View source for Propranolol

{{Short description|Beta blocker drug}}
{{Distinguish|Propanol|Propofol}}
{{Use dmy dates|date=February 2024}}
{{cs1 config|name-list-style=vanc|display-authors=6}}
{{Infobox drug
| Watchedfields = verified
| verifiedrevid = 464216937
| image = Propranolol.svg
| image_class = skin-invert-image
| width = 250px
| alt = 
| caption = 
| image2 = Propranolol-from-1977-crystal-structure-3D-balls-side.png
| width2 = 250px
| alt2 = <!-- Clinical data -->
| pronounce = {{IPAc-en|p|r|oʊ|ˈ|p|r|æ|n|ə|ˌ|l|ɒ|l}}
| tradename = Inderal, others
| Drugs.com = {{drugs.com|monograph|propranolol-hydrochloride}}
| DailyMedID = Propranolol
| MedlinePlus = 
| pregnancy_AU = C
| pregnancy_category = 
| routes_of_administration = [[Oral administration|By mouth]], [[rectal administration|rectal]], [[intravenous therapy|intravenous]]<ref name="Inderal-Label" /><ref name="KalamRasoolRehman2020" />
| class = [[Beta blocker]]
| ATC_prefix = C07
| ATC_suffix = AA05

<!-- Legal status -->| legal_AU = S4
| legal_UK = POM
| legal_US = Rx-only
| legal_EU = Rx-only
| legal_CA = Rx-only
| legal_status = <!-- Pharmacokinetic data -->
| bioavailability = 25%<ref name="Inderal-Label" /><ref name="Srinivasan2019" />
| protein_bound = 90% ([[human serum albumin|albumin]] and [[α1-acid glycoprotein|α<sub>1</sub>-acid glycoprotein]])<ref name="Inderal-Label" /><ref name="KalamRasoolRehman2020" />
| metabolism = [[Liver]] (extensive) [[CYP1A2]], [[CYP2D6]]; minor: [[CYP2C19]], [[CYP3A4]]; [[aromatic compound|aromatic]] [[hydroxylation]] (mainly 4-hydroxylation), ''N''-[[dealkylation]], [[side chain|side-chain]] [[oxidation]], [[glucuronidation]]<ref name="Inderal-Label" /><ref name="KalamRasoolRehman2020" />
| metabolites = ''N''-Desisopropylpropranolol; 4'-Hydroxypropanolol<ref name="KalamRasoolRehman2020" />
| elimination_half-life = ~4{{nbsp}}hours (range 3–8{{nbsp}}hours)<ref name="Inderal-Label" /><ref name="DrugBank" /><ref name="KalamRasoolRehman2020" />
| duration_of_action = Up to 12{{nbsp}}hours<ref name="PubChem" />
| excretion = [[Urine]]: 91%<ref name="DrugBank" /><ref name="KalamRasoolRehman2020" />

<!-- Identifiers -->| index2_label = as HCl
| CAS_number_Ref = {{cascite|correct|??}}
| CAS_number = 525-66-6
| PubChem = 4946
| IUPHAR_ligand = 564
| DrugBank_Ref = {{drugbankcite|correct|drugbank}}
| DrugBank = DB00571
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 4777
| UNII_Ref = {{fdacite|correct|FDA}}
| UNII = 9Y8NXQ24VQ
| KEGG_Ref = {{keggcite|correct|kegg}}
| KEGG = D08443
| KEGG2_Ref = {{keggcite|correct|kegg}}
| KEGG2 = D00483
| ChEBI_Ref = {{ebicite|correct|EBI}}
| ChEBI = 8499
| ChEMBL_Ref = {{ebicite|correct|EBI}}
| ChEMBL = 27
| synonyms = AY-20694; AY20694

<!-- Chemical data -->| IUPAC_name = (''RS'')-1-(propan-2-ylamino)-3-(1-naphthyloxy)propan-2-ol
| chirality = [[Racemic mixture]]
| C = 16
| H = 21
| N = 1
| O = 2
| SMILES = OC(COC1=C2C=CC=CC2=CC=C1)CNC(C)C
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI = 1S/C16H21NO2/c1-12(2)17-10-14(18)11-19-16-9-5-7-13-6-3-4-8-15(13)16/h3-9,12,14,17-18H,10-11H2,1-2H3
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = AQHHHDLHHXJYJD-UHFFFAOYSA-N

<!-- Physical data -->| melting_point = 96
}}
<!-- Definition and medical uses -->
'''Propranolol''' is a medication of the [[beta blocker]] class.<ref name="Srinivasan2019">{{cite journal | vauthors = Srinivasan AV | title = Propranolol: A 50-Year Historical Perspective | journal = Ann Indian Acad Neurol | volume = 22 | issue = 1 | pages = 21–26 | date = 2019 | pmid = 30692755 | pmc = 6327687 | doi = 10.4103/aian.AIAN_201_18 | doi-access = free | url = }}</ref><ref name="AHFS2015" /><ref name="Inderal-Label">{{Cite web | url=https://www.accessdata.fda.gov/drugsatfda_docs/label/2011/016418s080,016762s017,017683s008lbl.pdf | title=Inderal (propranolol hydrochloride) Tablets | website=www.accessdata.fda.gov}}</ref> It is used to treat [[hypertension|high blood pressure]], some types of [[cardiac dysrhythmia|irregular heart rate]], [[thyrotoxicosis]], [[capillary hemangioma]]s, [[akathisia]], [[performance anxiety]], and [[essential tremor]]s,<ref name="AHFS2015" /><ref name="Dav2006">{{cite journal | vauthors = Davidson JR | title = Pharmacotherapy of social anxiety disorder: what does the evidence tell us? | journal = The Journal of Clinical Psychiatry | volume = 67 | issue = Suppl 12 | pages = 20–26 | date = 2006 | pmid = 17092192 | doi = 10.1016/j.genhosppsych.2005.07.002 }}</ref><ref name="Chinnadurai2016">{{cite journal | vauthors = Chinnadurai S, Fonnesbeck C, Snyder KM, Sathe NA, Morad A, Likis FE, McPheeters ML | title = Pharmacologic Interventions for Infantile Hemangioma: A Meta-analysis | journal = Pediatrics | volume = 137 | issue = 2 | article-number = e20153896 | date = February 2016 | pmid = 26772662 | doi = 10.1542/peds.2015-3896 | s2cid = 30459652 | url = http://pediatrics.aappublications.org/content/pediatrics/137/2/e20153896.full.pdf | doi-access = free }}</ref><ref>{{Cite journal |last=Blaisdell |first=G. D. |date=July 1994 |title=Akathisia: A Comprehensive Review and Treatment Summary |url=https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-2007-1014294 |journal=Pharmacopsychiatry |language=en |volume=27 |issue=4 |pages=139–146 |doi=10.1055/s-2007-1014294 |pmid=7972345 |issn=0176-3679|url-access=subscription }}</ref> as well as to prevent [[migraine headaches]], and to prevent further heart problems in those with [[angina]] or previous [[myocardial infarction|heart attacks]].<ref name="AHFS2015">{{cite web | title = Propranolol hydrochloride | work = Monograph | url = https://www.drugs.com/monograph/propranolol-hydrochloride.html | publisher = The American Society of Health-System Pharmacists | access-date = 1 January 2015 | url-status = live | archive-url = https://web.archive.org/web/20150101152631/http://www.drugs.com/monograph/propranolol-hydrochloride.html | archive-date = 1 January 2015 }}</ref> It can be taken [[oral administration|orally]], [[rectal administration|rectally]], or by [[intravenous injection]].<ref name="AHFS2015" /><ref name="KalamRasoolRehman2020" /> The formulation that is taken orally comes in short-acting and long-acting versions.<ref name="AHFS2015" /> Propranolol appears in the blood after 30 minutes and has a maximum effect between 60 and 90 minutes when taken orally.<ref name="AHFS2015" /><ref>{{cite book| vauthors = Bryson PD |title=Comprehensive review in toxicology for emergency clinicians|date=1997|publisher=Taylor & Francis|location=Washington, DC|isbn=978-1-56032-612-0|page=167|edition=3|url=https://books.google.com/books?id=f7009NkJv70C&pg=PA167|url-status=live|archive-url=https://web.archive.org/web/20170324020627/https://books.google.com/books?id=f7009NkJv70C&pg=PA167|archive-date=24 March 2017}}</ref>

<!-- Side effects and mechanism -->
Common [[side effect]]s include [[nausea]], [[abdominal pain]], and [[constipation]].<ref name=AHFS2015/> It may worsen the symptoms of [[asthma]].<ref name=AHFS2015/> Propranolol may cause [[teratogen|harmful effect]]s for the baby if taken during [[pregnancy]];<ref>{{cite web|title=Prescribing medicines in pregnancy database|url=http://www.tga.gov.au/hp/medicines-pregnancy.htm|work=Australian Government|access-date=22 April 2014|date=3 March 2014|url-status=live|archive-url=https://web.archive.org/web/20140408040902/http://www.tga.gov.au/hp/medicines-pregnancy.htm#.U1Yw8Bc3tqw|archive-date=8 April 2014}}</ref> however, its use during [[breastfeeding]] is generally considered to be safe.<ref>{{cite book| vauthors = Briggs GG, Freeman RK, Yaffe SJ |title=Drugs in pregnancy and lactation: a reference guide to fetal and neonatal risk|date=2011|publisher=Wolters Kluwer Health/Lippincott Williams & Wilkins |location=Philadelphia |isbn=978-1-60831-708-0 |page=1226|edition=9th|url=https://books.google.com/books?id=OIgTE4aynrMC&pg=PA1226|url-status=live|archive-url=https://web.archive.org/web/20170214212837/https://books.google.ca/books?id=OIgTE4aynrMC&pg=PA1226|archive-date=14 February 2017}}</ref> It is a non-selective beta blocker which works by blocking [[β-adrenergic receptors]].<ref name=AHFS2015/>

