Kauduagonistid

Kauduagonistid is a term used in pharmacology to describe agents that produce receptor activation not by directly binding to the receptor’s orthosteric site, but by acting through indirect mechanisms that increase or modulate the activity of endogenous ligands. In practice, kauduagonistid are contrasted with direct agonists, which activate receptors through direct receptor binding.

Mechanisms of action attributed to kauduagonistid include increasing the concentration of endogenous neurotransmitters at the synapse (for example by promoting release or inhibiting reuptake), slowing or preventing the breakdown of these ligands (such as by inhibiting degrading enzymes), or enhancing receptor signaling in a manner that amplifies the natural ligand’s effect without occupying the primary binding site. Some kauduagonistid also encompass positive allosteric modulators that heighten the receptor’s response to endogenous agonists rather than triggering activation by themselves.

In terminology used in English-language pharmacology, the concept is often described as indirect agonism or indirect-acting agonism. The distinction from direct agonists can be nuanced, because indirect agents can still yield receptor-mediated effects that resemble direct activation, but the key difference lies in whether receptor occupancy occurs at the orthosteric site or via modulation of endogenous ligand levels and signaling pathways. The term kauduagonistid appears mainly in Estonian pharmacology literature and is less common in international usage, where indirect agonists and allosteric modulators are more standard.

Examples commonly discussed in related contexts include agents that increase endogenous transmitter availability (such as precursor substrates or reuptake inhibitors) and enzymes that elevate transmitter levels by reducing breakdown.