Noradrenaline

169.18

169.18

4231961

205-750-4

X4W3ENH1CV

757246

DTXSID5023378

C2321

Colorless microcrystals

C01CA03|C - Cardiovascular system

2922509090

86.7

-1.24

off-white to tan crystalline

1.4±0.1 g/cm3

217 °C (decomp)

442.6±40.0 °C at 760 mmHg

221.5±27.3 °C

1.659

soluble in alkali and dilute hydrochloric acid. Slightly soluble in water, ethanol anddiethyl ether.

2-8°C

7.5X10-8 mm Hg at 25 deg C (est)

dni-hmn:oth 5800 nmol/L CNREA8 40,1414,80

D25 -37.3° (c = 5 in water with 1 equiv HCl)

8.58None

Henry's Law constant = 3.2X10-19 atm-cu m/mol at 25 °C (est)

8.58|pKa = 8.58 (conjugate acid)|pKa1 = 8.64; pKa2 = 9.70|pKa1 = 8.55 (phenol); pKa2 = 10.32 (amine); pKa3 = 13.49 (phenol) (est)

137.3 Ų [M+H-H2O]+ [CCS Type: DT, Method: single field calibrated with Agilent tune mix (Agilent)]|136.8 Ų [M+H-H2O]+ [CCS Type: DT, Method: single field calibrated with Agilent tune mix (Agilent)]|131.99 Ų [M-H]- [CCS Type: DT, Method: single field calibrated with Agilent tune mix (Agilent)]|137.2 Ų [M-H2O+H]+ [CCS Type: DT, Method: single field calibrated with ESI Low Concentration Tuning Mix (Agilent)]|134.2 Ų [M-H]- [CCS Type: DT, Method: single field calibrated with ESI Low Concentration Tuning Mix (Agilent)]|132.6 Ų [M+H-H2O]+ [CCS Type: TW, Method: calibrated with polyalanine and drug standards]|134.4 Ų [M-H]-

Hydroxyl radical reaction rate constant = 9.5X10-11 cu cm/molec-sec at 25 °C (est)

II

6.1

UN 2811 6.1/PG 2

3

26/27/28-34-11-28

28-36/37-45-36/37/39-26-16-20

DN5950000

T+,C,F

Stable, but may be light-sensitive. Incompatible with acids, bases, oxidizing agents. Store at -20C.

P260-P264-P280-P284-P302 + P350-P310

H300-H310-H330

SRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.|SRP: At the time of review, regulatory criteria for small quantity disposal are subject to significant revision, however, household quantities of waste pharmaceuticals may be managed as follows: Mix with wet cat litter or coffee grounds, double bag in plastic, discard in trash.

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, incl norepinephrine bitartrate, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Norepinephrine bitartrate/

|Danger|H300 (97.78%): Fatal if swallowed [Danger Acute toxicity, oral]|P260, P262, P264, P270, P271, P280, P284, P301+P310, P302+P350, P304+P340, P310, P320, P321, P322, P330, P361, P363, P403+P233, P405, and P501|Aggregated GHS information provided by 45 companies from 3 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Wear approved respiratory protection, chemically compatible gloves and protective clothing. /Norepinephrine bitartrate/

This material is assumed to be combustible. /Norepinephrine bitartrate/

Water spray, dry chemical, carbon dioxide or foam as appropriate for surrounding fire and materials. This material is assumed to be combustible. As with all dry powders it is advisable to ground mechanical equipment in contact with dry material to dissipate the potential buildup of static electricity. As with all fires, evacuate personnel to a safe area. Firefighters should use self-contained breathing equipment and protective clothing. /Norepinephrine bitartrate/

Wipe up spillage or collect spillage using a high efficiency vacuum cleaner. Avoid breathing dust. Place spillage in appropriately-labelled container for disposal. Wash spill site. /Norepinephrine bitartrate/

SRP: The scientific literature for the use of contact lenses by industrial workers is inconsistent. The benefits or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.

Eye, skin, ... and/or respiratory tract irritation. /Norepinephrine bitartrate/

In high dose and especially when it is combined with other vasopressors, it can lead to limb ischemia and limb death.

