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Agonism occurs when a drug binds to a receptor and causes a biological response.
Agonist drugs typically bind to the same place on the receptor as the substance that naturally
activates the receptor, or the endogenous agonist.
Agonists that can generate a maximal response at a receptor are called full agonists.
Partial agonists are only able to generate a fraction of the possible response at a receptor.
In some cases, an agonist may bind to a receptor and cause a decrease in signaling at that
receptor.
These substances are called inverse agonists, and they can produce effects that are opposite
to those of an agonist.
Receptor antagonism occurs when a drug binds to a receptor but does not activate the receptor;
in the process, it interferes with the ability of agonists to activate the receptor.
The most common type of antagonism is reversible competitive antagonism, where a drug competes
with an agonist for its binding site, in the process limiting the amount of agonist that
can bind to the receptor at the same time.
Reversible competitive antagonists frequently unbind and rebind to receptors.
An agonist can replace the antagonist while it is unbound, allowing the antagonist’s
effects to be overcome with the addition of more agonist.
Irreversible competitive antagonists, sometimes called non-competitive antagonists, also bind
to the site where an agonist binds but unbind from the receptor very slowly, if at all.
They can reduce the maximal effect an agonist has, regardless of how much agonist is present.
Some drugs may bind to a receptor at a different site from where an agonist binds and influence
the function of the receptor.
These drugs, often called allosteric modulators, may increase or decrease the likelihood of
an agonist binding to a receptor, enhance or reduce the effects an agonist has when
it does bind, or activate the receptor on their own.