View source for Midodrine

{{Short description|Antihypotensive medication}}
{{Use dmy dates|date=August 2021}}
{{cs1 config|name-list-style=vanc|display-authors=6}}
{{Infobox drug
| Verifiedfields = verified
| Watchedfields = verified
| verifiedrevid = 462252266
| image = Midodrine.svg
| width = 250px
| caption = Above: molecular structure of midodrine
Below: 3D representation of a midodrine molecule
| image2 = Midodrine 3D.png
| chirality = [[Racemic mixture]]

<!-- Clinical data -->| pronounce = 
| tradename = Amatine, Gutron, Orvaten, ProAmatine, others
| Drugs.com = {{drugs.com|monograph|midodrine-hydrochloride}}
| MedlinePlus = a616030
| DailyMedID = Midodrine
| pregnancy_AU = C
| pregnancy_AU_comment = 
| pregnancy_category = 
| routes_of_administration = [[Oral administration|By mouth]]<ref name="DrugBank" />
| class = [[Alpha-1 adrenergic receptor|α<sub>1</sub>-Adrenergic receptor]] [[agonist]]; [[Antihypotensive agent]]
| ATC_prefix = C01
| ATC_suffix = CA17
| ATC_supplemental = <!-- Legal status -->
| legal_AU = S4
| legal_AU_comment = 
| legal_BR = <!-- OTC, A1, A2, A3, B1, B2, C1, C2, C3, C4, C5, D1, D2, E, F -->
| legal_BR_comment = 
| legal_CA = <!-- OTC, Rx-only, Schedule I, II, III, IV, V, VI, VII, VIII -->
| legal_CA_comment = 
| legal_DE = <!-- Anlage I, II, III or Unscheduled -->
| legal_DE_comment = 
| legal_NZ = <!-- Class A, B, C -->
| legal_NZ_comment = 
| legal_UK = <!-- GSL, P, POM, CD, CD Lic, CD POM, CD No Reg POM, CD (Benz) POM, CD (Anab) POM or CD Inv POM / Class A, B, C -->
| legal_UK_comment = 
| legal_US = Rx-only
| legal_US_comment = <ref>{{cite web | title=Proamatine- midodrine hydrochloride tablet | website=DailyMed | url=https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=9e8874f0-ad2e-41ce-8a35-bed819615a5d | access-date=14 August 2021}}</ref>
| legal_EU = 
| legal_EU_comment = 
| legal_UN = <!-- N I, II, III, IV / P I, II, III, IV -->
| legal_UN_comment = 
| legal_status = <!-- For countries not listed above -->

<!-- Pharmacokinetic data -->| bioavailability = 93% (as [[desglymidodrine]])<ref name="Midodrine-Label" /><ref name="Gilden2004">{{cite book | vauthors = Gilden JL | title=Primer on the Autonomic Nervous System | chapter=Midodrine and Other Sympathomimetics | publisher=Elsevier | date=2004 | isbn=978-0-12-589762-4 | doi=10.1016/b978-012589762-4/50113-4 | pages=413–415}}</ref><ref name="DrugBank" />
| protein_bound = 
| metabolism = Deglycination<ref name="Midodrine-Label" /><ref name="DrugBank" /><ref name="Gilden2004" />
| metabolites = • [[Desglymidodrine]]<ref name="Midodrine-Label" /><ref name="DrugBank" /><ref name="Gilden2004" />
| onset = ≤1 hour<ref name="Midodrine-Label" />
| elimination_half-life = Midodrine: 0.5{{nbsp}}hours<ref name="Gilden2004" /><br />Desglymidodrine: 2–4{{nbsp}}hours<ref name="Gilden2004" /><ref name="DrugBank" />
| duration_of_action = 2–6{{nbsp}}hours<ref name="Midodrine-Label" /><ref name="Gilden2004" />
| excretion = <!-- Identifiers -->
| CAS_number_Ref = {{cascite|correct|CAS}}
| CAS_number = 42794-76-3
| CAS_supplemental = 
| PubChem = 4195
| IUPHAR_ligand = 7240
| DrugBank_Ref = {{drugbankcite|correct|drugbank}}
| DrugBank = DB00211
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 4050
| UNII_Ref = {{fdacite|correct|FDA}}
| UNII = 6YE7PBM15H
| KEGG_Ref = {{keggcite|correct|kegg}}
| KEGG = D08220
| ChEBI_Ref = {{ebicite|correct|EBI}}
| ChEBI = 6933
| ChEMBL_Ref = {{ebicite|correct|EBI}}
| ChEMBL = 1201212
| NIAID_ChemDB = 
| PDB_ligand = 
| synonyms = ST-1085; TS-701; 3,6-Dimethoxy-β-hydroxy-''N''-aminoethanonyl-2-phenylethylamine; 2-Amino-''N''-[2-(2,5-dimethoxyphenyl)-2-hydroxyethyl]acetamide; 1-2',5'-Dimethoxyphenyl-1)-2 glycinamidoethanol