Cyclopropane and halothane anesthetics increase cardiac autonomic irritability and therefore seem to sensitize the myocardium to the action of intravenously administered epinephrine or norepinephrine bitartrate injection. Hence, the use of norepinephrine bitartrate injection during cyclopropane and halothane anesthesia is generally considered contraindicated because of the risk of producing ventricular tachycardia or fibrillation.|Enhanced pressor response may occur in patients taking monoamine oxidase (MAO) inhibitors owing to inhibition of neuronal metabolic degradation.|Administration of furosemide or other diuretics may decrease arterial responsiveness to pressor drugs such as norepinephrine.|Tricyclic antidepressants (e.g., imipramine), some antihistamines (especially diphenhydramine, tripelennamine, and dexchlorpheniramine), parenteral ergot alkaloids, guanethidine, or methyldopa may potentiate the pressor effects of norepinephrine, resulting in severe, prolonged hypertension. Norepinephrine should be given cautiously and in small doses to patients receiving these drugs. Potentiation may result from inhibition of tissue uptake of norepinephrine or by increased adrenoreceptor sensitivity to the drug. Monoamine oxidase (MAO) is one of the enzymes responsible for norepinephrine metabolism. Although some clinicians have reported that MAO inhibitors do not appear to potentiate the effects of norepinephrine to a clinically important extent, the manufacturer states that norepinephrine should be administered with extreme caution to patients receiving an MAO inhibitor because severe, prolonged hypertension may result.|For more Interactions (Complete) data for Norepinephrine (8 total), please visit the HSDB record page.

LD50 Rat iv 100 ug/kg|LD50 Mouse oral 20 mg/kg|LD50 Mouse ip 6 mg/kg|LD50 Mouse sc 5 mg/kg|LD50 Mouse iv 550 ug/kg

Norepinephrine is a naturally occurring neurotransmitter in the periphery and in adrenergic neurons in the central nervous system, which is released from sympathetic nerve terminals(1).

Norepinephrine's production and use as adrenergic and antihypotensive medicines(1) may result in its release to the environment through various waste streams(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 5.0(SRC), determined from a log Kow of -1.24(2) and a regression-derived equation(3), indicates that norepinephrine is expected to have very high mobility in soil(SRC). Values for pKa1 and pKa2 of 8.64 and 9.70, respectively(4), indicate that norepinephrine will exist partially in the cation form in the environment and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(5). Volatilization of norepinephrine from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 3.2X10-19 atm-cu m/mole(SRC), using a fragment constant estimation method(6). Norepinephrine is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 7.5X10-8 mm Hg at 25 °C(SRC), determined from a fragment constant method(7). Biodegradation data for norepinephrine were not available(SRC,2009).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 5.0(SRC), determined from a log Kow of -1.24(2) and a regression-derived equation(3), indicates that norepinephrineis not expected to adsorb to suspended solids and sediment(SRC). Values for pKa1 and pKa2 of 8.64 and 9.70, respectively(4), indicate that norepinephrine will exist partially in the cation form at pH values of 5 to 9 and therefore volatilization from water surfaces is not expected to be an important fate process(5). According to a classification scheme(6), an estimated BCF of 3.2(SRC), from its log Kow(2) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Biodegradation data for norepinephrine were not available(SRC,2009).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), norepinephrine, which has an estimated vapor pressure of 7.5X10-8 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase norepinephrine may be removed from the air by wet or dry deposition(SRC). Norepinephrine is unstable in light and air, especially at neutral and alkaline pH; oxidation to noradrenochrome occurs(3).

The rate constant for the vapor-phase reaction of norepinephrine with photochemically-produced hydroxyl radicals has been estimated as 9.5X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 4.1 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Norepinephrine is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(2). Norepinephrine is unstable in light and air, especially at neutral and alkaline pH; oxidation to noradrenochrome occurs(3).

An estimated BCF of 3.2 was calculated for norepinephrine(SRC), using a log Kow of -1.24(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

The Koc of norepinephrine is estimated as 5.0(SRC), using a log Kow of -1.24(1) and a regression-derived equation(2). According to a classification scheme(3), this estimated Koc value suggests that norepinephrine is expected to have very high mobility in soil. Values for pKa1 and pKa2 of 8.64 and 9.70, respectively(4), indicate that norepinephrine will exist partially in the cation form in the environment and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(5).

The Henry's Law constant for norepinephrine is estimated as 3.2X10-19 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that neutral norepinephrine is expected to be essentially nonvolatile from water surfaces(2). Norepinephrine's Henry's Law constant indicates that volatilization from moist soil surfaces is not expected to occur(SRC). Furthermore, values for pKa1 and pKa2 of 8.64 and 9.70, respectively(3), indicate that norepinephrine will exist partially in the cation form at pH values of 5 to 9 and therefore volatilization from water surfaces is not expected to be an important fate process(4). Norepinephrine is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 7.5X10-8 mm Hg(SRC), determined from a fragment constant method(5).

