Midodrine: Difference between revisions
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'''|Bull |
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'' |
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| verifiedrevid = 462252266 |
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| IUPAC_name = (''RS'')- ''N''-[2-(2,5-dimethoxyphenyl)-2-hydroxyethyl]glycinamide |
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| image = Midodrine.svg |
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| width = 200px |
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| imagename = 1 : 1 mixture (racemate) |
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| drug_name = Midodrine |
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<!--Clinical data--> |
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| tradename = Proamatine |
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| Drugs.com = {{drugs.com|monograph|midodrine-hydrochloride}} |
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| MedlinePlus = a602023 |
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<!--Identifiers--> |
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| CASNo_Ref = {{cascite|correct|CAS}} |
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| CAS_number_Ref = {{cascite|correct|??}} |
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| CAS_number = 133163-28-7 |
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| ATC_prefix = C01 |
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| ATC_suffix = CA17 |
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| PubChem = 4195 |
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| DrugBank_Ref = {{drugbankcite|correct|drugbank}} |
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| DrugBank = DB00211 |
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| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}} |
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| ChemSpiderID = 4050 |
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| UNII_Ref = {{fdacite|correct|FDA}} |
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| UNII = 6YE7PBM15H |
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| KEGG_Ref = {{keggcite|correct|kegg}} |
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| KEGG = D08220 |
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| ChEBI_Ref = {{ebicite|correct|EBI}} |
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| ChEBI = 6933 |
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| ChEMBL_Ref = {{ebicite|changed|EBI}} |
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| ChEMBL = 1076 |
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<!--Chemical data--> |
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| C=12 | H=18 | N=2 | O=4 |
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| molecular_weight = 254.282 g/mol |
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| smiles = O=C(NCC(O)c1cc(OC)ccc1OC)CN |
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| InChI = 1/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) |
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| InChIKey = PTKSEFOSCHHMPD-UHFFFAOYAG |
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| StdInChI_Ref = {{stdinchicite|correct|chemspider}} |
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| 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) |
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| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}} |
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| StdInChIKey = PTKSEFOSCHHMPD-UHFFFAOYSA-N |
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| synonyms = <small>2-amino-''N''-[2-(2,5-dimethoxyphenyl)-2-hydroxy-ethyl]-acetamide</small> |
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}} |
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'''Midodrine''' (brand names '''Amatine''', '''ProAmatine''', '''Gutron''') is a [[vasopressor]]/[[antihypotensive]] agent. Midodrine was approved in the United States by the [[Food and Drug Administration]] (FDA) in 1996 for the treatment of [[dysautonomia]] and [[orthostatic hypotension]]. In August 2010, the FDA proposed withdrawing this approval because the manufacturer, [[Shire plc]], has failed to complete required studies after the medicine reached the market.<ref>[http://uk.reuters.com/article/idUKTRE67F3SE20100816 U.S. proposes withdrawal of Shire hypotension drug], Aug 16, 2010.</ref><ref>{{cite web|last=O'Riordan|first=Michael|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|accessdate=1 April 2011}}.</ref> |
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In September 2010, the FDA reversed its decision to remove Midodrine from the market and has allowed it to remain available to patients while Shire plc collects 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] September 10, 2010.</ref> Shire plc announced on September 27, 2011 that it was continuing the process to work with the FDA towards a final approval of the drug.<ref>[http://www.sacbee.com/2011/09/22/3930671/shire-provides-update-on-proamatine.html Shire Announces Update on ProAmatime] September 27, 2011.</ref> |
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==Chemical properties== |
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Midodrine is an odorless, white, crystalline powder, soluble in water and sparingly soluble in [[methanol]]. |
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==Mechanism of action== |
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Midodrine is a [[prodrug]] which forms an active [[metabolite]], desglymidodrine, which is an [[Alpha-1 adrenergic receptor|α<sub>1</sub>-receptor]] [[agonist]] and exerts its actions via activation of the [[alpha-adrenergic receptor]]s of the arteriolar and venous vasculature, producing an increase in vascular tone and elevation of blood pressure. Desglymidodrine does not stimulate cardiac [[beta-adrenergic receptor]]s. Desglymidodrine diffuses poorly across the [[blood–brain barrier]], and is therefore not associated with effects on the [[central nervous system]]. |
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[[File:Desglymidodrine.svg|thumb|none|Metabolite desglymidodrine]]{{clear left}} |
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==Metabolism== |
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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 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 4 hours. The absolute bioavailability of midodrine (measured as desglymidodrine) is 93%. |
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==Indications== |
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Midodrine hydrochloride tablets are 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]].<ref>{{cite journal|last1=Izcovich|first1=A.|last2=Gonzalez Malla|first2=C.|last3=Manzotti|first3=M.|last4=Catalano|first4=H. N.|last5=Guyatt|first5=G.|title=Midodrine for orthostatic hypotension and recurrent reflex syncope: A systematic review|journal=Neurology|date=22 August 2014|volume=83|issue=13|pages=1170–1177|doi=10.1212/WNL.0000000000000815|pmid=25150287}}</ref> Small studies have also shown that midodrine can be used to prevent excessive drops in blood pressure in people requiring [[dialysis]].<ref>{{cite journal|last1=Prakash|first1=S|last2=Garg|first2=AX|last3=Heidenheim|first3=AP|last4=House|first4=AA|title=Midodrine appears to be safe and effective for dialysis-induced hypotension: a systematic review.|journal=Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association|date=Oct 2004|volume=19|issue=10|pages=2553–8|doi=10.1093/ndt/gfh420|pmid=15280522|url=http://ndt.oxfordjournals.org/content/19/10/2553.long}}</ref> |
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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|last1=Karwa|first1=R.|last2=Woodis|first2=C B.|title=Midodrine and Octreotide in Treatment of Cirrhosis-Related Hemodynamic Complications|journal=Annals of Pharmacotherapy|date=31 March 2009|volume=43|issue=4|pages=692–699|doi=10.1345/aph.1L373|pmid=19299324}}</ref> |
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==Contraindications== |
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Midodrine is contraindicated in patients with severe organic heart disease, acute renal disease, urinary retention, pheochromocytoma or thyrotoxicosis. Midodrine should not be used in patients with persistent and excessive supine hypertension. |
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==Side effects== |
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Headache; feeling of pressure/fullness in the head, vasodilation/flushing face, confusion/thinking abnormality, dry mouth; nervousness/anxiety and rash.{{Citation needed|date=August 2010}} |
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==See also== |
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* [[Lisdexamphetamine]] |
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==References== |
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{{Reflist}} |
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==External links== |
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* [http://www.drugs.com/pro/midodrine.html Midodrine] at drugs.com |
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{{Adrenergic agonists}} |
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{{Adrenergic and dopaminergic agents}} |
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[[Category:Alpha-adrenergic agonists]] |
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[[Category:Cardiac stimulants]] |
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[[Category:Phenethylamines]] |
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[[Category:Prodrugs]] |
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[[Category:Phenol ethers]] |
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[[Category:Acetamides]] |
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Revision as of 15:37, 1 December 2014
{{Drugbox |Bull