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Details

Stereochemistry ACHIRAL
Molecular Formula C8H11NO2
Molecular Weight 153.1784
Optical Activity NONE
Defined Stereocenters 0 / 0
E/Z Centers 0
Charge 0

SHOW SMILES / InChI
Structure of DOPAMINE

SMILES

NCCC1=CC=C(O)C(O)=C1

InChI

InChIKey=VYFYYTLLBUKUHU-UHFFFAOYSA-N
InChI=1S/C8H11NO2/c9-4-3-6-1-2-7(10)8(11)5-6/h1-2,5,10-11H,3-4,9H2

HIDE SMILES / InChI

Molecular Formula C8H11NO2
Molecular Weight 153.1784
Charge 0
Count
Stereochemistry ACHIRAL
Additional Stereochemistry No
Defined Stereocenters 0 / 0
E/Z Centers 0
Optical Activity NONE

Description
Curator's Comment: Description was created based on several sources, including https://www.ncbi.nlm.nih.gov/pubmed/21303898

Dopamine, a sympathomimetic amine vasopressor, is the naturally occurring immediate precursor of norepinephrine. G protein-coupled dopamine receptors (D1, D2, D3, D4, and D5) mediate all of the physiological functions of the catecholaminergic neurotransmitter dopamine, ranging from voluntary movement and reward to hormonal regulation and hypertension. Dopamine HCl is indicated for the correction of hemodynamic imbalances present in the shock syndrome due to myocardial infarction, trauma, endotoxic septicemia, open-heart surgery, renal failure, and chronic cardiac decompensation as in congestive failure.

Originator

Curator's Comment: reference retrieved from https://link.springer.com/chapter/10.1007%2F978-3-642-56051-4_2 | http://www.drugfuture.com/chemdata/dopamine.html

Approval Year

Targets

Targets

Primary TargetPharmacologyConditionPotency
Conditions

Conditions

ConditionModalityTargetsHighest PhaseProduct
Primary
DOPAMINE HYDROCHLORIDE

Approved Use

Dopamine HCl is indicated for the correction of hemodynamic imbalances present in the shock syndrome due to myocardial infarction, trauma, endotoxic septicemia, open-heart surgery, renal failure, and chronic cardiac decompensation as in congestive failure. Patients most likely to respond adequately to dopamine HCl are those in whom physiological parameters, such as urine flow, myocardial function, and blood pressure, have not undergone profound deterioration. Multiclinic trials indicate that the shorter the time interval between onset of signs and symptoms and initiation of therapy with blood volume correction and dopamine HCl, the better the prognosis. Where appropriate, blood volume restoration with a suitable plasma expander or whole blood should be accomplished prior to administration of dopamine HCl. Poor Perfusion of Vital Organs – Urine flow appears to be one of the better diagnostic signs by which adequacy of vital organ perfusion can be monitored. Nevertheless, the physician should also observe the patient for signs of reversal of confusion or reversal of comatose condition. Loss of pallor, increase in toe temperature, and/or adequacy of nail bed capillary filling may also be used as indices of adequate dosage. Clinical studies have shown that when dopamine HCl is administered before urine flow has diminished to levels of approximately 0.3 mL/minute, prognosis is more favorable. Nevertheless, in a number of oliguric or anuric patients, administration of dopamine HCl has resulted in an increase in urine flow, which in some cases reached normal levels. Dopamine HCl may also increase urine flow in patients whose output is within normal limits and thus may be of value in reducing the degree of pre-existing fluid accumulation. It should be noted that at doses above those optimal for the individual patient, urine flow may decrease, necessitating reduction of dosage. Low Cardiac Output – Increased cardiac output is related to dopamine’s direct inotropic effect on the myocardium. Increased cardiac output at low or moderate doses appears to be related to a favorable prognosis. Increase in cardiac output has been associated with either static or decreased systemic vascular resistance (SVR). Static or decreased SVR associated with low or moderate movements in cardiac output is believed to be a reflection of differential effects on specific vascular beds with increased resistance in peripheral beds (e.g., femoral) and concomitant decreases in mesenteric and renal vascular beds. Redistribution of blood flow parallels these changes so that an increase in cardiac output is accompanied by an increase in mesenteric and renal blood flow. In many instances the renal fraction of the total cardiac output has been found to increase. Increase in cardiac output produced by dopamine is not associated with substantial decreases in systemic vascular resistance as may occur with isoproterenol. Hypotension – Hypotension due to inadequate cardiac output can be managed by administration of low to moderate doses of dopamine HCl which have little effect on SVR. At high therapeutic doses, dopamine’s alpha-adrenergic activity becomes more prominent and thus may correct hypotension due to diminished SVR. As in the case of other circulatory decompensation states, prognosis is better in patients whose blood pressure and urine flow have not undergone profound deterioration. Therefore, it is suggested that the physician administer dopamine HCl as soon as a definite trend toward decreased systolic and diastolic pressure becomes evident.
Cmax

