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Details

Stereochemistry ACHIRAL
Molecular Formula C8H11NO2.BrH
Molecular Weight 234.09
Optical Activity NONE
Defined Stereocenters 0 / 0
E/Z Centers 0
Charge 0

SHOW SMILES / InChI
Structure of Dopamine hydrobromide

SMILES

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

InChI

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

HIDE SMILES / InChI

Molecular Formula BrH
Molecular Weight 80.912
Charge 0
Count
Stereochemistry ACHIRAL
Additional Stereochemistry No
Defined Stereocenters 0 / 0
E/Z Centers 0
Optical Activity NONE

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
Role of dopamine D1 and D2 receptors in the micturition reflex in conscious rats.
2001
The effects of nitric oxide on the oxidations of l-dopa and dopamine mediated by tyrosinase and peroxidase.
2001 Apr 6
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
Lymphocyte populations in Parkinson's disease and in rat models of parkinsonism.
2001 Feb 1
Organization and neurochemistry of vagal preganglionic neurons innervating the lower esophageal sphincter in ferrets.
2001 Feb 5
Dopamine D-1/D-5 receptor activation is required for long-term potentiation in the rat neostriatum in vitro.
2001 Jan
Association analysis of a functional catechol-o-methyltransferase gene polymorphism in schizophrenic patients in Taiwan.
2001 Jan
Monoamine compounds in cerebrospinal fluid of healthy subjects punctured without preceding strict bed rest: a pilot study.
2001 Jan
The effects of water-odor preference conditioning in the preadolescent nucleus accumbens septi.
2001 Jan
In vivo measurement of haloperidol affinity to dopamine D2/D3 receptors by [123I]IBZM and single photon emission computed tomography.
2001 Jan
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
Investigation of non-linear properties of multichannel EEG in the early stages of Parkinson's disease.
2001 Jan
Changes of biogenic amine levels in haemolymph during diapausing and non-diapausing status in Pieris brassicae L.
2001 Jan
Characterization of acute inhibition of Na/H exchanger NHE-3 by dopamine in opossum kidney cells.
2001 Jan
Dopamine induces ERK activation in renal epithelial cells through H2O2 produced by monoamine oxidase.
2001 Jan
The central aromatic amino acid DOPA decarboxylase inhibitor, NSD-1015, does not inhibit L-DOPA-induced circling in unilateral 6-OHDA-lesioned-rats.
2001 Jan
Colocalization of tyrosine hydroxylase and GAD65 mRNA in mesostriatal neurons.
2001 Jan
Injury induced c-Jun expression and phosphorylation in the dopaminergic nigral neurons of the rat: correlation with neuronal death and modulation by glial-cell-line-derived neurotrophic factor.
2001 Jan
Alteration of catecholamines in pheochromocytoma (PC12) cells in vitro by the metabolites of chlorotriazine herbicide.
2001 Jan
Adenosine activates aromatic L-amino acid decarboxylase activity in the kidney and increases dopamine.
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
The antidepressant-sensitive dopamine transporter in Drosophila melanogaster: a primordial carrier for catecholamines.
2001 Jan
Effect of inhibition of MAO and COMT on intrarenal dopamine and serotonin and on renal function.
2001 Jan
Effects of hyperprolactinemia on rat prostate growth: evidence of androgeno-dependence.
2001 Jan
Pharmacological agents for the treatment of urinary incontinence due to overactive bladder.
2001 Jan
Regulation by the medial amygdala of copulation and medial preoptic dopamine release.
2001 Jan 1
Motivational effects of ethanol in DARPP-32 knock-out mice.
2001 Jan 1
Prepulse inhibition deficits and perseverative motor patterns in dopamine transporter knock-out mice: differential effects of D1 and D2 receptor antagonists.
2001 Jan 1
Characterization of extracellular dopamine clearance in the medial prefrontal cortex: role of monoamine uptake and monoamine oxidase inhibition.
2001 Jan 1
Toxic effects of apomorphine on rat cultured neurons and glial C6 cells, and protection with antioxidants.
2001 Jan 1
Nicotine prevents striatal dopamine loss produced by 6-hydroxydopamine lesion in the substantia nigra.
2001 Jan 12
The human dopamine transporter gene: the 5'-flanking region reveals five diallelic polymorphic sites in a Caucasian population sample.
2001 Jan 12
M100,907, a selective 5-HT(2A) antagonist, attenuates dopamine release in the rat medial prefrontal cortex.
2001 Jan 5
Striatal preprotachykinin mRNA levels are regulated by stimulatory agents and dopamine D1 receptor manipulation in rodent organotypic slice cultures.
2001 Jan 5
Autoregulation of dopamine synthesis in subregions of the rat nucleus accumbens.
2001 Jan 5
The effects of LY393613, nimodipine and verapamil, in focal cerebral ischaemia.
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
Early ultrastructural findings and superoxide dismutase levels in experimental ischemic optic neuropathy: effect of hypertension and hypotension on ischemic changes.
2001 Jan-Feb
Gyroxin fails to modify in vitro release of labelled dopamine and acetylcholine from rat and mouse striatal tissue.
2001 Jun
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 Sat Dec 16 09:22:08 GMT 2023
Edited
by admin
on Sat Dec 16 09:22:08 GMT 2023
Record UNII
MT86RG32QV
Record Status Validated (UNII)
Record Version
  • Download
Name Type Language
Dopamine hydrobromide
Systematic Name English
NSC-44457
Code English
3,4-Dihydroxy-phenethylamine hydrobromide
Systematic Name English
1,2-Benzenediol, 4-(2-aminoethyl)-, hydrobromide
Common Name English
1,2-Benzenediol, 4-(2-aminoethyl)-, hydrobromide (1:1)
Systematic Name English
Pyrocatechol, 4-(2-aminoethyl)-, hydrobromide
Systematic Name English
3-Hydroxytyramine hydrobromide
Systematic Name English
Code System Code Type Description
EPA CompTox
DTXSID20214748
Created by admin on Sat Dec 16 09:22:08 GMT 2023 , Edited by admin on Sat Dec 16 09:22:08 GMT 2023
PRIMARY
CAS
645-31-8
Created by admin on Sat Dec 16 09:22:08 GMT 2023 , Edited by admin on Sat Dec 16 09:22:08 GMT 2023
PRIMARY
PUBCHEM
71564
Created by admin on Sat Dec 16 09:22:08 GMT 2023 , Edited by admin on Sat Dec 16 09:22:08 GMT 2023
PRIMARY
ECHA (EC/EINECS)
211-436-8
Created by admin on Sat Dec 16 09:22:08 GMT 2023 , Edited by admin on Sat Dec 16 09:22:08 GMT 2023
PRIMARY
NSC
44457
Created by admin on Sat Dec 16 09:22:08 GMT 2023 , Edited by admin on Sat Dec 16 09:22:08 GMT 2023
PRIMARY
FDA UNII
MT86RG32QV
Created by admin on Sat Dec 16 09:22:08 GMT 2023 , Edited by admin on Sat Dec 16 09:22:08 GMT 2023
PRIMARY