While data specific to norepinephrine were not located(SRC, 2009), the literature suggests that some pharmaceutically active compounds originating from human and veterinary therapy are not eliminated completely in municipal sewage treatment plants and are therefore discharged into receiving waters(1). Wastewater treatment processes often were not designed to remove them from the effluent(2). Selected organic waste compounds may be degrading to new and more persistent compounds that may be released instead of or in addition to the parent compound(2). Studies have indicated that several polar pharmaceutically active compounds can leach through soils(1).

NIOSH (NOES Survey 1981-1983) has statistically estimated that 613 workers (175 of these were female) were potentially exposed to norepinephrine in the US(1). Occupational exposure to norepinephrine may occur through inhalation of dust and dermal contact with this compound at workplaces where norepinephrine is produced or used. Exposure to norepinephrine among the general population may be limited to those administered drug containing norepinephrine, a catecholamine(SRC).

In eight cases of injection of norepinephrine into healthy volunteers age 22 to 26 years old, blood plasma samples contained a mean norepinephrine concentration of 0.48 ng/mL (control), 0.58 ng/mL (1 mg/kg ethanol), 0.85 ng/mL (24 ng/kg/min IV for 20 min), 1.22 ng/mL (24 ng/kg/min IV for 20 min, after 1 mg/kg ethanol), 1.26 ng/mL (48 ng/kg/min IV for 20 min), 1.76 ng/mL (48 ng/kg/min IV for 20 min, after 1 mg/kg ethanol), 2.06 ng/mL (90 ng/kg/min IV for 20 min), and 2.49 ng/mL (90 ng/kg/min IV for 20 min, after 1 mg/kg ethanol)(1).

Mainly used to treat patients in vasodilatory shock states such as septic shock and neurogenic shock and has shown a survival benefit over dopamine. Also used as a vasopressor medication for patients with critical hypotension.

Norepinephrine is used to produce vasoconstriction and cardiac stimulation as an adjunct to correct hemodynamic imbalances in the treatment of shock that persists after adequate fluid volume replacement. /Included in US product label/|Epinephrine is the drug of choice in the emergency treatment of severe acute anaphylactic reactions, including anaphylactic shock. Once adequate ventilation is assured, maintenance of blood pressure in patients with anaphylactic shock may be achieved with other pressor agents, such as norepinephrine. /Included in US product label/|In hypotension associated with myocardial infarction, cautious administration of norepinephrine may be of value and some clinicians consider it to be the pressor drug of choice. However, this type of shock generally has a poor prognosis even when pressor agents are used, and norepinephrine-induced increases in myocardial oxygen demand and the work of the heart may outweigh the beneficial effects of the drug. In addition, cardiac arrhythmias due to the drug are more likely to occur in patients with myocardial infarction. If severe congestive heart failure is also present, dopamine may be preferable because it increases renal blood flow as well as stroke volume. If peripheral vascular resistance is elevated, isoproterenol may be used in conjunction with norepinephrine, but dosage of both drugs must be carefully adjusted according to the specific hemodynamic imbalances present. /Included in US product label/|Norepinephrine may be used to treat hypotension occurring during spinal anesthesia, but other vasopressors having a longer duration of action and which can be administered IM such as metaraminol, methoxamine, or phenylephrine are more commonly used. Norepinephrine may be used to treat hypotension occurring during general anesthesia; however, the possibility of cardiac arrhythmias should be considered. /Included in US product label/|For more Therapeutic Uses (Complete) data for Norepinephrine (7 total), please visit the HSDB record page.

Norepinephrine can cause severe peripheral and visceral vasoconstriction, reduced blood flow to vital organs, decreased renal perfusion and therefore decreased urine output, tissue hypoxia, and metabolic acidosis. These effects are most likely to occur in hypovolemic patients. In addition, prolonged use of norepinephrine may cause plasma volume depletion which may result in perpetuation of the shock state or recurrence of hypotension when the drug is discontinued.|Prolonged administration of norepinephrine has caused edema, hemorrhage, focal myocarditis, subpericardial hemorrhage, necrosis of the intestine, or hepatic and renal necrosis. These effects have generally occurred in patients with severe shock and it is not clear if the drug or the shock state itself was the cause.|Norepinephrine can cause tissue necrosis and sloughing at the site of injection as a result of local vasoconstriction. Impairment of circulation and sloughing of tissue may also occur without obvious extravasation. Gangrene of the extremities has been reported rarely and has occurred in a lower extremity when norepinephrine was injected into an ankle vein.|Norepinephrine increases myocardial oxygen consumption and the work of the heart. Cardiac output may be decreased following prolonged use of the drug or administration of large doses because venous return to the heart may be diminished because of increased peripheral vascular resistance. Decreased cardiac output may be especially harmful to elderly patients or those with initially poor cerebral or coronary circulation. Norepinephrine may cause palpitation and bradycardia as well as potentially fatal cardiac arrhythmias, including ventricular tachycardia, bigeminal rhythm, nodal rhythm, atrioventricular dissociation, and fibrillation. Bradycardia may be treated by administration of atropine. Arrhythmias are especially likely to occur in patients with acute myocardial infarction, hypoxia, or hypercapnia, or those receiving other drugs which may increase cardiac irritability such as cyclopropane or halogenated hydrocarbon general anesthetics.|For more Drug Warnings (Complete) data for Norepinephrine (19 total), please visit the HSDB record page.