<!-- History, society and culture -->
Propranolol was patented in 1962 and approved for medical use in 1964.<ref>{{cite book | vauthors = Fischer J, Ganellin CR |title=Analogue-based Drug Discovery |date=2006 |publisher=John Wiley & Sons |isbn=978-3-527-60749-5 |page=460 |url=https://books.google.com/books?id=FjKfqkaKkAAC&pg=PA460 }}</ref> It is on the [[WHO Model List of Essential Medicines|World Health Organization's List of Essential Medicines]].<ref name="WHO21st">{{cite book | vauthors = ((World Health Organization)) | title = World Health Organization model list of essential medicines: 21st list 2019 | year = 2019 | hdl = 10665/325771 | author-link = World Health Organization | publisher = World Health Organization | location = Geneva | id = WHO/MVP/EMP/IAU/2019.06. License: CC BY-NC-SA 3.0 IGO }}</ref> Propranolol is available as a [[generic medication]].<ref name=AHFS2015/> In 2023, it was the 69th most commonly prescribed medication in the United States, with more than 9{{nbsp}}million prescriptions.<ref name="Top300Drugs">{{cite web | title=Top 300 of 2023 | url=https://clincalc.com/DrugStats/Top300Drugs.aspx | website=ClinCalc | access-date=12 August 2025 | archive-date=12 August 2025 | archive-url=https://web.archive.org/web/20250812130026/https://clincalc.com/DrugStats/Top300Drugs.aspx | url-status=live }}</ref><ref>{{cite web | title = Propranolol Drug Usage Statistics, United States, 2013 - 2023 | website = ClinCalc | url = https://clincalc.com/DrugStats/Drugs/Propranolol | access-date = 18 August 2025 }}</ref>

==Medical uses==
[[Image:Propranolol 80mg.png|thumb|right|An 80&nbsp;mg capsule of [[Time release technology|extended-release]] propranolol]]
[[Image:Propranolol tablets.png|thumb|right|A mixture of 20&nbsp;mg and 10&nbsp;mg extended-release propranolol tablets]]
[[File:Propranolol hci sandoz 10mg.jpg|thumb|Propranolol blister pack]]

Propranolol is used for treating various conditions, including:

===Cardiovascular===
* [[Hypertension]] (high blood pressure)
* [[Angina pectoris]] (with the exception of [[Prinzmetal's angina|variant angina]])
* [[Myocardial infarction]]
* [[Tachycardia]] (and other [[sympathetic nervous system]] symptoms, such as [[muscle tremor]]) associated with various conditions, including [[anxiety]], [[panic]], [[hyperthyroidism]], and [[lithium pharmacology|lithium therapy]]
* [[Portal hypertension]], to lower [[Hepatic portal vein|portal vein]] pressure
* Prevention of [[esophageal varices|esophageal variceal]] bleeding and [[ascites]]
* [[Anxiety]]
* [[Hypertrophic cardiomyopathy]]

While once a first-line treatment for hypertension, the role of beta blockers was downgraded in June 2006 in the [[United Kingdom]] to fourth-line, as they do not perform as well as other drugs, particularly in the elderly, and evidence is increasing that the most frequently used beta blockers at usual doses carry an unacceptable risk of provoking [[Diabetes mellitus type 2|type 2 diabetes]].<ref>{{cite web | vauthors = Ladva S | title=NICE and BHS launch updated hypertension guideline | url=http://www.nice.org.uk/download.aspx?o=335988 | date=28 June 2006 | publisher=[[National Institute for Health and Clinical Excellence]] | access-date=11 October 2009 | archive-url=https://web.archive.org/web/20060924003311/http://www.nice.org.uk/download.aspx?o=335988 | archive-date=24 September 2006 }}</ref>

Propranolol is not recommended for the treatment of high blood pressure by the Eighth Joint National Committee (JNC 8) because a higher rate of the primary composite outcome of cardiovascular death, [[myocardial infarction]], or [[stroke]] compared to an angiotensin receptor blocker was noted in one study.<ref>{{cite journal | vauthors = James PA, Oparil S, Carter BL, Cushman WC, Dennison-Himmelfarb C, Handler J, Lackland DT, LeFevre ML, MacKenzie TD, Ogedegbe O, Smith SC, Svetkey LP, Taler SJ, Townsend RR, Wright JT, Narva AS, Ortiz E | title = 2014 evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8) | journal = JAMA | volume = 311 | issue = 5 | pages = 507–520 | date = February 2014 | pmid = 24352797 | doi = 10.1001/jama.2013.284427 | doi-access = free }}</ref>

===Anxiety and related disorders===
{{See also|Beta blocker#Anxiety}}

Propranolol is occasionally used to treat performance anxiety,<ref name=Dav2006/> although evidence to support its use in any anxiety disorders is poor.<ref name="Steenenvan Wijk2015">{{cite journal | vauthors = Steenen SA, van Wijk AJ, van der Heijden GJ, van Westrhenen R, de Lange J, de Jongh A | title = Propranolol for the treatment of anxiety disorders: Systematic review and meta-analysis | journal = Journal of Psychopharmacology | volume = 30 | issue = 2 | pages = 128–139 | date = February 2016 | pmid = 26487439 | pmc = 4724794 | doi = 10.1177/0269881115612236 }}</ref> Its efficacy in managing [[panic disorder]] appears similar to [[benzodiazepine]]s, while carrying lower risks for addiction or abuse.<ref name="Steenenvan Wijk2015"/> Although beta-blockers such as propranolol have been suggested to be beneficial in managing [[Sympathetic nervous system|physical symptoms]] of anxiety, its [[efficacy#Medicine|efficacy]] in treating [[generalized anxiety disorder]] and panic disorder remain unestablished.<ref>{{cite journal | title = Beta-blockers in anxiety disorders | vauthors = Peggy H, Charles S | doi = 10.1016/0165-0327(87)90017-6 | url = https://www.sciencedirect.com/science/article/abs/pii/0165032787900176 | journal = Journal of Affective Disorders | volume = 13 | issue = 2 | date = October 1987 | pages = 119–130| pmid = 2890677 | url-access = subscription }}</ref> It is thought that beta blockers do not directly treat psychological symptoms of anxiety, but can help control physical symptoms such as [[palpitation]]s, and this may interfere with a positive feedback loop to indirectly reduce psychological anxiety.<ref name="ArcherWilesKessler2025" />

A 2025 [[systematic review]] and [[meta-analysis]] found widespread prescription of beta blockers, namely propranolol, for treatment of anxiety disorders, but found no evidence of a beneficial effect relative to placebo or [[benzodiazepine]]s in people with [[social phobia]] or panic disorder.<ref name="ArcherWilesKessler2025">{{cite journal | vauthors = Archer C, Wiles N, Kessler D, Turner K, Caldwell DM | title = Beta-blockers for the treatment of anxiety disorders: A systematic review and meta-analysis | journal = J Affect Disord | volume = 368 | issue = | pages = 90–99 | date = January 2025 | pmid = 39271062 | doi = 10.1016/j.jad.2024.09.068 | url = | doi-access = free }}</ref> However, the [[quality of evidence]], including both numbers of studies and patients as well as quality and risk of [[statistical bias|bias]] of those studies, was limited.<ref name="ArcherWilesKessler2025" /> Findings were similar in a previous 2016 systematic review and meta-analysis.<ref name="SteenenvanWijkvanderHeijden2016">{{cite journal | vauthors = Steenen SA, van Wijk AJ, van der Heijden GJ, van Westrhenen R, de Lange J, de Jongh A | title = Propranolol for the treatment of anxiety disorders: Systematic review and meta-analysis | journal = J Psychopharmacol | volume = 30 | issue = 2 | pages = 128–139 | date = February 2016 | pmid = 26487439 | pmc = 4724794 | doi = 10.1177/0269881115612236 | url = }}</ref>

Other beta blockers that have been used to treat anxiety disorders besides propranolol include [[atenolol]], [[betaxolol]], [[nadolol]], [[oxprenolol]], and [[pindolol]].<ref name="ArcherWilesKessler2025" /><ref name="BoyceBalloneCerta2021">{{cite journal | vauthors = Boyce TG, Ballone NT, Certa KM, Becker MA | title = The Use of β-Adrenergic Receptor Antagonists in Psychiatry: A Review | journal = J Acad Consult Liaison Psychiatry | volume = 62 | issue = 4 | pages = 404–412 | date = 2021 | pmid = 34210401 | doi = 10.1016/j.jaclp.2020.12.009 | url = }}</ref>

Some experimentation has been conducted in other psychiatric areas:<ref name="pmid17200914">{{cite journal | vauthors = Kornischka J, Cordes J, Agelink MW | title = 40 years beta-adrenoceptor blockers in psychiatry | language = de | journal = Fortschritte der Neurologie-Psychiatrie | volume = 75 | issue = 4 | pages = 199–210 | date = April 2007 | pmid = 17200914 | doi = 10.1055/s-2006-944295 | s2cid = 260156607 | url = https://www.thieme-connect.de/products/ejournals/abstract/10.1055/s-2006-944295| url-access = subscription }}</ref>

* [[Post-traumatic stress disorder]] (PTSD) and [[specific phobia]]s
* [[Aggressive behavior]] of patients with [[acquired brain injury|brain injuries]]<ref name="pmid7903928">{{cite journal | vauthors = Thibaut F, Colonna L | title = [Anti-aggressive effect of beta-blockers] | language = fr | journal = L'Encephale | volume = 19 | issue = 3 | pages = 263–267 | year = 1993 | pmid = 7903928 }}</ref>
* Treating the excessive drinking of fluids in [[psychogenic polydipsia]]<ref name="pmid7737786">{{cite journal | vauthors = Vieweg V, Pandurangi A, Levenson J, Silverman J | title = The consulting psychiatrist and the polydipsia-hyponatremia syndrome in schizophrenia | journal = International Journal of Psychiatry in Medicine | volume = 24 | issue = 4 | pages = 275–303 | year = 1994 | pmid = 7737786 | doi = 10.2190/5WG5-VV1V-BXAD-805K | s2cid = 22703210 }}</ref><ref name="pmid9844835">{{cite journal | vauthors = Kishi Y, Kurosawa H, Endo S | title = Is propranolol effective in primary polydipsia? | journal = International Journal of Psychiatry in Medicine | volume = 28 | issue = 3 | pages = 315–325 | year = 1998 | pmid = 9844835 | doi = 10.2190/QPWL-14H7-HPGG-A29D | s2cid = 25222454 }}</ref>