Cmax

ValueDoseCo-administeredAnalytePopulation
1712 ng/mL
250 mg single, oral
dose: 250 mg
route of administration: Oral
experiment type: SINGLE
co-administered:
DOPAMINE plasma
Homo sapiens
population: HEALTHY
age: ADULT
sex: MALE
food status: FASTED
AUC

AUC

ValueDoseCo-administeredAnalytePopulation
2926 ng × h/mL
250 mg single, oral
dose: 250 mg
route of administration: Oral
experiment type: SINGLE
co-administered:
DOPAMINE plasma
Homo sapiens
population: HEALTHY
age: ADULT
sex: MALE
food status: FASTED
T1/2

T1/2

ValueDoseCo-administeredAnalytePopulation
1.6 h
250 mg single, oral
dose: 250 mg
route of administration: Oral
experiment type: SINGLE
co-administered:
DOPAMINE plasma
Homo sapiens
population: HEALTHY
age: ADULT
sex: MALE
food status: FASTED
Overview

Overview

CYP3A4CYP2C9CYP2D6hERG

OverviewOther

Other InhibitorOther SubstrateOther Inducer





Drug as victim
Sourcing

Sourcing

Vendor/AggregatorIDURL
PubMed

PubMed

TitleDatePubMed
[Pharmacological studies of antipsychotic drug, penfluridol. 2. General pharmacological properties].
1976 Jul
Kappa-opioid receptor activation prevents alterations in mesocortical dopamine neurotransmission that occur during abstinence from cocaine.
2000
Estrogen priming modulates autoreceptor-mediated potentiation of dopamine uptake.
2000 Aug 11
A novel phenylaminotetralin (PAT) recognizes histamine H1 receptors and stimulates dopamine synthesis in vivo in rat brain.
2000 Jan 3
Sulfation of environmental estrogen-like chemicals by human cytosolic sulfotransferases.
2000 Jan 7
L-Dopa uptake and dopamine production in proximal tubular cells are regulated by beta(2)-adrenergic receptors.
2000 Jul
Role of heme oxygenase-1 in the regulation of manganese superoxide dismutase gene expression in oxidatively-challenged astroglia.
2000 Oct
Comparison between the role of the neuronal and inducible nitric oxide synthase in methamphetamine-induced neurotoxicity and sensitization.
2000 Sep
Repeated adenosine pre-treatment potentiates the acute effect of methamphetamine in rats.
2000 Sep
Dopamine deficiency in mice.
2000 Sep
A hypertensive reaction induced by concurrent use of selegiline and dopamine.
2000 Sep
Role of dopamine D1 and D2 receptors in the micturition reflex in conscious rats.
2001
SCH 23390 affords protection against soman-evoked seizures in the freely moving guinea-pig: a concomitant neurochemical, electrophysiological and behavioural study.
2001
Identification of the aromatic L-amino acid decarboxylase (AADC) gene and its expression in the attachment and metamorphosis of the barnacle, Balanus amphitrite.
2001 Feb
The reverse transport of DA, what physiological significance?
2001 Feb
Neurotensin gene expression and behavioral responses following administration of psychostimulants and antipsychotic drugs in dopamine D(3) receptor deficient mice.
2001 Feb
Pharmacology and behavioral pharmacology of the mesocortical dopamine system.
2001 Feb
Inhibition of a Gi-activated potassium channel (GIRK1/4) by the Gq-coupled m1 muscarinic acetylcholine receptor.
