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
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
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 |
DescriptionSources: http://labeling.pfizer.com/ShowLabeling.aspx?id=4429Curator's Comment: Description was created based on several sources, including
https://www.ncbi.nlm.nih.gov/pubmed/21303898
Sources: http://labeling.pfizer.com/ShowLabeling.aspx?id=4429
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.
Approval Year
Targets
Primary Target | Pharmacology | Condition | Potency |
---|---|---|---|
Target ID: CHEMBL2096905 Sources: https://www.ncbi.nlm.nih.gov/pubmed/21303898 |
Conditions
Condition | Modality | Targets | Highest Phase | Product |
---|---|---|---|---|
Primary | DOPAMINE HYDROCHLORIDE Approved UseDopamine 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
Value | Dose | Co-administered | Analyte | Population |
---|---|---|---|---|
1712 ng/mL EXPERIMENT https://www.ncbi.nlm.nih.gov/pubmed/2775615 |
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
Value | Dose | Co-administered | Analyte | Population |
---|---|---|---|---|
2926 ng × h/mL EXPERIMENT https://www.ncbi.nlm.nih.gov/pubmed/2775615 |
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
Value | Dose | Co-administered | Analyte | Population |
---|---|---|---|---|
1.6 h EXPERIMENT https://www.ncbi.nlm.nih.gov/pubmed/2775615 |
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
CYP3A4 | CYP2C9 | CYP2D6 | hERG |
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OverviewOther
Other Inhibitor | Other Substrate | Other Inducer |
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Drug as victim
Target | Modality | Activity | Metabolite | Clinical evidence |
---|---|---|---|---|
Page: - |
yes | |||
Sources: https://pubmed.ncbi.nlm.nih.gov/10386253/ Page: - |
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Sources: https://dmd.aspetjournals.org/content/37/4/768.short Page: - |
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PubMed
Title | Date | PubMed |
---|---|---|
[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 |
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Estrogen priming modulates autoreceptor-mediated potentiation of dopamine uptake. | 2000 Aug 11 |
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A novel phenylaminotetralin (PAT) recognizes histamine H1 receptors and stimulates dopamine synthesis in vivo in rat brain. | 2000 Jan 3 |
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Sulfation of environmental estrogen-like chemicals by human cytosolic sulfotransferases. | 2000 Jan 7 |
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L-Dopa uptake and dopamine production in proximal tubular cells are regulated by beta(2)-adrenergic receptors. | 2000 Jul |
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Role of heme oxygenase-1 in the regulation of manganese superoxide dismutase gene expression in oxidatively-challenged astroglia. | 2000 Oct |
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Comparison between the role of the neuronal and inducible nitric oxide synthase in methamphetamine-induced neurotoxicity and sensitization. | 2000 Sep |
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Repeated adenosine pre-treatment potentiates the acute effect of methamphetamine in rats. | 2000 Sep |
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Dopamine deficiency in mice. | 2000 Sep |
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A hypertensive reaction induced by concurrent use of selegiline and dopamine. | 2000 Sep |
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Role of dopamine D1 and D2 receptors in the micturition reflex in conscious rats. | 2001 |
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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 |
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The reverse transport of DA, what physiological significance? | 2001 Feb |
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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 |
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Inhibition of a Gi-activated potassium channel (GIRK1/4) by the Gq-coupled m1 muscarinic acetylcholine receptor. | 2001 Feb 23 |
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Ascorbic acid increases the yield of dopaminergic neurons derived from basic fibroblast growth factor expanded mesencephalic precursors. | 2001 Jan |
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Nicotinic agonists stimulate acetylcholine release from mouse interpeduncular nucleus: a function mediated by a different nAChR than dopamine release from striatum. | 2001 Jan |
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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 |
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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 |
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Ethanol acts synergistically with a D2 dopamine agonist to cause translocation of protein kinase C. | 2001 Jan |
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Dopamine D2 receptor regulation of the dopamine transporter expressed in Xenopus laevis oocytes is voltage-independent. | 2001 Jan |
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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 |
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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 |
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Autoregulation of dopamine synthesis in subregions of the rat nucleus accumbens. | 2001 Jan 5 |
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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
In Vivo Use Guide
Sources: http://labeling.pfizer.com/ShowLabeling.aspx?id=4429
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
Substance Class |
Chemical
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Record UNII |
VTD58H1Z2X
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Record Status |
Validated (UNII)
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NCI_THESAURUS |
C88516
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13733-1
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DSLD |
4132 (Number of products:1)
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NDF-RT |
N0000007715
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14703-3
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12.4
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2217-8
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2216-0
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44316-8
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15059-9
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C01CA04
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N0000175570
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27212-0
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QC01CA04
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44918-1
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D004298
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DTXSID6022420
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VTD58H1Z2X
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Dopamine (medication)
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200-110-0
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DOPAMINE
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C62025
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100000080782
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m4740
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59905
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940
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Dopamine
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18243
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Related Record | Type | Details | ||
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TRANSPORTER -> SUBSTRATE |
BINDING
IC50
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TARGET -> AGONIST |
Ki
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TARGET -> AGONIST |
Ki
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TARGET -> AGONIST |
D2R concentration levels were significantly lower in AD patients than in healthy controls (SMD = ?1.13, 95%CI: ?1.52 to ?0.74), with low heterogeneity (I2 = 7.80%), when USA studies were considered.
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CONSTITUENT ALWAYS PRESENT -> PARENT |
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TARGET -> AGONIST |
Ki
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TARGET -> AGONIST |
Ki
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METABOLIC ENZYME -> SUBSTRATE |
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TRANSPORTER -> SUBSTRATE |
Ki
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TRANSPORTER -> SUBSTRATE |
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METABOLIC ENZYME -> SUBSTRATE |
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ACTIVATOR OF RELEASE->TARGET |
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METABOLIC ENZYME -> SUBSTRATE |
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SALT/SOLVATE -> PARENT |
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TRANSPORTER -> SUBSTRATE |
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TARGET -> AGONIST |
Ki
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Related Record | Type | Details | ||
---|---|---|---|---|
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METABOLITE -> PARENT |
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PRODRUG -> METABOLITE ACTIVE |
PLASMA; URINE
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PRODRUG -> METABOLITE ACTIVE |
MAJOR
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METABOLITE INACTIVE -> PARENT |
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PRODRUG -> METABOLITE ACTIVE |
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METABOLITE TOXIC -> PARENT |
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PRODRUG -> METABOLITE ACTIVE |
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PARENT -> METABOLITE ACTIVE |
MINOR
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METABOLITE TOXIC -> PARENT |
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PRODRUG -> METABOLITE ACTIVE |
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METABOLITE -> PARENT |
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Related Record | Type | Details | ||
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PARENT -> IMPURITY | |||
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PARENT -> IMPURITY |
CHROMATOGRAPHIC PURITY (HPLC/UV)
EP
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Related Record | Type | Details | ||
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ACTIVE MOIETY |
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