====Post-traumatic stress disorder and phobias====
Propranolol is being investigated as a potential treatment for PTSD.<ref>{{cite web |url=http://www.nbcnews.com/id/10806799 |archive-url=https://web.archive.org/web/20131112233001/http://www.nbcnews.com/id/10806799/ |archive-date=12 November 2013 |title=Doctors test a drug to ease traumatic memories - Mental Health - NBC News |website=[[NBC News]] |access-date=30 June 2007 }}</ref><ref>{{cite journal | vauthors = Brunet A, Orr SP, Tremblay J, Robertson K, Nader K, Pitman RK | title = Effect of post-retrieval propranolol on psychophysiologic responding during subsequent script-driven traumatic imagery in post-traumatic stress disorder | journal = Journal of Psychiatric Research | volume = 42 | issue = 6 | pages = 503–506 | date = May 2008 | pmid = 17588604 | doi = 10.1016/j.jpsychires.2007.05.006 }}</ref><ref>{{Cite book | vauthors = Young C, Butcher R |url=https://www.ncbi.nlm.nih.gov/books/NBK562942/ |title=Propranolol for Post-Traumatic Stress Disorder: A Review of Clinical Effectiveness |date=2020 |publisher=Canadian Agency for Drugs and Technologies in Health |series=CADTH Rapid Response Reports |location=Ottawa (ON) |pmid=33074615}}</ref> Propranolol works to inhibit the actions of [[norepinephrine]] (noradrenaline), a [[neurotransmitter]] that enhances [[memory consolidation]].<ref>{{Cite web |title=DocFilm – DW |url=https://www.dw.com/en/docfilm/program-294010 |access-date=2 August 2023 |website=dw.com |language=en}}</ref> In one small study, individuals given propranolol immediately after trauma experienced fewer stress-related symptoms and lower rates of PTSD than respective control groups who did not receive the drug.<ref>{{cite journal | vauthors = Vaiva G, Ducrocq F, Jezequel K, Averland B, Lestavel P, Brunet A, Marmar CR | title = Immediate treatment with propranolol decreases posttraumatic stress disorder two months after trauma | journal = Biological Psychiatry | volume = 54 | issue = 9 | pages = 947–949 | date = November 2003 | pmid = 14573324 | doi = 10.1016/s0006-3223(03)00412-8 | s2cid = 3064619 }}</ref> Due to the fact that memories and their emotional content are reconsolidated in the hours after they are recalled or re-experienced, propranolol can also diminish the emotional impact of already formed memories; for this reason, it is also being studied in the treatment of [[specific phobia]]s, such as [[arachnophobia]], [[dental fear]], and [[social phobia]].<ref name="Steenenvan Wijk2015" /> It has also been found to be helpful for some individuals with [[misophonia]].<ref>{{cite journal | vauthors = Webb J | title = β-Blockers for the Treatment of Misophonia and Misokinesia | journal = Clinical Neuropharmacology | volume = 45 | issue = 1 | pages = 13–14 | date = Jan–Feb 2022 | pmid = 35029865 | doi = 10.1097/WNF.0000000000000492 | s2cid = 245932937 }}</ref>

Ethical and legal questions have been raised surrounding the use of propranolol-based medications for use as a "memory damper", including altering memory-recalled evidence during an investigation, modifying the behavioral response to past (albeit traumatic) experiences, the regulation of these drugs, and others.<ref>{{cite journal| vauthors = Kolber AJ | title=Therapeutic Forgetting: The Legal and Ethical Implications of Memory Dampening |journal=Vanderbilt Law Review, San Diego Legal Studies Paper No. 07-37. |volume=59 |page=1561 |year=2006}}</ref> However, Hall and Carter have argued that many such objections are "based on wildly exaggerated and unrealistic scenarios that ignore the limited action of propranolol in affecting memory, underplay the debilitating impact that PTSD has on those who suffer from it, and fail to acknowledge the extent to which drugs like [[alcohol (drug)|alcohol]] are already used for this purpose".<ref>{{cite journal | vauthors = Hall W, Carter A | title = Debunking alarmist objections to the pharmacological prevention of PTSD | journal = The American Journal of Bioethics | volume = 7 | issue = 9 | pages = 23–25 | date = September 2007 | pmid = 17849333 | doi = 10.1080/15265160701551244 | s2cid = 27063524 }}</ref>

===Other uses===
* [[Essential tremor]]. However, evidence for use for [[akathisia]] is insufficient.<ref>{{cite journal | vauthors = Lima AR, Bacalcthuk J, Barnes TR, Soares-Weiser K | title = Central action beta-blockers versus placebo for neuroleptic-induced acute akathisia | journal = The Cochrane Database of Systematic Reviews | issue = 4 | article-number = CD001946 | date = October 2004 | volume = 2004 | pmid = 15495022 | pmc = 6599862 | doi = 10.1002/14651858.CD001946.pub2 }}</ref>
* [[Migraine]] and [[cluster headache]] prevention<ref>{{cite journal | vauthors = Shields KG, Goadsby PJ | title = Propranolol modulates trigeminovascular responses in thalamic ventroposteromedial nucleus: a role in migraine? | journal = Brain | volume = 128 | issue = Pt 1 | pages = 86–97 | date = January 2005 | pmid = 15574468 | doi = 10.1093/brain/awh298 | doi-access = free }}</ref><ref>{{cite book |title=The Biochemistry of Migraine | vauthors = Eadie M, Tyrer JH |year=1985 |publisher=Springer |location=New York |isbn=978-0-85200-731-0 |page=148 |oclc=11726870 |url= https://books.google.com/books?id=JYeyCc9M6acC&q=Propranolol+migraine+mechanism%2C&pg=PA148 |url-status=live |archive-url=https://web.archive.org/web/20170324030406/https://books.google.com/books?id=JYeyCc9M6acC&pg=PA148&lpg=PA148&dq=Propranolol+migraine+mechanism,&source=bl&ots=Ep2oSjxpAo&sig=7H_KHF3xoIP0nBKJJaqsDl_IhAs&hl=en&ei=TXVPTuu6DKHE4gT6gLnXBw&sa=X&oi=book_result&ct=result&resnum=4&ved=0CCoQ6AEwAzgK#v=onepage&q=Propranolol%20migraine%20mechanism%2C&f=false |archive-date=24 March 2017 }}</ref> and in primary exertional headache<ref name=AHFS2015/><ref>{{cite web | vauthors = Chan C, Goadsby PJ | veditors = Silberstein SD | date = 26 September 1996 | title = Primary exercise headache | work = MedLink | url = https://www.medlink.com/articles/primary-exercise-headache }}</ref>
* [[Hyperhidrosis]] (excessive sweating){{cn|date=June 2023}}
* [[Infantile hemangioma]]<ref>{{cite journal | vauthors = Chen T, Gudipudi R, Nguyen SA, Carroll W, Clemmens C | title = Should Propranolol Remain the Gold Standard for Treatment of Infantile Hemangioma? A Systematic Review and Meta-Analysis of Propranolol Versus Atenolol | journal = The Annals of Otology, Rhinology, and Laryngology | pages = 332–340 | date = April 2022 | volume = 132 | issue = 3 | pmid = 35466712 | doi = 10.1177/00034894221089758 | s2cid = 248375711 }}</ref>
* [[Glaucoma]]{{cn|date=June 2023}}
* [[Thyrotoxicosis]] by [[deiodinase]] inhibition{{cn|date=June 2023}}

Propranolol may be used to treat severe [[infantile hemangioma]]s (IHs). This treatment shows promise as being superior to [[corticosteroid]]s when treating IHs. Extensive clinical case evidence and a small controlled trial support its efficacy.<ref>{{cite journal |journal= Current Dermatology Reports |year= 2012 |doi= 10.1007/s13671-012-0026-6 |title= Propranolol for Infantile Hemangiomas: A Review | vauthors = Hogeling M |page= Online-first |volume=1|issue= 4 |doi-access= free }}</ref>

Propranolol is useful in the treatment of acute [[cardiovascular]] [[toxicity]] (e.g. in [[overdose]]) caused by [[sympathomimetic]]s like [[amphetamine]], [[methamphetamine]], [[cocaine]], [[ephedrine]], and [[pseudoephedrine]], including reducing elevations in [[heart rate]] and [[blood pressure]] caused by these agents.<ref name="RichardsAlbertsonDerlet2015">{{cite journal | vauthors = Richards JR, Albertson TE, Derlet RW, Lange RA, Olson KR, Horowitz BZ | title = Treatment of toxicity from amphetamines, related derivatives, and analogues: a systematic clinical review | journal = Drug Alcohol Depend | volume = 150 | issue = | pages = 1–13 | date = May 2015 | pmid = 25724076 | doi = 10.1016/j.drugalcdep.2015.01.040 | url = }}</ref><ref name="RichardsHollanderRamoska2017">{{cite journal | vauthors = Richards JR, Hollander JE, Ramoska EA, Fareed FN, Sand IC, Izquierdo Gómez MM, Lange RA | title = β-Blockers, Cocaine, and the Unopposed α-Stimulation Phenomenon | journal = J Cardiovasc Pharmacol Ther | volume = 22 | issue = 3 | pages = 239–249 | date = May 2017 | pmid = 28399647 | doi = 10.1177/1074248416681644 | url = }}</ref> Other beta blockers are also used.<ref name="RichardsAlbertsonDerlet2015" /><ref name="RichardsHollanderRamoska2017" /> However, the controversial yet possible phenomenon of "unopposed α-stimulation" with administration of selective beta blockers to block non-selective sympathomimetics potentially makes dual [[alpha-1 blocker|alpha-1]] and beta blockers like [[labetalol]] and [[carvedilol]] more favorable for such purposes than selective beta blockers like propranolol.<ref name="RichardsAlbertsonDerlet2015" /><ref name="RichardsHollanderRamoska2017" /> The rate of unopposed α-stimulation with selective beta blockers has been reported to be 0.4%,<ref name="RichardsAlbertsonDerlet2015" /> whereas no cases of unopposed α-stimulation have been reported with dual alpha and beta blockers like labetalol.<ref name="RichardsHollanderRamoska2017" />

===Available forms===
Propranolol is available in the form of 10, 20, 40, 60, and 80{{nbsp}}mg (as propranolol [[hydrochloride]]) [[oral administration|oral]] [[tablet (pharmacy)|tablet]]s, among other formulations.<ref name="Inderal-Label" /><ref name="DrugBank" />

