Agonist–Antagonist Dose-Response Simulator

Agonist

Concentration [A] 10.0 nM

Hill coefficient n 1.0

Antagonist

Concentration [B] 0.0 nM

Live Readouts

Occupancy

Response

Apparent EC50

10.0 nM

Apparent Emax

100%

No antagonist Current curve

How it works

A drug's effect follows the classic occupancy-response (Emax/Hill) model. Fractional receptor occupancy and the resulting response both rise sigmoidally with the log of agonist concentration [A]:

Response = Emax · [A]^n / (EC50^n + [A]^n)

where EC50 is the concentration producing a half-maximal effect and n is the Hill coefficient (steepness, ≈ cooperativity of binding).

A competitive antagonist occupies the same site and can be displaced by enough agonist — it shifts the curve rightward (raises the apparent EC50) without lowering the ceiling:

EC50' = EC50 · (1 + [B] / Ki)     Emax unchanged

A noncompetitive antagonist binds elsewhere (or irreversibly) and removes functional receptors from the pool regardless of agonist concentration — it lowers the ceiling (Emax) without shifting EC50:

Emax' = Emax · Ki / (Ki + [B])     EC50 unchanged

Concentration slider — moves the agonist dose on a log axis (0.1–1000 nM); the receptor field and curve marker update live.
Hill slider — steepens or flattens the sigmoid, mimicking cooperative binding between multiple receptor sites.
Antagonist mode — switches between the two classic pharmacological mechanisms and redraws the shifted curve against the unshifted baseline.

Real-world relevance: this is the exact model pharmacologists use to characterise every receptor-targeted drug — from beta-blockers competing with adrenaline to naloxone displacing opioids — and to read Ki and mechanism straight off a lab dose-response assay.

Agonist-bound receptor Antagonist-bound receptor Free receptor

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