<!-- Chemical data -->| IUPAC_name = (''RS'')-''N''-[2-(2,5-Dimethoxyphenyl)-2-hydroxyethyl]glycinamide
| C = 12
| H = 18
| N = 2
| O = 4
| SMILES = O=C(NCC(O)c1cc(OC)ccc1OC)CN
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI = 1S/C12H18N2O4/c1-17-8-3-4-11(18-2)9(5-8)10(15)7-14-12(16)6-13/h3-5,10,15H,6-7,13H2,1-2H3,(H,14,16)
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = PTKSEFOSCHHMPD-UHFFFAOYSA-N

<!-- Physical data -->| density = 
| density_notes = 
| melting_point = 
| melting_high = 
| melting_notes = 
| boiling_point = 
| boiling_notes = 
| solubility = 
| sol_units = 
| specific_rotation = 
}}
<!-- Definition and medical uses -->
'''Midodrine''', sold under the brand names '''ProAmatine''' and '''Orvaten''' among others, is an [[antihypotensive]] [[medication]] used to treat [[orthostatic hypotension]] (low blood pressure when standing) and [[urinary incontinence]].<ref name="Midodrine-Label">{{cite web | title=ProAmatine® (midodrine hydrochloride) Tablets | publisher=Food and Drug Administration | website=fda.gov | url=https://www.accessdata.fda.gov/drugsatfda_docs/label/2017/019815s010lbl.pdf | archive-url=https://web.archive.org/web/20210405140728/https://www.accessdata.fda.gov/drugsatfda_docs/label/2017/019815s010lbl.pdf | url-status=dead | archive-date=5 April 2021 | access-date=28 August 2024}}</ref><ref name="AdisInsight">{{cite web | title=GE Healthcare | website=AdisInsight | date=21 October 2021 | url=https://adisinsight.springer.com/drugs/800007027 | access-date=28 August 2024}}</ref><ref name="DrugBank" /> It is taken [[oral administration|by mouth]].<ref name="Midodrine-Label" /><ref name="DrugBank" />

<!-- Side effects and mechanism of action -->
[[Side effect]]s of midodrine include [[hypertension]] (high blood pressure), [[paresthesia]], [[pruritus|itching]], [[goosebumps]], [[chills]], [[urinary urgency]], [[urinary retention]], and [[urinary frequency]].<ref name="Midodrine-Label" /> Midodrine is a [[prodrug]] of its [[active metabolite]] [[desglymidodrine]].<ref name="Midodrine-Label" /><ref name="DrugBank" /> This [[metabolite]] acts as a [[binding selectivity|selective]] [[agonist]] of the [[alpha-1 adrenergic receptor|α<sub>1</sub>-adrenergic receptor]].<ref name="Midodrine-Label" /><ref name="DrugBank" /> This in turn results in [[vasoconstriction]] and increased [[blood pressure]].<ref name="Midodrine-Label" /><ref name="DrugBank" />