2001 Feb 23
Ascorbic acid increases the yield of dopaminergic neurons derived from basic fibroblast growth factor expanded mesencephalic precursors.
2001 Jan
Nicotinic agonists stimulate acetylcholine release from mouse interpeduncular nucleus: a function mediated by a different nAChR than dopamine release from striatum.
2001 Jan
N-methyl-D-aspartate receptors mediating hippocampal noradrenaline and striatal dopamine release display differential sensitivity to quinolinic acid, the HIV-1 envelope protein gp120, external pH and protein kinase C inhibition.
2001 Jan
Neurotrophic and neurotoxic effects of nitric oxide on fetal midbrain cultures.
2001 Jan
Radiosynthesis of [123I]betaCIT, a selective ligand for the study of the dopaminergic and serotoninergic systems in human brain.
2001 Jan
D2 receptor imaging in neonates using I-123 iodobenzamide brain SPECT.
2001 Jan
Characterization of acute inhibition of Na/H exchanger NHE-3 by dopamine in opossum kidney cells.
2001 Jan
The subthalamic nucleus, hemiballismus and Parkinson's disease: reappraisal of a neurosurgical dogma.
2001 Jan
Catecholaminergic regulation of Na-K-Cl cotransport in pigmented ciliary epithelium: differences between PE and NPE.
2001 Jan
Ethanol acts synergistically with a D2 dopamine agonist to cause translocation of protein kinase C.
2001 Jan
Dopamine D2 receptor regulation of the dopamine transporter expressed in Xenopus laevis oocytes is voltage-independent.
2001 Jan
Biochemical and immunohistological changes in the brain of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mouse.
2001 Jan
A study of the binding requirements of calyculin A and dephosphonocalyculin A with PP1, development of a molecular recognition model for the binding interactions of the okadaic acid class of compounds with PP1.
2001 Jan
Iboga interactions with psychomotor stimulants: panacea in the paradox?
2001 Jan
Regulation by the medial amygdala of copulation and medial preoptic dopamine release.
2001 Jan 1
Glutaredoxin protects cerebellar granule neurons from dopamine-induced apoptosis by activating NF-kappa B via Ref-1.
2001 Jan 12
M100,907, a selective 5-HT(2A) antagonist, attenuates dopamine release in the rat medial prefrontal cortex.
2001 Jan 5
Autoregulation of dopamine synthesis in subregions of the rat nucleus accumbens.
2001 Jan 5
Activation of dopamine D(1)-like receptor causes phosphorylation of alpha(1)-subunit of Na(+),K(+)-ATPase in rat renal proximal tubules.
2001 Jan 5
Helium-oxygen pressure induces striatal glutamate increase: a microdialysis study in freely-moving rats.
2001 Jan 5
Indirubins inhibit glycogen synthase kinase-3 beta and CDK5/p25, two protein kinases involved in abnormal tau phosphorylation in Alzheimer's disease. A property common to most cyclin-dependent kinase inhibitors?
2001 Jan 5
Early ultrastructural findings and superoxide dismutase levels in experimental ischemic optic neuropathy: effect of hypertension and hypotension on ischemic changes.
2001 Jan-Feb
Patents

