the receptor's side. A full agonist can drive the tissue to its maximal response, as morphine is taught to do at the mu opioid receptor. A partial agonist cannot: even with every receptor occupied, it plateaus below the maximum, as buprenorphine does at the mu receptor. Drug C is a partial agonist. Give a partial agonist with a full agonist and they compete for the same receptors, so the partial agonist acts as an antagonist, pulling the response toward its own lower ceiling, though enough full agonist can still win. An inverse agonist is different: some receptors are active even with no ligand. An inverse agonist stabilizes the inactive form, so the response falls below baseline: a negative efficacy. A plain antagonist just blocks, and leaves the baseline alone.
2:51Practice question
Your turn. A pharmacologist tests three agonists at one receptor. The tissue's maximum is 100%. Drug K: EC50 4 nanomolar, maximal response 100%. Drug L: EC50 0.5 nanomolar, maximal response 35%. Drug M: EC50 30 nanomolar, maximal response 100%. Which statement is most accurate? A, drug K is more potent than drug L, because it produces the greater maximal response. B, drug M is more efficacious than drug K, because it needs a higher concentration. C, drug L is the most potent and the least efficacious. D, drugs K and M differ in efficacy but have equal potency. E, drug L is an inverse agonist, because its maximal response is the lowest. Pause here and decide.
3:59The answer
A is out: maximal response is efficacy, not potency, and L has the lowest EC50. B is out: K and M reach the same maximum, so their efficacy is equal; M's higher EC50 makes it less potent. D is out: K and M differ in potency, not in efficacy. E is out: an inverse agonist pushes below baseline, but L gives a positive 35%: a partial agonist. So the answer is C. Drug L has the lowest EC50, so the highest potency, and the lowest maximum, so the lowest efficacy.
4:40Recap and next lesson
Three things to keep. One: the EC50 sets potency, how far left the curve sits; the E max sets efficacy, how high it reaches. Two: potency and efficacy are independent, so a drug can be potent but weak, or the reverse. Three: a full agonist reaches the maximum, a partial agonist plateaus below it, and an inverse agonist pushes below baseline. Next: competitive and noncompetitive antagonists, and how they bend these curves.
Sources
Numbers in the text, e.g. [1], point here- Europe PMC PMC13608559 (J Pers Med 2026): loop diuretic dose equivalence. europepmc.org/article/PMC/PMC13608559
- Europe PMC PMC13729087 (Clin Cardiol 2026): furosemide 40 mg = torsemide 20 mg = bumetanide 1 mg. europepmc.org/article/PMC/PMC13729087
- Deranged Physiology. Potency and efficacy; Graded dose-response curves; Full agonists, partial agonists and inverse agonists. derangedphysiology.com/main/cicm-primary-exam/pharmacodynamics/Chapter-415/potency-and-efficacy · derangedphysiology.com/main/cicm-primary-exam/pharmacodynamics/Chapter-412/graded-dose-response-curves · derangedphysiology.com/main/cicm-primary-exam/pharmacodynamics/Chapter-417/full-agonists-partial-agonists-and-inverse-agonists
- MSD Manual Professional Version. Dose-Response Relationships. msdmanuals.com/professional/clinical-pharmacology/pharmacodynamics/dose-response-relationships
- MSD Manual Professional Version. Drug-Receptor Interactions. msdmanuals.com/professional/clinical-pharmacology/pharmacodynamics/drug-receptor-interactions
- Wikipedia (secondary). Dose-response relationship; Agonist. en.wikipedia.org/wiki/Agonist
- Europe PMC PMC12971109 (2026): buprenorphine as a partial agonist. europepmc.org/article/PMC/PMC12971109
The practice question is original and its patient is synthetic. Every fact is checked against the sources above in independent accuracy reviews. Always follow your local guidelines and your own laboratory’s ranges.
Corrections. None so far. Spotted an error? Email info@medservatory.com with the lesson code MS-S1-PHARM-009.
For exam study only, not medical advice. Read the medical disclaimer.
In this series
Playlist on YouTube- EP 01Potency vs efficacy: EC50, Emax and agonist types5:17
- EP 02Competitive vs noncompetitive antagonists: effect on EC50 and Emax5:01
- EP 03Therapeutic index explained: TD50 / ED505:01
- EP 04First-pass metabolism and bioavailability: calculating oral F from AUC5:18
- EP 05Volume of distribution: why Vd can be bigger than the body5:17
- EP 06Clearance and half-life: t½ = 0.693 × Vd / CL5:01
- EP 07Zero-order vs first-order elimination explained5:12
- EP 08Loading dose and maintenance dose, explained5:02
- EP 09CYP450 inducers and inhibitors: how they change drug levels5:16
- EP 10Autonomic receptors: alpha, beta and muscarinic5:33
- EP 11Beta blocker selectivity: beta-1, ISA and alpha blockade5:24
- EP 12Vasopressors compared: receptors, pressure and heart rate5:46
- EP 13Organophosphate poisoning: muscarinic vs nicotinic signs5:36
- EP 14Receptor desensitization, downregulation and upregulation5:01
- EP 15Beta-lactams and vancomycin: enzyme versus substrate5:04
- EP 16Protein synthesis inhibitors: 30S vs 50S antibiotics5:07