Midodrine

Midodrine

Clinical data
Trade names	Proamatine
AHFS/Drugs.com	Monograph
MedlinePlus	a602023
ATC code	C01CA17 (WHO)
Identifiers
IUPAC name (RS)- N-[2-(2,5-Dimethoxyphenyl)-2-hydroxyethyl]glycinamide
Synonyms	2-amino-N-[2-(2,5-dimethoxyphenyl)-2-hydroxy-ethyl]-acetamide
CAS Number	133163-28-7 Y
PubChem CID	4195
IUPHAR/BPS	7240
DrugBank	DB00211 Y
ChemSpider	4050 Y
UNII	6YE7PBM15H
KEGG	D08220 Y
ChEBI	CHEBI:6933 Y
ChEMBL	CHEMBL1076 N
Chemical and physical data
Formula	C12H18N2O4
Molar mass	254.282 g/mol
3D model (Jmol)	Interactive image
Chirality	Racemic mixture
SMILES O=C(NCC(O)c1cc(OC)ccc1OC)CN
InChI InChI=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) Y Key:PTKSEFOSCHHMPD-UHFFFAOYSA-N Y
NY (what is this?)

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.

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. 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.

Midodrine is an odorless, white, crystalline powder, soluble in water and sparingly soluble in methanol.

Midodrine is a prodrug which forms an active metabolite, desglymidodrine, which is an α₁-receptor agonist and exerts its actions via activation of the alpha-adrenergic receptors of the arteriolar and venous vasculature, producing an increase in vascular tone and elevation of blood pressure. Desglymidodrine does not stimulate cardiac beta-adrenergic receptors. Desglymidodrine diffuses poorly across the blood–brain barrier, and is therefore not associated with effects on the central nervous system.

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%.