Editing Partial agonist

{{Short description|Agonist drug having partial efficacy at a receptor}}
[[File:Agonist 2.png|thumb|Relationship between percentage activity and concentration of full agonists and partial agonists]]
In [[pharmacology]], '''partial agonists''' are drugs that bind to and activate a given [[Receptor (biochemistry)|receptor]], but have only partial [[Intrinsic activity|efficacy]] at the receptor relative to a [[full agonist]]. They may also be considered [[Ligand (biochemistry)|ligands]] which display both [[agonistic]] and [[Receptor antagonist|antagonist]]ic effects—when both a full agonist and partial agonist are present, the partial agonist actually acts as a [[competitive antagonist]],{{Citation needed|reason= plenty of partial agonists, if not the majority, do not seem to behave this way. Drugs such as varenicline and psilocin do not function as antagonists when full agonists are present. I'm not aware of any partial agonists besides buprenorphine that act as antagonists when a full agonist is present.|date=April 2022}}  competing with the full agonist for receptor occupancy and producing a net decrease in the receptor activation observed with the full agonist alone.<ref>{{cite book |first1=Norman |last1=Calvey |first2=Norton |last2=Williams | name-list-style = vanc |year=2009 |chapter=Partial agonists |chapter-url=https://books.google.com/books?id=lnRlU12Q4h8C&pg=PA62 |page=62 |title=Principles and Practice of Pharmacology for Anaesthetists |publisher=John Wiley & Sons |isbn=978-1-4051-9484-6}}</ref> Clinically, partial agonists can be used to activate receptors to give a desired submaximal response when inadequate amounts of the endogenous ligand are present, or they can reduce the overstimulation of receptors when excess amounts of the endogenous ligand are present.<ref>{{cite journal | vauthors = Zhu BT | title = Mechanistic explanation for the unique pharmacologic properties of receptor partial agonists | journal = Biomedicine & Pharmacotherapy | volume = 59 | issue = 3 | pages = 76–89 | date = April 2005 | pmid = 15795100 | doi = 10.1016/j.biopha.2005.01.010 }}</ref>

Some currently common drugs that have been classed as partial agonists at particular receptors include [[buspirone]], [[aripiprazole]], [[buprenorphine]], [[nalmefene]] and [[norclozapine]]. Examples of ligands activating [[peroxisome proliferator-activated receptor gamma]] as partial agonists are [[honokiol]] and [[falcarindiol]].<ref>{{cite journal | vauthors = Atanasov AG, Wang JN, Gu SP, Bu J, Kramer MP, Baumgartner L, Fakhrudin N, Ladurner A, Malainer C, Vuorinen A, Noha SM, Schwaiger S, Rollinger JM, Schuster D, Stuppner H, Dirsch VM, Heiss EH | title = Honokiol: a non-adipogenic PPARγ agonist from nature | journal = Biochimica et Biophysica Acta (BBA) - General Subjects | volume = 1830 | issue = 10 | pages = 4813–9 | date = October 2013 | pmid = 23811337 | pmc = 3790966 | doi = 10.1016/j.bbagen.2013.06.021 }}</ref><ref>{{cite journal | vauthors = Atanasov AG, Blunder M, Fakhrudin N, Liu X, Noha SM, Malainer C, Kramer MP, Cocic A, Kunert O, Schinkovitz A, Heiss EH, Schuster D, Dirsch VM, Bauer R | title = Polyacetylenes from Notopterygium incisum--new selective partial agonists of peroxisome proliferator-activated receptor-gamma | journal = PLOS ONE | volume = 8 | issue = 4 | pages = e61755 | year = 2013 | pmid = 23630612 | pmc = 3632601 | doi = 10.1371/journal.pone.0061755 | bibcode = 2013PLoSO...861755A | doi-access = free }}</ref> Delta 9-tetrahydrocannabivarin ([[Tetrahydrocannabivarin|THCV]]) is a partial agonist at [[Cannabinoid receptor type 2|CB2 receptors]] and this activity might be implicated in ∆9-THCV-mediated [[anti-inflammatory]] effects.<ref>{{Cite web|url=http://insubriaspace.cineca.it/bitstream/10277/269/1/Phd_thesis_bolognini_completa.pdf|title=PHARMACOLOGICAL PROPERTIES OF THE PHYTOCANNABINOIDS ∆9-TETRAHYDROCANNABIVARIN AND CANNABIDIOL - Phd thesis of: Dr. Daniele Bolognini - PDF|date=2010}}</ref> Additionally, Delta-9-Tetrahydrocannabinol ([[Tetrahydrocannabinol|THC]]) is a partial agonist at both the [[Cannabinoid receptor type 1|CB1]] and CB2 receptors, with the former being responsible for its psychoactive effects.

== See also ==
*[[Competitive antagonist]]
*[[Beta blocker#Intrinsic sympathomimetic activity|Intrinsic sympathomimetic activity]] of [[beta blocker]]s
*[[Inverse agonist]]
*[[Mixed agonist/antagonist]]

== References ==
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{{Pharmacology}}

[[Category:Pharmacodynamics]]


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