Sample Use Guides

Rate of Administration – Dopamine Hydrochloride Injection, USP after dilution, is administered intravenously by infusion via a suitable I.V. catheter or needle. When administering Dopamine Hydrochloride (or any potent medication) by continuous intravenous infusion, it is advisable to use a precision volume control I.V. set. Each patient must be individually titrated to the desired hemodynamic or renal response to dopamine. In titrating to the desired increase in systolic blood pressure, the optimum dosage rate for renal response may be exceeded, thus necessitating a reduction in rate after the hemodynamic condition is stabilized. Administration at rates greater than 50 mcg/kg/min have safely been used in advanced circulatory decompensation states. If unnecessary fluid expansion is of concern, adjustment of drug concentration may be preferred over increasing the flow rate of a less concentrated dilution. Suggested Regimen: 1. When appropriate, increase blood volume with whole blood or plasma until central venous pressure is 10 to 15 cm H2O or pulmonary wedge pressure is 14 to 18 mm Hg. 2. Begin infusion of diluted solution at doses of 2 – 5 mcg/kg/min of Dopamine Hydrochloride in patients who are likely to respond to modest increments of heart force and renal perfusion. In more seriously ill patients, begin infusion of diluted solution at doses of 5 mcg/kg/min of Dopamine Hydrochloride and increase gradually using 5 to 10 mcg/kg/min increments up to a rate of 20 to 50 mcg/kg/min as needed. If doses in excess of 50 mcg/kg/min are required, it is advisable to check urine output frequently. Should urinary flow begin to decrease in the absence of hypotension, reduction of dopamine dosage should be considered. Multiclinic trials have shown that more than 50 percent of patients have been satisfactorily maintained on doses less than 20 mcg/kg/min. In patients who do not respond to these doses with adequate arterial pressures or urine flow, additional increments of dopamine may be given in an effort to produce an appropriate arterial pressure and central perfusion. 3. Treatment of all patients requires constant evaluation of therapy in terms of blood volume, augmentation of cardiac contractility, and distribution of peripheral perfusion. Dosage of dopamine should be adjusted according to the patient’s response, with particular attention to diminution of established urine flow rate, increasing tachycardia or development of new dysrhythmias as indices for decreasing or temporarily suspending the dosage. 4. As with all potent intravenously administered drugs, care should be taken to control the rate of administration to avoid inadvertent administration of a bolus of the drug. Parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration, whenever solution and container permit.
Route of Administration: Intravenous
In Vitro Use Guide
Unknown
Substance Class Chemical
Created
by admin
on Mon Mar 31 17:48:27 GMT 2025
Edited
by admin
on Mon Mar 31 17:48:27 GMT 2025
Record UNII
VTD58H1Z2X
Record Status Validated (UNII)
Record Version
  • Download
Name Type Language
MEDOPA
Preferred Name English
DOPAMINE
HSDB   INN   MI   VANDF   WHO-DD  
INN  
Official Name English
4-(2-AMINOETHYL)PYROCATECHOL
Systematic Name English
NORADRENALINE TARTRATE IMPURITY C [EP IMPURITY]
Common Name English
DOBUTAMINE A
Common Name English
DOBUTAMINE HYDROCHLORIDESPECIFIED IMPURITY A [EP IMPURITY]
Common Name English
dopamine [INN]
Common Name English
A-DOPAMINE
Common Name English
DOPAMINE [VANDF]
Common Name English
HYDROXYTYRAMINE
Systematic Name English
OXYTYRAMINE
Common Name English
DOPAMINE [MI]
Common Name English
Dopamine [WHO-DD]
Common Name English
1,2-BENZENEDIOL, 4-(2-AMINOETHYL)-
Systematic Name English
DOBUTAMINE HYDROCHLORIDE IMPURITY A [EP IMPURITY]
Common Name English
NSC-173182
Code English
DOPAMINE [HSDB]
Common Name English
Classification Tree Code System Code
NCI_THESAURUS C88516
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LOINC 13733-1
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DSLD 4132 (Number of products:1)
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NDF-RT N0000007715
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LOINC 14703-3
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LOINC 15058-1
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LOINC 25906-9
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WHO-ESSENTIAL MEDICINES LIST 12.4
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LOINC 2217-8
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LOINC 24524-1
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LOINC 2218-6
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LOINC 2216-0
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LOINC 44316-8
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LOINC 15059-9
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WHO-ATC C01CA04
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LOINC 33873-1
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LOINC 74904-4
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NDF-RT N0000175570
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LOINC 27212-0
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WHO-VATC QC01CA04
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LOINC 44918-1
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Code System Code Type Description
MESH
D004298
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PRIMARY
EPA CompTox
DTXSID6022420
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PRIMARY
DAILYMED
VTD58H1Z2X
Created by admin on Mon Mar 31 17:48:27 GMT 2025 , Edited by admin on Mon Mar 31 17:48:27 GMT 2025
PRIMARY
WIKIPEDIA
Dopamine (medication)
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PRIMARY
ECHA (EC/EINECS)
200-110-0
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PRIMARY
WIKIPEDIA
DOPAMINE
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PRIMARY
NCI_THESAURUS
C62025
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PRIMARY
SMS_ID
100000080782
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PRIMARY
PUBCHEM
681
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PRIMARY
HSDB
3068
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PRIMARY
ChEMBL
CHEMBL59
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PRIMARY
FDA UNII
VTD58H1Z2X
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PRIMARY
RXCUI
3628
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PRIMARY RxNorm
MERCK INDEX
m4740
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PRIMARY Merck Index
CHEBI
59905
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PRIMARY
IUPHAR
940
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PRIMARY
NSC
173182
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PRIMARY
LACTMED
Dopamine
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PRIMARY
INN
2417
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PRIMARY
DRUG BANK
DB00988
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PRIMARY
CAS
51-61-6
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PRIMARY
DRUG CENTRAL
947
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PRIMARY
EVMPD
SUB06365MIG
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PRIMARY
CHEBI
18243
Created by admin on Mon Mar 31 17:48:27 GMT 2025 , Edited by admin on Mon Mar 31 17:48:27 GMT 2025
PRIMARY
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