<!-- History, society, and culture -->
Midodrine was discovered by 1971<ref name="Elks2014" /> and was introduced for medical use in the [[United States]] in 1996.<ref>{{cite journal | vauthors = Kymes SM, Sullivan C, Jackson K, Raj SR | title = Real-world droxidopa or midodrine treatment persistence in patients with neurogenic orthostatic hypotension or orthostatic hypotension | language = English | journal = Autonomic Neuroscience | volume = 225 | pages = 102659 | date = May 2020 | pmid = 32200263 | doi = 10.1016/j.autneu.2020.102659 | doi-access = free }}</ref>

==Medical uses==
Midodrine is indicated for the treatment of symptomatic orthostatic hypotension. It can reduce dizziness and faints by about a third, but can be limited by troublesome [[goose bumps]], [[pruritus|skin itch]], gastrointestinal discomfort, chills, elevated blood pressure while lying down, and [[urinary retention]].<ref>{{cite journal | vauthors = Izcovich A, González Malla C, Manzotti M, Catalano HN, Guyatt G | title = Midodrine for orthostatic hypotension and recurrent reflex syncope: A systematic review | journal = Neurology | volume = 83 | issue = 13 | pages = 1170–1177 | date = September 2014 | pmid = 25150287 | doi = 10.1212/WNL.0000000000000815 | s2cid = 5439767 }}</ref> A meta-analysis of clinical trials of midodrine or droxidopa in patients with [[neurogenic orthostasis|low blood pressure when standing]] found that midodrine increased standing blood pressure more than [[droxidopa]] but that midodrine but not droxidopa increased the risk of high blood pressure when lying down.<ref>{{cite journal | vauthors = Chen JJ, Han Y, Tang J, Portillo I, Hauser RA, Dashtipour K | title = Standing and Supine Blood Pressure Outcomes Associated With Droxidopa and Midodrine in Patients With Neurogenic Orthostatic Hypotension: A Bayesian Meta-analysis and Mixed Treatment Comparison of Randomized Trials | journal = The Annals of Pharmacotherapy | volume = 52 | issue = 12 | pages = 1182–1194 | date = December 2018 | pmid = 29972032 | doi = 10.1177/1060028018786954 | s2cid = 49674644 }}</ref> Small studies have also shown that midodrine can be used to prevent excessive drops in blood pressure in people requiring [[Kidney dialysis|dialysis]].<ref>{{cite journal | vauthors = Prakash S, Garg AX, Heidenheim AP, House AA | title = Midodrine appears to be safe and effective for dialysis-induced hypotension: a systematic review | journal = Nephrology, Dialysis, Transplantation | volume = 19 | issue = 10 | pages = 2553–2558 | date = October 2004 | pmid = 15280522 | doi = 10.1093/ndt/gfh420 | doi-access = }}</ref>

Midodrine has been used in the complications of [[cirrhosis]]. It is also used with [[octreotide]] for [[hepatorenal syndrome]]; the proposed mechanism is constriction of splanchnic vessels and dilation of renal vasculature. Studies have not been sufficiently well conducted to show a clear place for midodrine.<ref>{{cite journal | vauthors = Karwa R, Woodis CB | title = Midodrine and octreotide in treatment of cirrhosis-related hemodynamic complications | journal = The Annals of Pharmacotherapy | volume = 43 | issue = 4 | pages = 692–699 | date = April 2009 | pmid = 19299324 | doi = 10.1345/aph.1L373 | s2cid = 207263346 }}</ref>