==Contraindications==
{{See also|Beta blocker#Contraindications}}

[[Contraindication]]s of propranolol include [[cardiogenic shock]], [[sinus bradycardia]] (slow heart rate; <60 beats/minute), [[heart block]] greater than first degree, [[bronchial asthma]], overt [[heart failure]], and known [[hypersensitivity]] to propranolol.<ref name="Inderal-Label" /> Other contraindications include reversible airway diseases, particularly [[asthma]] or [[chronic obstructive pulmonary disease]] (COPD), [[sick sinus syndrome]], [[atrioventricular block]] ([[second-degree atrioventricular block|second-]] or [[third-degree atrioventricular block|third-degree]]), [[shock (circulatory)|circulatory shock]], and severe [[hypotension]] (low blood pressure).<ref name="Rossi" />

Propranolol should be used with caution in people with:<ref name="Rossi">{{cite book | veditors = Rossi S | title = [[Australian Medicines Handbook]] | date = 2006 | location = Adelaide | publisher = Australian Medicines Handbook }}</ref>

* [[Diabetes mellitus]] or [[hyperthyroidism]], since signs and symptoms of [[hypoglycemia]] may be masked
* [[Peripheral artery disease]] and [[Raynaud syndrome]], which may be exacerbated
* [[Phaeochromocytoma]], as [[hypertension]] may be aggravated without prior [[alpha blocker]] therapy
* [[Myasthenia gravis]], which may be worsened
* Other drugs with [[bradycardia|bradycardic]] effects

==Side effects==
{{See also|Beta blocker#Adverse effects}}

===Pregnancy and lactation===
Propranolol, like other beta-blockers, is classified as [[pregnancy category]] C in the United States and [[Australian Drug Evaluation Committee|ADEC]] category C in Australia. β-blocking agents in general reduce [[perfusion]] of the [[placenta]], which may lead to adverse outcomes for the [[neonate]], including [[human lung|lung]] or [[human heart|heart]] complications, or [[premature birth]]. The newborn may experience additional adverse effects such as [[hypoglycemia|low blood sugar]] and a [[bradycardia|slower than normal heart rate]].<ref name="Martindale">{{Cite book| veditors = Sweetman SC |chapter=Cardiovascular Drugs|title=Martindale: The complete drug reference |edition=36th |year=2009|pages=1226–1381|publisher=Pharmaceutical Press |location=London|isbn=978-0-85369-840-1|title-link=Martindale: The complete drug reference}}</ref>

Most β-blocking agents appear in the milk of [[lactation|lactating]] women. However, propranolol is highly [[plasma protein binding|bound to proteins in the bloodstream]] and is distributed into [[breast milk]] at very low levels.<ref name="LactMed">[No authors listed] (2007). "Propranolol". In: ''Drugs and Lactation Database.'' U.S. [[National Library of Medicine]] Toxicology Data Network. Retrieved 25 February 2013.</ref> These low levels are not expected to pose any risk to the breastfeeding infant, and the [[American Academy of Pediatrics]] considers propranolol therapy "generally compatible with [[breastfeeding]]."<ref name="Martindale"/><ref name="LactMed"/><ref>{{cite journal |author=Committee on Drugs | title = Transfer of drugs and other chemicals into human milk | journal = Pediatrics | volume = 108 | issue = 3 | pages = 776–789 | date = September 2001 | pmid = 11533352 | doi = 10.1542/peds.108.3.776| s2cid = 27763768 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Spencer JP, Gonzalez LS, Barnhart DJ | title = Medications in the breast-feeding mother | journal = American Family Physician | volume = 64 | issue = 1 | pages = 119–126 | date = July 2001 | pmid = 11456429 }}</ref>

==Overdose==
Propranolol [[overdose]] has been associated with [[symptom]]s including [[bradycardia]] and [[hypotension]].<ref name="Inderal-Label" /> These symptoms may be managed by drugs including [[glucagon]], [[isoprenaline]] (isoproterenol), [[dopamine (medication)|medication]], [[phosphodiesterase inhibitor]]s, or [[atropine]], whereas [[epinephrine (medication)|epinephrine]] may provoke uncontrolled [[hypertension]] due to unopposed alpha stimulation and is not indicated.<ref name="Inderal-Label" /> Propranolol overdose has also been associated with [[seizure]]s.<ref>{{cite journal | vauthors = Reith DM, Dawson AH, Epid D, Whyte IM, Buckley NA, Sayer GP | title = Relative toxicity of beta blockers in overdose | journal = Journal of Toxicology. Clinical Toxicology | volume = 34 | issue = 3 | pages = 273–278 | date = 1996 | pmid = 8667464 | doi = 10.3109/15563659609013789 }}</ref> [[Cardiac arrest]] may occur in propranolol overdose due to sudden [[ventricular arrhythmias]], or [[cardiogenic shock]] which may ultimately culminate in bradycardic [[Pulseless electrical activity|PEA]].<ref>{{cite journal | vauthors = Holstege CP, Eldridge DL, Rowden AK | title = ECG manifestations: the poisoned patient | journal = Emergency Medicine Clinics of North America | volume = 24 | issue = 1 | pages = 159–77, vii | date = February 2006 | pmid = 16308118 | doi = 10.1016/j.emc.2005.08.012 }}</ref>

==Interactions==
===Pharmacodynamic interactions===
Since beta blockers are known to relax the [[cardiac muscle]] and constrict the [[smooth muscle]], they have an additive effect with other drugs that decrease blood pressure or decrease [[cardiac contractility]] or conductivity.<ref name="Inderal-Label" /><ref name="MaideenRajkapoorMuthusamy2021">{{cite journal | vauthors = Maideen NM, Rajkapoor B, Muthusamy S, Ramanathan S, Thangadurai SA, Sughir AA | title = A Review on Pharmacokinetic and Pharmacodynamic Drug Interactions of Adrenergic β-blockers with Clinically Relevant Drugs-An Overview | journal = Curr Drug Metab | volume = 22 | issue = 9 | pages = 672–682 | date = 2021 | pmid = 34182907 | doi = 10.2174/1389200222666210614112529 | url = }}</ref> Pharmacodynamic interactions may occur with other drugs affecting the cardiovascular system, including [[propafenone]], [[quinidine]], [[amiodarone]], [[cardiac glycoside]]s, [[calcium channel blocker]]s like [[verapamil]] and [[diltiazem]], [[ACE inhibitor]]s, [[alpha blocker]]s like [[prazosin]], [[catecholamine-depleting drug]]s like [[reserpine]], [[ergot alkaloid]]s, and [[adrenergic receptor agonist]]s including [[epinephrine]] (adrenaline), [[isoprenaline]] (isoproterenol), [[dobutamine]], [[beta-2 adrenergic receptor agonist|β<sub>2</sub>-adrenergic receptor agonist]]s like [[salbutamol]], [[levosalbutamol]], [[formoterol]], [[salmeterol]], and [[clenbuterol]], and [[alpha-2 adrenergic receptor|α<sub>2</sub>-adrenergic receptor]] agonists like [[clonidine]].<ref name="Inderal-Label" /><ref name="Rossi" /> [[Tricyclic antidepressant]]s (TCAs) and [[monoamine oxidase inhibitor]]s (MAOIs) have [[hypotensive]] [[side effect]]s and these may be exacerbated by propranolol.<ref name="Inderal-Label" /> Hypotension and [[cardiac arrest]] have been reported with the combination of propranolol and [[haloperidol]].<ref name="Inderal-Label" /> [[Nonsteroidal anti-inflammatory drug]]s (NSAIDs), which include drugs like [[ibuprofen]], [[naproxen]], and [[aspirin]], have been reported to blunt the [[antihypertensive]] effects of beta blockers like propranolol.<ref name="Inderal-Label" /> The NSAID [[indomethacin]] specifically may reduce the efficacy of propranolol in decreasing heart rate and blood pressure.<ref name="Inderal-Label" />

===Effects of drugs on propranolol===
Propranolol is [[drug metabolism|metabolized]] by [[cytochrome P450]] [[enzyme]]s including [[CYP2D6]], [[CYP1A2]], and [[CYP2C19]].<ref name="Inderal-Label" /><ref name="KalamRasoolRehman2020" /><ref name="MaideenRajkapoorMuthusamy2021" /> Levels of propranolol may be increased by CYP2D6 [[enzyme inhibitor|inhibitor]]s such as [[amiodarone]], [[bupropion]], [[cimetidine]], [[duloxetine]], [[fluoxetine]], [[paroxetine]], [[propafenone]], [[quinidine]], and [[ritonavir]], by CYP1A2 inhibitors such as [[imipramine]], cimetidine, [[ciprofloxacin]], [[fluvoxamine]], [[isoniazid]], [[theophylline]], [[zileuton]], [[zolmitriptan]], and [[rizatriptan]], and by CYP2C19 inhibitors such as [[fluconazole]], cimetidine, fluoxetine, [[fluvoxamine]], [[teniposide]], and [[tolbutamide]].<ref name="Inderal-Label" /><ref name="KalamRasoolRehman2020" /><ref name="MaideenRajkapoorMuthusamy2021" /><ref name="ShinHillsFinley2020">{{cite journal | vauthors = Shin J, Hills NK, Finley PR | title = Combining Antidepressants with β-Blockers: Evidence of a Clinically Significant CYP2D6 Drug Interaction | journal = Pharmacotherapy | volume = 40 | issue = 6 | pages = 507–516 | date = June 2020 | pmid = 32342526 | doi = 10.1002/phar.2406 | url = }}</ref><ref name="Zhou2009" /> No interactions with propranolol were observed with [[ranitidine]], [[lansoprazole]], or [[omeprazole]].<ref name="Inderal-Label" /> Propranolol levels may be reduced by [[enzyme inducer|inducer]]s of [[liver|hepatic]] metabolism including [[rifampin]], [[alcohol (drug)|alcohol]], [[phenytoin]], [[phenobarbital]], and [[cigarette smoking]].<ref name="Inderal-Label" /><ref name="MaideenRajkapoorMuthusamy2021" />

