Agonists: full, partial, inverse and biased
Explains drugs that activate receptors: how much they can activate them (full vs partial), drugs that push activity below baseline (inverse), and drugs that activate only some of a receptor's signals (biased).
Where this fitsConnects to 3 · Unlocks 2
- Connects to
- How drugs bind: affinity, shape and binding site — Agonism is one of the two things binding can do: mimic.
- Receptor types: autoreceptors, heteroreceptors and location — Agonists at autoreceptors can turn a synapse down instead of up.
- Fast doors and slow keypads: ionotropic and metabotropic receptors — Biased agonism only applies to metabotropic (G protein-coupled) receptors.
- Unlocks
- Dose-response curves: potency, efficacy, slope and variability — Full vs partial agonists are two different efficacies on a dose-response curve.
- Treating addiction: substitution, antagonists, glutamate, vaccines — and the model's limits — Methadone (full) and buprenorphine (partial) treat opioid addiction for exactly these reasons.
- Full agonist
- Partial agonist
- Antagonist
- Inverse agonist
Walk through
Full agonist
A full agonist activates the receptor as much as the system allows — the curve climbs to the top. Examples: heroin and oxycodone at μ-opioid receptors; classical psychedelics at 5-HT2A.
Analogy and worked example
Analogy: Think of a dimmer switch. A full agonist turns the lights all the way up. A partial agonist can only turn them to half, no matter how hard you push. An antagonist is a hand covering the switch — it doesn't change the light, it just stops anyone else from touching it. An inverse agonist turns the lights below the 'night-light' level the room normally sits at.
Buprenorphine is a partial μ-opioid agonist. Why does that make it useful — and safer — for treating opioid addiction?
- It activates μ-opioid receptors enough to ease craving and withdrawal.
Tip: the ← and → keys move through the lesson.
Full lesson: Reversible receptor binding