Midodrine is used [[off-label use|off-label]] to increase blood pressure in the treatment of [[postural orthostatic tachycardia syndrome]] (POTS) where increased transduction of venous alpha 1 adrenergic receptors increases venous return.<ref name="NarasimhanAggarwalSatish2022">{{cite journal | vauthors = Narasimhan B, Aggarwal D, Satish P, Kantharia B, Aronow WS | title = Postural orthostatic tachycardia syndrome: pathophysiology, management, and experimental therapies | journal = Expert Opin Investig Drugs | volume = 31 | issue = 10 | pages = 1017–1025 | date = October 2022 | pmid = 36094001 | doi = 10.1080/13543784.2022.2121697 | url = }}</ref><ref name="VasavadaVermaSheggari2023">{{cite journal | vauthors = Vasavada AM, Verma D, Sheggari V, Ghetiya S, Chirumamilla PC, Kotak RA, Mahapatra SS, Patel T, Jain M | title = Choices and Challenges With Drug Therapy in Postural Orthostatic Tachycardia Syndrome: A Systematic Review | journal = Cureus | volume = 15 | issue = 5 | pages = e38887 | date = May 2023 | pmid = 37313107 | pmc = 10259876 | doi = 10.7759/cureus.38887 | doi-access = free | url = }}</ref><ref name="Benarroch2012">{{cite journal | vauthors = Benarroch EE | title = Postural tachycardia syndrome: a heterogeneous and multifactorial disorder | journal = Mayo Clin Proc | volume = 87 | issue = 12 | pages = 1214–1225 | date = December 2012 | pmid = 23122672 | pmc = 3547546 | doi = 10.1016/j.mayocp.2012.08.013 | url = }}</ref>

===Available forms===
Midodrine is available in the [[pharmaceutical form|form]] of 2.5, 5, and 10{{nbsp}}mg [[oral administration|oral]] [[tablet (pharmacy)|tablet]]s.<ref name="Midodrine-Label" /><ref name="DrugBank" />

==Contraindications==
Midodrine is contraindicated in patients with severe organic heart disease, acute kidney disease, [[urinary retention]], [[pheochromocytoma]] or [[thyrotoxicosis]]. Midodrine should not be used in patients with persistent and excessive supine hypertension.<ref>{{Cite web |title=Midodrine - FDA prescribing information, side effects and uses |url=https://www.drugs.com/pro/midodrine.html |access-date=2022-06-30 |website=Drugs.com |language=en}}</ref>

==Side effects==
Headache, feeling of pressure or fullness in the head, vasodilation or flushing face, scalp tingling, confusion or thinking abnormality, dry mouth, anxiety, and rash, among others.<ref>{{Cite web|url=https://www.mayoclinic.org/drugs-supplements/midodrine-oral-route/side-effects/drg-20064821|title=Midodrine (Oral Route) Side Effects - Mayo Clinic|website=www.mayoclinic.org}}</ref>

==Pharmacology==
===Mechanism of action===
Midodrine is a [[prodrug]] which forms the [[active metabolite]], [[desglymidodrine]], which is an [[Alpha-1 adrenergic receptor|α<sub>1</sub>-adrenergic receptor]] [[agonist]] and exerts its actions via activation of α<sub>1</sub>-adrenergic receptors of the arteriolar and venous vasculature, producing an increase in vascular tone and elevation of blood pressure. Desglymidodrine does not stimulate cardiac [[β-adrenergic receptor]]s.{{Citation needed|date=February 2025}}

[[File:Desglymidodrine.svg|thumb|none|Chemical structure of [[desglymidodrine]].]]{{clear left}}

===Pharmacokinetics===
After oral administration, midodrine is rapidly absorbed. The plasma levels of the prodrug peak after about half an hour, and decline with a half-life of approximately 25{{nbsp}}minutes, while the metabolite reaches peak blood concentrations about 1 to 2 hours after a dose of midodrine and has a half-life of about 3 to{{nbsp}}4 hours. The absolute [[bioavailability]] of midodrine (measured as [[desglymidodrine]]) is 93%.<ref name="DrugBank" />