The CYP2D6 inhibitor quinidine has been found to increase propranolol levels by 2- to 3-fold.<ref name="Inderal-Label" /><ref name="Zhou2009" /> The CYP1A2 inhibitor fluvoxamine has been found to increase propranolol levels by 5-fold.<ref name="vanHarten1995">{{cite journal | vauthors = van Harten J | title = Overview of the pharmacokinetics of fluvoxamine | journal = Clinical Pharmacokinetics | volume = 29 | issue = Suppl 1 | pages = 1–9 | year = 1995 | pmid = 8846617 | doi = 10.2165/00003088-199500291-00003 | s2cid = 71812133 }}</ref> The [[calcium channel blocker]] [[nisoldipine]] increased peak levels of propranolol by 1.5-fold and area-under-the-curve levels by 1.3-fold, while [[nicardipine]] increased propranolol peak levels by 1.8-fold and area-under-the-curve levels by 1.5-fold.<ref name="Inderal-Label" /> Conversely, [[verapamil]] does not affect the [[pharmacokinetics]] of propranolol and vice-versa.<ref name="Inderal-Label" /> The CYP1A2 inhibitor zolmitriptan increased peak propranolol levels by 1.4-fold and area-under-the-curve levels by 1.56-fold, while the CYP1A2 inhibitor [[rizatriptan]] increased propranolol peak levels by 1.8-fold and area-under-the-curve levels by 1.7-fold.<ref name="Inderal-Label" /> [[Chlorpromazine]] has been found to increase propranolol levels by 1.7-fold.<ref name="Inderal-Label" /> The [[binding selectivity|non-selective]] CYP450 inhibitor cimetidine has been found to increase peak propranolol levels by 1.4-fold and area-under-the-curve levels by 1.5-fold.<ref name="Inderal-Label" /> Cigarette smoking, which induces CYP1A2, has been found to reduce the [[clearance (pharmacology)|clearance]] of propranolol by 77%, in turn resulting in decreased propranolol concentrations.<ref name="Inderal-Label" /><ref name="MaideenRajkapoorMuthusamy2021" /> The lipid-lowering drug [[cholestyramine]] or [[colestipol]] decreased propranolol levels by up to 50%.<ref name="Inderal-Label" /> [[Aluminum hydroxide]] gel may decrease propranolol levels.<ref name="Inderal-Label" /> Alcohol may increase propranolol levels.<ref name="Inderal-Label" />

===Effects of propranolol on other drugs===
Propranolol has been found to increase [[area-under-the-curve (pharmacokinetics)|area-under-the-curve]] levels of [[propafenone]] by more than 3-fold.<ref name="Inderal-Label" /> It has been found to increase [[lidocaine]] levels by 1.3-fold.<ref name="Inderal-Label" /> The drug has been found to increase peak and area-under-the-curve levels of nifedipine by 1.6-fold and 1.8-fold, respectively.<ref name="Inderal-Label" /> Propranolol decreases [[theophylline]] clearance by 30 to 52%.<ref name="Inderal-Label" /> Propranolol inhibits the metabolism of the benzodiazepine [[diazepam]] and can increase exposure to diazepam.<ref name="Inderal-Label" /> Conversely, propranolol does not affect various other [[benzodiazepines]], including [[oxazepam]], [[triazolam]], [[lorazepam]], and [[alprazolam]].<ref name="Inderal-Label" /> High-dose long-acting propranolol has been found to increase [[thioridazine]] levels by 1.6- to 4.7-fold and levels of its metabolite [[mesoridazine]] by 1.3- to 3.1-fold.<ref name="Inderal-Label" /> Propranolol decreased [[lovastatin]] or [[pravastatin]] area-under-the-curve levels by 18 to 23% but did not affect [[fluvastatin]].<ref name="Inderal-Label" /> It may decrease [[triiodothyronine]] (T<sub>3</sub>) levels when taken with [[thyroxine]] (T<sub>4</sub>).<ref name="Inderal-Label" /> Propranolol has been found to increase the [[bioavailability]] and effects of [[warfarin]].<ref name="Inderal-Label" />

