agonistit

Agonistit, in English commonly referred to as agonists, are substances that bind to a receptor and activate it to produce a biological response. They can be endogenous, such as neurotransmitters and hormones, or exogenous, such as drugs. Agonists are contrasted with antagonists, which bind without activating the receptor, and with inverse agonists, which reduce constitutive receptor activity.

Agonists are classified by their efficacy. Full agonists generate the maximal possible response when they occupy receptors, whereas partial agonists produce a submaximal response even at full receptor occupancy. Inverse agonists decrease baseline activity of receptors that display constitutive activity. Some ligands act as biased agonists, preferentially triggering certain signaling pathways over others after receptor binding.

Mechanistically, agonists bind to the receptor’s active or allosteric site and stabilize conformations associated with activation. Receptors they target include G protein–coupled receptors, ion channels, and enzyme-linked receptors. The resulting signaling cascades lead to physiological effects such as altered heart rate, muscle contraction, or neurotransmitter release.

Potency and efficacy are key pharmacodynamic concepts for agonists. Potency describes the concentration required to achieve a given effect (often expressed as EC50), while efficacy refers to the maximal effect achievable by the drug. Selectivity for receptor subtypes influences tissue-specific responses and adverse effects.

Clinical relevance is broad: agonists are used to stimulate physiological processes in conditions such as acute hypotension (vasopressors), asthma (beta-adrenergic agonists), pain control (opioid receptor agonists), and metabolic regulation (serotonin or dopamine receptor agonists). Tolerance, desensitization, and receptor regulation can affect long-term responses to agonists.