Midodrine and desglymidodrine diffuse poorly across the [[blood–brain barrier]] and are therefore [[peripherally selective drug|peripherally selective]] and are not associated with effects in the [[central nervous system]].<ref name="Costa-PintoJonesUdy2022">{{cite journal | vauthors = Costa-Pinto R, Jones DA, Udy AA, Warrillow SJ, Bellomo R | title = Midodrine use in critically ill patients: a narrative review | journal = Crit Care Resusc | volume = 24 | issue = 4 | pages = 298–308 | date = December 2022 | pmid = 38047013 | pmc = 10692611 | doi = 10.51893/2022.4.R | url = }}</ref><ref name="Cruz2000">{{cite journal | vauthors = Cruz DN | title = Midodrine: a selective alpha-adrenergic agonist for orthostatic hypotension and dialysis hypotension | journal = Expert Opin Pharmacother | volume = 1 | issue = 4 | pages = 835–840 | date = May 2000 | pmid = 11249519 | doi = 10.1517/14656566.1.4.835 | url = }}</ref><ref name="McClellanWisemanWilde1998">{{cite journal | vauthors = McClellan KJ, Wiseman LR, Wilde MI | title = Midodrine. A review of its therapeutic use in the management of orthostatic hypotension | journal = Drugs Aging | volume = 12 | issue = 1 | pages = 76–86 | date = January 1998 | pmid = 9467688 | doi = 10.2165/00002512-199812010-00007 | url = }}</ref>

Neither midodrine nor desglymidodrine are [[substrate (biochemistry)|substrate]]s of [[monoamine oxidase]].<ref name="Midodrine-Label" />

==Chemistry==
Midodrine, also known as 3,6-dimethoxy-β-hydroxy-''N''-aminoethanonyl-2-phenylethylamine, is a [[substituted phenethylamine]] [[chemical derivative|derivative]].<ref name="Gilden2004" />

Midodrine is an odorless, white, crystalline powder, soluble in water and sparingly soluble in [[methanol]].<ref>{{Cite web |title=DailyMed - MIDODRINE HCL- midodrine hydrochloride tablet |url=https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=24847065-0be0-46eb-a084-7e5425a8be73 |access-date=2023-01-05 |website=[[DailyMed]]}}</ref>

Midodrine's experimental [[partition coefficient|log P]] is -0.5 and its predicted log P ranges from -0.49 to -0.95.<ref name="PubChem">{{cite web | title=Midodrine | website=PubChem | url=https://pubchem.ncbi.nlm.nih.gov/compound/4195 | access-date=1 August 2024}}</ref><ref name="DrugBank">{{cite web | title=Midodrine: Uses, Interactions, Mechanism of Action | website=DrugBank Online | date=31 December 1992 | url=https://go.drugbank.com/drugs/DB00211 | access-date=1 August 2024}}</ref> The predicted log P of its [[active metabolite]] [[desglymidodrine]] ranges from -0.01 to 0.15.<ref name="PubChem-Desglymidodrine">{{cite web | title=Desglymidodrine | website=PubChem | url=https://pubchem.ncbi.nlm.nih.gov/compound/43260 | access-date=1 August 2024}}</ref><ref name="DrugBank-Desglymidodrine">{{cite web | title=Metabolite desglymidodrine | website=DrugBank Online | url=https://go.drugbank.com/metabolites/DBMET00829 | access-date=1 August 2024}}</ref>

===Stereochemistry===
Midodrine contains a stereocenter and consists of two [[enantiomer]]s, making it a [[racemate]]; ''i.e.'', a 1:1 mixture of (''R'')- and (''S'')-forms:<ref name="Rote Liste">Rote Liste Service GmbH (Hrsg.): ''Rote Liste 2017 – Arzneimittelverzeichnis für Deutschland (einschließlich EU-Zulassungen und bestimmter Medizinprodukte)''. Rote Liste Service GmbH, Frankfurt/Main, 2017, Aufl. 57, {{ISBN|978-3-946057-10-9}}, S. 196.</ref>