==Pharmacology==
===Pharmacodynamics===
{| class="wikitable floatright" style="font-size:small;"
|+ Propranolol activities
|-
! Site !! K<sub>i</sub> (nM) !! Species !! Ref
|-
| [[5-HT1A receptor|5-HT<sub>1A</sub>]] || 55–272 (K<sub>i</sub>)<br />29 ({{abbr|–|(–)-propranolol}}) (K<sub>i</sub>)<br />128 ({{abbr|–|(–)-propranolol}}) ({{Abbrlink|EC<sub>50</sub>|half-maximal effective concentration}})<br />15% ({{abbr|–|(–)-propranolol}}) ({{Abbrlink|E<sub>max</sub>|maximal efficacy}}) || Human<br />Human<br />Human<br />Human || <ref name="pmid2078271">{{cite journal | vauthors = Hamon M, Lanfumey L, el Mestikawy S, Boni C, Miquel MC, Bolaños F, Schechter L, Gozlan H | title = The main features of central 5-HT1 receptors | journal = Neuropsychopharmacology | volume = 3 | issue = 5–6 | pages = 349–360 | year = 1990 | pmid = 2078271 }}</ref><ref name="pmid9686407">{{cite journal | vauthors = Toll L, Berzetei-Gurske IP, Polgar WE, Brandt SR, Adapa ID, Rodriguez L, Schwartz RW, Haggart D, O'Brien A, White A, Kennedy JM, Craymer K, Farrington L, Auh JS | title = Standard binding and functional assays related to medications development division testing for potential cocaine and opiate narcotic treatment medications | journal = NIDA Research Monograph | volume = 178 | pages = 440–466 | date = March 1998 | pmid = 9686407 }}</ref><br /><ref name="Newman-TancrediConteChaput1997" /><br /><ref name="Newman-TancrediConteChaput1997" /><br /><ref name="Newman-TancrediConteChaput1997" />
|-
| [[5-HT1B receptor|5-HT<sub>1B</sub>]] || 56–85 || Rat || <ref name="pmid1968985">{{cite journal | vauthors = Tsuchihashi H, Nakashima Y, Kinami J, Nagatomo T | title = Characteristics of 125I-iodocyanopindolol binding to beta-adrenergic and serotonin-1B receptors of rat brain: selectivity of beta-adrenergic agents | journal = Japanese Journal of Pharmacology | volume = 52 | issue = 2 | pages = 195–200 | date = February 1990 | pmid = 1968985 | doi = 10.1254/jjp.52.195 | doi-access = free }}</ref><ref name="pmid2936965">{{cite journal | vauthors = Engel G, Göthert M, Hoyer D, Schlicker E, Hillenbrand K | title = Identity of inhibitory presynaptic 5-hydroxytryptamine (5-HT) autoreceptors in the rat brain cortex with 5-HT1B binding sites | journal = Naunyn-Schmiedeberg's Archives of Pharmacology | volume = 332 | issue = 1 | pages = 1–7 | date = January 1986 | pmid = 2936965 | doi = 10.1007/bf00633189 | s2cid = 5999838 }}</ref>
|-
| [[5-HT1D receptor|5-HT<sub>1D</sub>]] || 4,070 || Pig || <ref name="pmid2797214">{{cite journal | vauthors = Schlicker E, Fink K, Göthert M, Hoyer D, Molderings G, Roschke I, Schoeffter P | title = The pharmacological properties of the presynaptic serotonin autoreceptor in the pig brain cortex conform to the 5-HT1D receptor subtype | journal = Naunyn-Schmiedeberg's Archives of Pharmacology | volume = 340 | issue = 1 | pages = 45–51 | date = July 1989 | pmid = 2797214 | doi = 10.1007/bf00169206 | s2cid = 2287040 }}</ref>
|-
| [[5-HT2A receptor|5-HT<sub>2A</sub>]] || 4,280 || Human || <ref name="pmid2723656">{{cite journal | vauthors = Elliott JM, Kent A | title = Comparison of [125I]iodolysergic acid diethylamide binding in human frontal cortex and platelet tissue | journal = Journal of Neurochemistry | volume = 53 | issue = 1 | pages = 191–196 | date = July 1989 | pmid = 2723656 | doi = 10.1111/j.1471-4159.1989.tb07313.x | s2cid = 25820829 }}</ref>
|-
| [[5-HT2B receptor|5-HT<sub>2B</sub>]] || 457–513 ({{abbr|+|(+)-propranolol}})<br />166–316 ({{abbr|–|(–)-propranolol}}) || Human<br />Human || <ref name="pmid8743744">{{cite journal | vauthors = Schmuck K, Ullmer C, Kalkman HO, Probst A, Lubbert H | title = Activation of meningeal 5-HT2B receptors: an early step in the generation of migraine headache? | journal = The European Journal of Neuroscience | volume = 8 | issue = 5 | pages = 959–967 | date = May 1996 | pmid = 8743744 | doi = 10.1111/j.1460-9568.1996.tb01583.x | s2cid = 19578349 }}</ref><br /><ref name="pmid8743744" />
|-
| [[5-HT2C receptor|5-HT<sub>2C</sub>]] || 61,700 ({{abbr|+|(+)-propranolol}})<br /> 5,010 ({{abbr|–|(–)-propranolol}})<br />736–2,457 || Human<br />Human<br />Rodent || <ref name="pmid8743744" /><br /><ref name="pmid8743744" /><br /><ref name="pmid4078623">{{cite journal | vauthors = Yagaloff KA, Hartig PR | title = 125I-lysergic acid diethylamide binds to a novel serotonergic site on rat choroid plexus epithelial cells | journal = The Journal of Neuroscience | volume = 5 | issue = 12 | pages = 3178–3183 | date = December 1985 | pmid = 4078623 | pmc = 6565215 | doi = 10.1523/JNEUROSCI.05-12-03178.1985 }}</ref><ref name="pmid9686407" />
|-
| [[5-HT3 receptor|5-HT<sub>3</sub>]] || >10,000 || Human || <ref name="pmid2809591">{{cite journal | vauthors = Barnes JM, Barnes NM, Costall B, Ironside JW, Naylor RJ | title = Identification and characterisation of 5-hydroxytryptamine 3 recognition sites in human brain tissue | journal = Journal of Neurochemistry | volume = 53 | issue = 6 | pages = 1787–1793 | date = December 1989 | pmid = 2809591 | doi = 10.1111/j.1471-4159.1989.tb09244.x | s2cid = 46356673 }}</ref>
|-
| [[Alpha-1 adrenergic receptor|α<sub>1</sub>]] || {{abbr|ND|No data}} || {{abbr|ND|No data}} || {{abbr|ND|No data}}
|-
| [[Alpha-2 adrenergic receptor|α<sub>2</sub>]] || 1,297–2,789 || Rat || <ref name="pmid2885406">{{cite journal | vauthors = Boyajian CL, Leslie FM | title = Pharmacological evidence for alpha-2 adrenoceptor heterogeneity: differential binding properties of [3H]rauwolscine and [3H]idazoxan in rat brain | journal = The Journal of Pharmacology and Experimental Therapeutics | volume = 241 | issue = 3 | pages = 1092–1098 | date = June 1987 | doi = 10.1016/S0022-5347(25)00190-9 | pmid = 2885406 }}</ref>
|-
| [[Beta-1 adrenergic receptor|β<sub>1</sub>]] || 0.02–2.69 || Human || <ref name="pmid8935801">{{cite journal | vauthors = Schotte A, Janssen PF, Gommeren W, Luyten WH, Van Gompel P, Lesage AS, De Loore K, Leysen JE | title = Risperidone compared with new and reference antipsychotic drugs: in vitro and in vivo receptor binding | journal = Psychopharmacology | volume = 124 | issue = 1–2 | pages = 57–73 | date = March 1996 | pmid = 8935801 | doi = 10.1007/bf02245606 | s2cid = 12028979 }}</ref><ref name="pmid7915318">{{cite journal | vauthors = Fraundorfer PF, Fertel RH, Miller DD, Feller DR | title = Biochemical and pharmacological characterization of high-affinity trimetoquinol analogs on guinea pig and human beta adrenergic receptor subtypes: evidence for partial agonism | journal = The Journal of Pharmacology and Experimental Therapeutics | volume = 270 | issue = 2 | pages = 665–674 | date = August 1994 | doi = 10.1016/S0022-3565(25)22397-7 | pmid = 7915318 }}</ref>
|-
| [[Beta-2 adrenergic receptor|β<sub>2</sub>]] || 0.01–0.61 || Human || <ref name="pmid8935801" /><ref name="pmid7915318" />
|-
| [[Beta-3 adrenergic receptor|β<sub>3</sub>]] || 450 || Mouse || <ref name="pmid1718744">{{cite journal | vauthors = Nahmias C, Blin N, Elalouf JM, Mattei MG, Strosberg AD, Emorine LJ | title = Molecular characterization of the mouse beta 3-adrenergic receptor: relationship with the atypical receptor of adipocytes | journal = The EMBO Journal | volume = 10 | issue = 12 | pages = 3721–3727 | date = December 1991 | pmid = 1718744 | pmc = 453106 | doi = 10.1002/j.1460-2075.1991.tb04940.x }}</ref>
|-
| [[D1 receptor|D<sub>1</sub>]] || >10,000 || Human || <ref name="pmid9686407" />
|-
| [[D2 receptor|D<sub>2</sub>]] || >10,000 || Human || <ref name="pmid9686407" />
|-
| [[H1 receptor|H<sub>1</sub>]] || >10,000 || Human || <ref name="pmid6146381">{{cite journal | vauthors = Kanba S, Richelson E | title = Histamine H1 receptors in human brain labelled with [3H]doxepin | journal = Brain Research | volume = 304 | issue = 1 | pages = 1–7 | date = June 1984 | pmid = 6146381 | doi = 10.1016/0006-8993(84)90856-4 | s2cid = 45303586 }}</ref>
|-
| {{abbrlink|SERT|Serotonin transporter}} || 3,700 || Rat || <ref name="pmid2970277">{{cite journal | vauthors = Kovachich GB, Aronson CE, Brunswick DJ, Frazer A | title = Quantitative autoradiography of serotonin uptake sites in rat brain using [3H]cyanoimipramine | journal = Brain Research | volume = 454 | issue = 1–2 | pages = 78–88 | date = June 1988 | pmid = 2970277 | doi = 10.1016/0006-8993(88)90805-0 | s2cid = 9586842 }}</ref>
|-
| {{abbrlink|NET|Norepinephrine transporter}} || 5,000 ({{abbrlink|IC<sub>50</sub>|Half-maximal inhibitory concentration}}) || Rat || <ref name="pmid2872325">{{cite journal | vauthors = Tuross N, Patrick RL | title = Effects of propranolol on catecholamine synthesis and uptake in the central nervous system of the rat | journal = The Journal of Pharmacology and Experimental Therapeutics | volume = 237 | issue = 3 | pages = 739–745 | date = June 1986 | doi = 10.1016/S0022-3565(25)24861-3 | pmid = 2872325 }}</ref>
|-
| {{abbrlink|DAT|Dopamine transporter}} || 29,000 ({{abbr|IC<sub>50</sub>|Half-maximal inhibitory concentration}}) || Rat || <ref name="pmid2872325" />
|-
| {{abbrlink|VDCC|Voltage-dependent calcium channel}} || >10,000 || Rat || <ref name="pmid2338642">{{cite journal | vauthors = Zobrist RH, Mecca TE | title = [3H]TA-3090, a selective benzothiazepine-type calcium channel receptor antagonist: in vitro characterization | journal = The Journal of Pharmacology and Experimental Therapeutics | volume = 253 | issue = 2 | pages = 461–465 | date = May 1990 | doi = 10.1016/S0022-3565(25)12990-X | pmid = 2338642 }}</ref>
|- class="sortbottom"
| colspan="4" style="width: 1px; background-color:#eaecf0; text-align: center;" | '''Notes:''' Values are K<sub>i</sub> (nM), unless otherwise noted. The smaller the value, the more avidly the drug binds to the site. '''Refs:''' <ref name="PDSPKiDatabase">{{cite web | title = PDSP K<sub>i</sub> Database | work = Psychoactive Drug Screening Program (PDSP)|author1-link=Bryan Roth | vauthors = Roth BL, Driscol J | publisher = University of North Carolina at Chapel Hill and the United States National Institute of Mental Health | access-date = 14 August 2017 | url = https://pdsp.unc.edu/databases/pdsp.php?knowID=0&kiKey=&receptorDD=&receptor=&speciesDD=&species=&sourcesDD=&source=&hotLigandDD=&hotLigand=&testLigandDD=&testFreeRadio=testFreeRadio&testLigand=propranolol&referenceDD=&reference=&KiGreater=&KiLess=&kiAllRadio=all&doQuery=Submit+Query}}</ref><ref name="BindingDB">{{Cite web | url=https://www.bindingdb.org/rwd/bind/chemsearch/marvin/MolStructure.jsp?monomerid=25761 | title=Activity Spreadsheet -- Enzyme Inhibition Constant Data from BindingDB | website=www.bindingdb.org}}</ref>
|}

Propranolol is classified as a competitive non-cardioselective sympatholytic [[beta blocker]] that crosses the [[blood–brain barrier]]. It is lipid soluble and also has sodium channel-blocking effects. Propranolol is a non-selective β-adrenergic receptor antagonist, or [[beta blocker]];<ref name="Propranolol">{{cite book | vauthors = Al-Majed AA, Bakheit AH, Abdel Aziz HA, Alajmi FM, AlRabiah H | title = Propranolol | series = Profiles of Drug Substances, Excipients and Related Methodology | volume = 42 | pages = 287–338 | date = 2017 | pmid = 28431779 | doi = 10.1016/bs.podrm.2017.02.006 | isbn = 978-0-12-812226-6 }}</ref> that is, it [[receptor antagonist|blocks]] the action of [[epinephrine]] (adrenaline) and [[norepinephrine]] (noradrenaline) at both [[Beta-1 adrenergic receptor|β<sub>1</sub>-]] and [[Beta-2 adrenergic receptor|β<sub>2</sub>-adrenergic receptor]]s. It has little [[Beta blocker#Intrinsic sympathomimetic activity|intrinsic sympathomimetic activity]], but has strong [[membrane stabilizing effect|membrane stabilizing activity]] (only at high blood concentrations, e.g. [[overdose]]).<ref>{{cite book| vauthors = Naish J, Court DS |title=Medical sciences|date=2014|isbn=978-0-7020-5249-1|page=150|publisher=Elsevier Health Sciences |edition=Second}}</ref> Propranolol can cross the [[blood–brain barrier]] and exert effects in the [[central nervous system]] in addition to its peripheral activity.<ref name="Steenenvan Wijk2015"/>

In addition to blockade of [[adrenergic receptor]]s, propranolol has very weak inhibitory effects on the [[norepinephrine transporter]] and/or weakly stimulates norepinephrine release (i.e., the concentration of norepinephrine is increased in the [[synapse]]).<ref name="YoungGlennon2008">{{cite journal | vauthors = Young R, Glennon RA | title = S(-)Propranolol as a discriminative stimulus and its comparison to the stimulus effects of cocaine in rats | journal = Psychopharmacology | volume = 203 | issue = 2 | pages = 369–382 | date = April 2009 | pmid = 18795268 | doi = 10.1007/s00213-008-1317-2 | doi-access = free }}</ref><ref name="pmid2872325"/> Since propranolol blocks β-adrenoceptors, the increase in synaptic norepinephrine only results in α-adrenoceptor activation, with the [[Alpha-1 adrenergic receptor|α<sub>1</sub>-adrenoceptor]] being particularly important for effects observed in [[animal model]]s.<ref name="YoungGlennon2008" /><ref name="pmid2872325" /> Therefore, it can be looked upon as a weak indirect α<sub>1</sub>-adrenoceptor [[agonist]] in addition to potent β-adrenoceptor antagonist.<ref name="YoungGlennon2008" /><ref name="pmid2872325" /> In addition to its effects on the adrenergic system, there is evidence that indicates that propranolol may act as a relatively weak [[receptor antagonist|antagonist]] of certain [[serotonin receptor]]s, namely the [[5-HT1A|5-HT<sub>1A</sub>]], [[5-HT1B receptor|5-HT<sub>1B</sub>]], and [[5-HT2B receptor|5-HT<sub>2B</sub> receptor]]s.<ref name="Glennon1987">{{cite journal | vauthors = Glennon RA | title = Central serotonin receptors as targets for drug research | journal = J Med Chem | volume = 30 | issue = 1 | pages = 1–12 | date = January 1987 | pmid = 3543362 | doi = 10.1021/jm00384a001 | url = | quote = Table II. Affinities of Selected Phenalkylamines for 5-HT1 and 5-HT2 Binding Sites}}</ref><ref name="pmid9064274">{{cite journal | vauthors = Davids E, Lesch KP | title = [The 5-HT1A receptor: a new effective principle in psychopharmacologic therapy?] | language = de | journal = Fortschritte der Neurologie-Psychiatrie | volume = 64 | issue = 11 | pages = 460–472 | date = November 1996 | pmid = 9064274 | doi = 10.1055/s-2007-996592 | s2cid = 147793142 }}</ref><ref name="pmid7938165">{{cite journal | vauthors = Hoyer D, Clarke DE, Fozard JR, Hartig PR, Martin GR, Mylecharane EJ, Saxena PR, Humphrey PP | title = International Union of Pharmacology classification of receptors for 5-hydroxytryptamine (Serotonin) | journal = Pharmacological Reviews | volume = 46 | issue = 2 | pages = 157–203 | date = June 1994 | doi = 10.1016/S0031-6997(25)06783-3 | pmid = 7938165 }}</ref><ref name="pmid8743744" /> The latter may be involved in the effectiveness of propranolol in the treatment of [[migraine]] at high doses.<ref name="pmid8743744" /> (–)-Propranolol is not a [[silent antagonist]] of the serotonin 5-HT<sub>1A</sub> receptor but is instead a very weak [[partial agonist]] of the receptor.<ref name="Newman-TancrediConteChaput1997">{{cite journal | vauthors = Newman-Tancredi A, Conte C, Chaput C, Verrièle L, Audinot-Bouchez V, Lochon S, Lavielle G, Millan MJ | title = Agonist activity of antimigraine drugs at recombinant human 5-HT1A receptors: potential implications for prophylactic and acute therapy | journal = Naunyn Schmiedebergs Arch Pharmacol | volume = 355 | issue = 6 | pages = 682–688 | date = June 1997 | pmid = 9205951 | doi = 10.1007/pl00005000 | url = }}</ref>

Both enantiomers of propranolol have a [[local anesthetic]] (topical) effect, which is normally mediated by blockade of [[voltage-gated sodium channel]]s. Studies have demonstrated propranolol's ability to block cardiac, neuronal, and skeletal voltage-gated sodium channels, accounting for its known membrane stabilizing effect and antiarrhythmic and other central nervous system effects.<ref>{{cite journal | vauthors = Wang DW, Mistry AM, Kahlig KM, Kearney JA, Xiang J, George AL | title = Propranolol blocks cardiac and neuronal voltage-gated sodium channels | journal = Frontiers in Pharmacology | volume = 1 | page = 144 | year = 2010 | pmid = 21833183 | pmc = 3153018 | doi = 10.3389/fphar.2010.00144 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Bankston JR, Kass RS | title = Molecular determinants of local anesthetic action of beta-blocking drugs: Implications for therapeutic management of long QT syndrome variant 3 | journal = Journal of Molecular and Cellular Cardiology | volume = 48 | issue = 1 | pages = 246–253 | date = January 2010 | pmid = 19481549 | pmc = 2813422 | doi = 10.1016/j.yjmcc.2009.05.012 }}</ref><ref>{{cite journal | vauthors = Desaphy JF, Pierno S, De Luca A, Didonna P, Camerino DC | title = Different ability of clenbuterol and salbutamol to block sodium channels predicts their therapeutic use in muscle excitability disorders | journal = Molecular Pharmacology | volume = 63 | issue = 3 | pages = 659–670 | date = March 2003 | pmid = 12606775 | doi = 10.1124/mol.63.3.659 | url = http://pdfs.semanticscholar.org/20af/2edd8d1cb9f3874aee83a478c5af152298c0.pdf | s2cid = 631197 | archive-url = https://web.archive.org/web/20190220073326/http://pdfs.semanticscholar.org/20af/2edd8d1cb9f3874aee83a478c5af152298c0.pdf | archive-date = 20 February 2019 }}</ref>

====Mechanism of action====
Propranolol is a non-selective beta receptor antagonist.<ref name="Propranolol"/> This means that it does not have preference to β<sub>1</sub> or β<sub>2</sub> receptors. It competes with sympathomimetic neurotransmitters for binding to receptors, which inhibits [[Sympathetic nervous system|sympathetic]] stimulation of the heart. Blockage of neurotransmitter binding to β<sub>1</sub> receptors on [[cardiac myocytes]] inhibits activation of adenylate cyclase, which in turn inhibits [[Cyclic adenosine monophosphate|cAMP]] synthesis leading to reduced [[Protein kinase A]] (PKA) activation. This results in less [[calcium]] influx to cardiac myocytes through [[Voltage-gated calcium channel|voltage-gated L-type calcium channels]], meaning there is a decreased sympathetic effect on cardiac cells, resulting in antihypertensive effects including reduced heart rate and lower arterial blood pressure.<ref name="DrugBank" /> Blocking neurotransmitter activity at β<sub>2</sub> receptors in vascular smooth muscle cells causes vasoconstriction, leading to [[hypertension]].

===Pharmacokinetics===
====Absorption====
Propranolol is rapidly and completely [[absorption (pharmacokinetics)|absorbed]], with peak plasma levels achieved about 2{{nbsp}}hours (range 1–3{{nbsp}}hours) after ingestion.<ref name="DrugBank" /><ref name="KalamRasoolRehman2020">{{cite journal | vauthors = Kalam MN, Rasool MF, Rehman AU, Ahmed N | title = Clinical Pharmacokinetics of Propranolol Hydrochloride: A Review | journal = Curr Drug Metab | volume = 21 | issue = 2 | pages = 89–105 | date = 2020 | pmid = 32286940 | doi = 10.2174/1389200221666200414094644 | url = }}</ref> Its oral [[bioavailability]] is approximately 25%.<ref name="Inderal-Label" /><ref name="Srinivasan2019" /> Despite complete absorption, propranolol has a variable [[bioavailability]] due to extensive [[first-pass metabolism]].<ref name="KalamRasoolRehman2020" /> [[Hepatic impairment]] therefore increases its bioavailability.<ref name="KalamRasoolRehman2020" /> Effective plasma concentrations are between 10 and 100{{nbsp}}mg/L.{{Citation needed|date=September 2017}} Toxic levels are associated with plasma concentrations above 2,000{{nbsp}}mg/L.{{Citation needed|date=September 2017}} Coadministration with food appears to enhance bioavailability but does not hasten its time to peak levels.<ref name="DrugBank" /><ref>{{cite book| vauthors = Rang HP |title=Rang & Dale's pharmacology|date=2011|publisher=Churchill Livingstone |location=Edinburgh |isbn=978-0-7020-3471-8 |page=106 |edition=7th }}</ref> Propranolol can be absorbed along the whole intestine with the main absorption site being the colon,<ref>{{cite journal | vauthors = Nagare N, Damre A, Singh KS, Mallurwar SR, Iyer S, Naik A, Chintamaneni M | title = Determination of site of absorption of propranolol in rat gut using in situ single-pass intestinal perfusion | journal = Indian Journal of Pharmaceutical Sciences | volume = 72 | issue = 5 | pages = 625–629 | date = September 2010 | pmid = 21694996 | pmc = 3116309 | doi = 10.4103/0250-474X.78533 | doi-access = free }}</ref> which means people who have lost their colon due to surgery may absorb less propranolol. Propranolol shows marked [[interindividual variability]] in [[pharmacokinetics]], with propranolol levels varying 20-fold in different individuals.<ref name="Shand1976">{{cite journal | vauthors = Shand DG | title = Pharmacokinetics of propranolol: a review | journal = Postgrad Med J | volume = 52 Suppl 4 | issue = | pages = 22–25 | date = 1976 | pmid = 787953 | doi = | url = }}</ref>

====Distribution====
The [[volume of distribution]] of propranolol is about 4{{nbsp}}L/kg or 320{{nbsp}}L.<ref name="DrugBank" /><ref name="KalamRasoolRehman2020" /> The [[plasma protein binding]] of propranolol is approximately 90%, with a range of 85 to 96% in different studies.<ref name="DrugBank" /><ref name="KalamRasoolRehman2020" /> Propranolol is a highly [[lipophilic]] drug achieving high concentrations in the brain.<ref name="Srinivasan2019" /><ref name="HeelBrogdenSpeight1979">{{cite journal | vauthors = Heel RC, Brogden RN, Speight TM, Avery GS | title = Atenolol: a review of its pharmacological properties and therapeutic efficacy in angina pectoris and hypertension | journal = Drugs | volume = 17 | issue = 6 | pages = 425–460 | date = June 1979 | pmid = 38096 | doi = 10.2165/00003495-197917060-00001 | url = }}</ref> The [[brain-to-blood ratio]] of propranolol in humans ranges from 15:1 to 33:1, whereas the ratio for the [[peripherally selective drug|peripherally selective]] beta blocker [[atenolol]] has been found to be 0.2:1.<ref name="Drayer1987">{{cite journal | vauthors = Drayer DE | title = Lipophilicity, hydrophilicity, and the central nervous system side effects of beta blockers | journal = Pharmacotherapy | volume = 7 | issue = 4 | pages = 87–91 | date = 1987 | pmid = 2891122 | doi = 10.1002/j.1875-9114.1987.tb04029.x | url = }}</ref><ref name="HeelBrogdenSpeight1979" />

====Metabolism====
Propranolol undergoes [[drug metabolism|metabolism]] via [[aromatic compound|aromatic]] [[hydroxylation]] (mainly 4-hydroxylation), ''N''-[[dealkylation]], [[side chain|side-chain]] [[oxidation]], and [[glucuronidation]].<ref name="Inderal-Label" /><ref name="DrugBank" /><ref name="KalamRasoolRehman2020" /> The metabolism of propranolol involves [[cytochrome P450]] [[enzyme]]s including [[CYP2D6]], [[CYP1A2]], and [[CYP2C19]].<ref name="Inderal-Label" /><ref name="KalamRasoolRehman2020" /><ref name="MaideenRajkapoorMuthusamy2021" /> CYP1A2 and CYP2D6 have a major role, while CYP2C19 and [[CYP3A4]] have a minor role.<ref name="MaideenRajkapoorMuthusamy2021" />{{Additional citation needed|date=June 2025}} The main [[metabolite]] 4-hydroxypropranolol, which has a longer [[elimination half-life]] than propranolol, is also pharmacologically active.<ref name="DrugBank" /><ref name="KalamRasoolRehman2020" />