{| class="wikitable" style="text-align:center"
|- class="hintergrundfarbe6"
! colspan="2"| Enantiomers of midodrine
|-
| [[File:(R)-Midodrin Structural Formula V1.svg|250 px]]<br />(''R'')-midodrine<br /><small> CAS number: 133163-25-4</small>
| [[File:(S)-Midodrin Structural Formula V1.svg|250 px]]<br />(''S'')-midodrine<br /><small> CAS number: 133267-39-7</small>
|}

===Synthesis===
Acylation of [[1,4-dimethoxybenzene]] with [[chloroacetyl chloride]] gives the chloroketone '''2'''. The halogen is then converted to the amine '''3''' by any set of standard schemes, and the ketone reduced to an alcohol with borohydride ('''4''').<ref>{{Cite journal | vauthors = Moreau P, Finiels A, Meric P |date=2000-03-20 |title=Acetylation of dimethoxybenzenes with acetic anhydride in the presence of acidic zeolites |url=https://www.sciencedirect.com/science/article/pii/S1381116999003738 |journal=Journal of Molecular Catalysis A: Chemical |language=en |volume=154 |issue=1 |pages=185–192 |doi=10.1016/S1381-1169(99)00373-8 |issn=1381-1169|url-access=subscription }}</ref> Acylation of the amino group in this last intermediate with [[chloroacetyl chloride]] affords the amide '''5'''. The halogen is then displaced with azide and the resulting product '''6''' reduced catalytically to the glycinamide, midodrine ('''7''').<ref>{{cite book | vauthors = Cao T, Martini ML, Park K, Kaniskan HÜ, Jin J | chapter = 8.02 - Pyrimidines and Their Benzo Derivatives |date=2022-01-01 | doi = 10.1016/B978-0-12-818655-8.00041-X | veditors = Black DS, Cossy J, Stevens CV | title = Comprehensive Heterocyclic Chemistry IV |pages=86–228 |place=Oxford |publisher=Elsevier |language=en |isbn=978-0-12-818656-5 }}</ref>

[[File:Midodrine synthesis.svg|thumb|center|700px|Synthesis of midodrine<ref>{{Cite patent | inventor = Zoelss G |country= DE |number= 2506110 | title = Phenylethanolamine derivs prepn. - by reducing azides, useful as hypertensives | assign1 = Lentia GmbH | gdate = 21 April 1983 | postscript = . }}</ref><ref>K. Wismayr et al., {{Cite patent |country= AT |number= 241435}}; eidem, {{US patent|3340298}} (1965, 1967 both to Chemie Linz Ag).</ref> See also:<ref>Zoelss & W. Karl-Anton Ing {{Cite patent |country= DE |number= 2523735}} (1974 to Lentia GmbH).</ref>]]

==History==
Midodrine was discovered by 1971.<ref name="Elks2014" /> It was approved in the United States by the [[Food and Drug Administration]] (FDA) in 1996 for the treatment of [[dysautonomia]] and [[orthostatic hypotension]].{{Citation needed|date=August 2024}}

In August 2010, the FDA proposed withdrawing this approval because the manufacturer, [[Shire plc]], failed to complete [[postmarketing surveillance|required studies]] after the medicine reached the market.<ref>[https://archive.today/20120720172637/http://uk.reuters.com/article/idUKTRE67F3SE20100816 U.S. proposes withdrawal of Shire hypotension drug], 16 August 2010.</ref><ref>{{cite web| vauthors = O'Riordan M |title=FDA recommends withdrawal of midodrine|url=http://www.theheart.org/article/1110411.do|work=Food and Drug Administration. FDA proposes withdrawal of low blood pressure drug [press release]. August 16, 2010.|publisher=TheHeart.org|access-date=1 April 2011}}</ref> In September 2010, the FDA reversed its decision to remove midodrine from the market and allowed it to remain available to patients while Shire plc collected further data regarding the efficacy and safety of the drug.<ref>[http://healthcare.utah.edu/pharmacy/alerts/497.htm Midodrine (ProAmatine, generic) Proposed Market Withdrawal – Update] {{Webarchive|url=https://web.archive.org/web/20120328072841/http://healthcare.utah.edu/pharmacy/alerts/497.htm |date=28 March 2012 }} 10 September 2010.</ref> Shire announced on September 22, 2011, that it was withdrawing completely from supplying midodrine. Midodrine remains available as a [[generic drug]].<ref>{{Cite press release|url=https://www.prnewswire.com/news-releases/shire-provides-update-on-proamatine-midodrine-hcl-130364128.html|title=Shire Provides Update on ProAmatine® (midodrine HCl)| author = Shire plc |website=www.prnewswire.com}}</ref>

==Society and culture==
===Names===
''Midodrine'' is the [[generic term|generic name]] of the drug and its {{Abbrlink|INN|International Nonproprietary Name}}, {{Abbrlink|BAN|British Approved Name}}, and {{Abbrlink|DCF|Dénomination Commune Française}}, while its {{Abbrlink|DCIT|Denominazione Comune Italiana}} is ''midodrina''.<ref name="Elks2014">{{cite book | vauthors = Elks J | title=The Dictionary of Drugs: Chemical Data: Chemical Data, Structures and Bibliographies | publisher=Springer US | year=2014 | isbn=978-1-4757-2085-3 | url=https://books.google.com/books?id=0vXTBwAAQBAJ&pg=PA824 | access-date=30 August 2024 | page=824}}</ref><ref name="MortonHall2012">{{cite book | vauthors = Morton IK, Hall JM | title=Concise Dictionary of Pharmacological Agents: Properties and Synonyms | publisher=Springer Netherlands | year=2012 | isbn=978-94-011-4439-1 | url=https://books.google.com/books?id=tsjrCAAAQBAJ&pg=PA137 | access-date=30 August 2024 | page=137}}</ref><ref name="IndexNominum2004">{{cite book | author=Schweizerischer Apotheker-Verein | title=Index Nominum: International Drug Directory | publisher=Medpharm Scientific Publishers | year=2004 | isbn=978-3-88763-101-7 | url=https://books.google.com/books?id=EgeuA47Ocm4C&pg=PA805 | access-date=30 August 2024 | page=805}}</ref> In the case of the [[hydrochloride]] [[salt (chemistry)|salt]], its generic name is ''midodrine hydrochloride'' and this is its {{Abbrlink|USAN|United States Adopted Name}}, {{Abbrlink|BANM|British Approved Name}}, and {{Abbrlink|JAN|Japanese Accepted Name}}.<ref name="Elks2014" /><ref name="IndexNominum2004" /> The drug is also known by its developmental code names ''ST-1085'' and ''TS-701''.<ref name="Elks2014" /><ref name="IndexNominum2004" /><ref name="Schlesser1990">{{cite book | vauthors = Schlesser JL | title=Drugs Available Abroad: A Guide to Therapeutic Drugs Available and Approved for Use Outside the U. S. | publisher=Gale Research | year=1990 | isbn=978-0-8103-7177-4 | url=https://books.google.com/books?id=2x1tAAAAMAAJ | access-date=30 August 2024 | pages=139,356}}</ref> Midodrine has been sold under brand names including ''Amatine'', ''Gutron'', ''Midamine'', ''Midon'', and ''ProAmatine'', among others.<ref name="Elks2014" /><ref name="IndexNominum2004" />

==Research==
Midodrine was under development for the treatment of [[chronic fatigue syndrome]], but no recent development for this indication has been reported.<ref name="AdisInsight" />

==References==
{{Reflist}}

==External links==
{{Commons category-inline}}

{{Cardiac stimulants excluding cardiac glycosides}}
{{Adrenergic receptor modulators}}
{{Phenethylamines}}
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[[Category:Antihypotensive agents]]
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[[Category:Methoxyphenethylamines]]
[[Category:Peripherally selective drugs]]
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[[Category:Sympathomimetics]]
[[Category:Vasoconstrictors]]