====Elimination====
Propranolol is [[elimination (pharmacology)|eliminated]] in [[urine]].<ref name="DrugBank">{{cite web |title=Propranolol |url=https://www.drugbank.ca/drugs/DB00571 |website=www.drugbank.ca |access-date=31 January 2019}}</ref><ref name="KalamRasoolRehman2020" /> Approximately 91% of an [[oral administration|oral]] dose of propranolol is eliminated in urine as 12{{nbsp}}[[metabolite]]s.<ref name="DrugBank" /><ref name="KalamRasoolRehman2020" /> Only about 1 to 4% of propranolol is [[excretion|excreted]] unchanged in urine or [[feces]].<ref name="KalamRasoolRehman2020" />

The [[elimination half-life]] of propranolol ranges from 2.8 to 8{{nbsp}}hours in different studies, with a typical half-life of around 4{{nbsp}}hours.<ref name="Inderal-Label" /><ref name="DrugBank" /><ref name="KalamRasoolRehman2020" /> The [[duration of action]] of a single oral dose is longer than the half-life and may be up to 12{{nbsp}}hours if the single dose is high enough (e.g., 80&nbsp;mg).<ref name="PubChem">{{cite web |title=Propranolol |url=https://pubchem.ncbi.nlm.nih.gov/compound/propranolol |website=pubchem.ncbi.nlm.nih.gov |access-date=31 January 2019 |language=en}}</ref>

===Pharmacogenomics===
There were no significance differences in area-under-the-curve levels of propranolol in [[CYP2D6]] [[poor metabolizer]]s versus [[extensive metabolizer]]s.<ref name="Zhou2009">{{cite journal | vauthors = Zhou SF | title = Polymorphism of human cytochrome P450 2D6 and its clinical significance: Part I | journal = Clin Pharmacokinet | volume = 48 | issue = 11 | pages = 689–723 | date = 2009 | pmid = 19817501 | doi = 10.2165/11318030-000000000-00000 | url = }}</ref> However, area-under-the-curve propranolol levels were ~2.5-fold higher in [[white people|Caucasian]] CYP2D6 poor metabolizers or [[Chinese people|Chinese]] people with a non-functional CYP2D6 gene.<ref name="Zhou2009" /> The contribution of CYP2D6 to the metabolism of propranolol is less than with [[metoprolol]] and is described as only "marginal".<ref name="Zhou2009" />

==Chemistry==
Propranolol is highly [[lipophilic]].<ref name="Srinivasan2019" /><ref name="KalamRasoolRehman2020" /> The experimental [[log P]] of propranolol is 3.0 to 3.48 and its predicted log P ranges from 2.20 to 3.10.<ref name="KalamRasoolRehman2020" /><ref name="DrugBank" /><ref name="PubChem" /><ref name="TekesSzegiHashemi2013">{{cite journal |vauthors=Tekes K, Szegi P, Hashemi F, Laufer R, Kalász H, Siddiq A, Ertsey C |date=2013 |title=Medicinal chemistry of antimigraine drugs |url= |journal=Curr Med Chem |volume=20 |issue=26 |pages=3300–3316 |doi=10.2174/0929867311320260012 |pmid=23746273}}</ref><ref name="ChemSpider">{{cite web |date=10 June 2024 |title=b-Propranolol |url=https://www.chemspider.com/Chemical-Structure.4777.html |access-date=22 June 2025 |website=ChemSpider}}</ref>

==History==
{{See also|Beta blocker#History|Discovery and development of beta-blockers}}

[[Scottish people|Scottish]] scientist [[James W. Black]] developed propranolol in the 1960s.<ref name="Srinivasan2019" /><ref name="Black JW, Crowther AF, Shanks RG, Smith LH, Dornhorst AC 1964 1080–1081">{{cite journal | vauthors = Black JW, Crowther AF, Shanks RG, Smith LH, Dornhorst AC | title = A New Adrenergic Beta-Receptor Antagonist | journal = Lancet | volume = 1 | issue = 7342 | pages = 1080–1081 | date = May 1964 | pmid = 14132613 | doi = 10.1016/S0140-6736(64)91275-9 }}</ref> It was the first beta-blocker effectively used in the treatment of [[coronary artery disease]] and [[hypertension]].<ref name=":0">{{Cite book|title=Basic & Clinical Pharmacology| vauthors = Benowitz NL |publisher=McGraw-Hill|year=2017|isbn=978-1-259-64115-2| veditors = Katzung BG |edition=14th|chapter=Antihypertensive Agents}}</ref>

Newer, more cardio-selective beta blockers (such as [[bisoprolol]], [[nebivolol]], [[carvedilol]], or [[metoprolol]]) are used preferentially in the treatment of hypertension.<ref name=":0" />

==Society and culture==
===Performance enhancement===
In a 1987 study by the International Conference of Symphony and Opera Musicians, it was reported that 27% of interviewed members said they used beta blockers such as propranolol for musical performances.<ref name= Fishbein>{{cite journal |vauthors=Fishbein M, Middlestadt SE, Ottati V, Straus S, Ellis A | year = 1988 | title = Medical problems among ICSOM musicians: overview of a national survey | journal = Med Probl Perform Artist | volume = 3| pages = 1–8}}</ref> For about 10 to 16% of performers, their degree of stage fright is considered pathological.<ref name= Fishbein/><ref>{{cite journal |vauthors=Steptoe A, Malik F, Pay C, Pearson P, Price C, Win Z | year = 1995 | title = The impact of stage fright on student actors | journal = Br J Psychol | volume = 86| pages = 27–39 | doi=10.1111/j.2044-8295.1995.tb02544.x}}</ref> Propranolol is used by musicians, actors, and public speakers for its ability to treat anxiety symptoms activated by the sympathetic nervous system.<ref>{{cite journal | vauthors = Lockwood AH | title = Medical problems of musicians | journal = The New England Journal of Medicine | volume = 320 | issue = 4 | pages = 221–227 | date = January 1989 | pmid = 2643048 | doi = 10.1056/nejm198901263200405 }}</ref> It has also been used as a [[Performance-enhancing substance|performance-enhancing drug]] in sports where high accuracy is required, including [[Target archery|archery]], [[Shooting sports|shooting]], [[golf]],<ref name="ogrady">{{cite news |author=Tim Glover |url=https://www.independent.co.uk/sport/golf-ogrady-says-players-use-betablockers-drugs-helped-win-majors-1368307.html |title=Golf: O'Grady says players use beta-blockers: Drugs 'helped win majors' |newspaper=[[The Independent]] |access-date=28 March 2017 |url-status=live |archive-url=https://web.archive.org/web/20150925223906/http://www.independent.co.uk/sport/golf-ogrady-says-players-use-betablockers-drugs-helped-win-majors-1368307.html |archive-date=25 September 2015 }}</ref> and [[snooker]].<ref name="ogrady"/> In the [[2008 Summer Olympics]], [[Shooting at the 2008 Summer Olympics – Men's 50 metre pistol|50-metre pistol]] silver medalist and [[Shooting at the 2008 Summer Olympics – Men's 10 metre air pistol|10-metre air pistol]] bronze medalist [[Kim Jong-su]] tested positive for propranolol and was stripped of his medals.<ref name="Guardian NK Doping">{{cite web| vauthors = Scott M |title=Olympics: North Korea's Kim Jong-su loses medals after positive drugs test |url= https://www.theguardian.com/sport/2008/aug/15/olympics2008.drugsinsport |website=The Guardian |publisher=Guardian News and Media Limited |access-date=7 March 2018 |date=15 August 2008}}</ref>

===Brand names===
Propranolol was first marketed under the brand name Inderal, manufactured by [[Imperial Chemical Industries|ICI Pharmaceuticals]] (now [[AstraZeneca]]), in 1965. "Inderal" is a quasi-[[anagram]] of "Alderlin", the trade name of pronethalol (which propranolol replaced); both names are an homage to [[Alderley Park]], the ICI headquarters where the drugs were first developed.<ref name=Quirke>{{cite journal |vauthors=Quirke V |title=Putting theory into practice: James Black, receptor theory and the development of the beta-blockers at ICI, 1958-1978 |journal=Med Hist |volume=50 |issue=1 |pages=69–92 |date=January 2006 |pmid=16502872 |pmc=1369014 |doi=10.1017/s0025727300009455}}</ref>

Propranolol is also marketed under brand names Avlocardyl, Deralin, Dociton, Inderalici, InnoPran XL, Indoblok,<ref>{{Cite web |title=Indoblok Tablet - Product - TabletWise.com |url=https://www.tabletwise.com/southafrica/indoblok-tablet |access-date=15 October 2022 |website=www.tabletwise.com |language=en}}</ref> Sumial, Anaprilin, and Bedranol SR ([[Sandoz]]). In India, it is marketed under brand names such as Ciplar and Ciplar LA by [[Cipla]]. Hemangeol, a 4.28&nbsp;mg/mL solution of propranolol, is indicated for the treatment of proliferating [[infantile hemangioma]].<ref>{{cite web|title=Hemangeol - Food and Drug Administration|url=https://www.accessdata.fda.gov/drugsatfda_docs/label/2014/205410s000lbl.pdf|access-date=23 March 2015|date=1 March 2014|url-status=live|archive-url=https://web.archive.org/web/20150402113709/https://www.accessdata.fda.gov/drugsatfda_docs/label/2014/205410s000lbl.pdf|archive-date=2 April 2015}}</ref>

==References==
{{Reflist}}

==Further reading==
* {{cite journal | vauthors = Stapleton MP | title = Sir James Black and propranolol. The role of the basic sciences in the history of cardiovascular pharmacology | journal = Texas Heart Institute Journal | volume = 24 | issue = 4 | pages = 336–342 | year = 1997 | pmid = 9456487 | pmc = 325477 }}

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