Noradrenaline acts on both alpha-1 and alpha-2 adrenergic receptors to cause vasoconstriction. Its effect in-vitro is often limited to the increasing of blood pressure through antagonising alpha-1 and alpha-2 receptors and causing a resultant increase in systemic vascular resistance.

Drugs that selectively bind to and activate alpha adrenergic receptors. (See all compounds classified as Adrenergic alpha-Agonists.)|Drugs that mimic the effects of stimulating postganglionic adrenergic sympathetic nerves. Included here are drugs that directly stimulate adrenergic receptors and drugs that act indirectly by provoking the release of adrenergic transmitters. (See all compounds classified as Sympathomimetics.)|Drugs used to cause constriction of the blood vessels. (See all compounds classified as Vasoconstrictor Agents.)

Norepinephrine localizes mainly in sympathetic nervous tissue. The drug crosses the placenta but not the blood-brain barrier.|Orally ingested norepinephrine is destroyed in the GI tract, and the drug is poorly absorbed after subcutaneous injection. After IV administration, a pressor response occurs rapidly. The drug has a short duration of action, and the pressor action stops within 1-2 minutes after the infusion is discontinued.|Norepinephrine, like epinephrine, is ineffective when given orally and is absorbed poorly from sites of subcutaneous injection. It is rapidly inactivated in the body by the same enzymes that methylate and oxidatively deaminate epinephrine. Small amounts normally are found in the urine. The excretion rate may be greatly increased in patients with pheochromocytoma.

The pharmacologic actions of norepinephrine are terminated primarily by uptake and metabolism in sympathetic nerve endings. The drug is metabolized in the liver and other tissues by a combination of reactions involving the enzymes catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO). The major metabolites are normetanephrine and 3-methoxy-4-hydroxy mandelic acid (vanillylmandelic acid, VMA), both of which are inactive. Other inactive metabolites include 3-methoxy-4-hydroxyphenylglycol, 3,4-dihydroxymandelic acid, and 3,4-dihydroxyphenylglycol. Norepinephrine metabolites are excreted in urine primarily as the sulfate conjugates and, to a lesser extent, as the glucuronide conjugates. Only small quantities of norepinephrine are excreted unchanged.

Norepinephrine functions as a peripheral vasoconstrictor by acting on alpha-adrenergic receptors. It is also an inotropic stimulator of the heart and dilator of coronary arteries as a result of it's activity at the beta-adrenergic receptors.|The pharmacological actions of norepinephrine and epinephrine have been extensively compared in vivo and in vitro. Both drugs are direct agonists on effector cells, and their actions differ mainly in the ratio of their effectiveness in stimulating alpha and beta2-receptors. They are approximately equipotent in stimulating beta1-receptors. Norepinephrine is a potent alpha agonist and has relatively little action on beta-2 receptors; however, it is somewhat less potent than epinephrine on the alpha receptors of most organs.|During cold exposures there is an immediate release of catecholamines (e.g., norepinephrine, dopamine), which activate the sympathetic nervous system to reduce heat loss via peripheral vasoconstriction and shift substrate utilization toward fatty acid metabolism for heat production.

Adrenaline|N-benzyl-1-phenylmethanamine|2-chloro-1-(3,4-dihydroxyphenyl)ethanone|2-(dibenzylamino)-1-(3,4-dihydroxyphenyl)ethanone|For more Impurities (Complete) data for Norepinephrine (7 total), please visit the HSDB record page.

Remove from exposure. Remove contaminated clothing. Persons developing serious hypersensitivity (anaphylactic) reactions must receive immediate medical attention. If person is not breathing give artificial respiration. If breathing is difficult give oxygen. Obtain medical attention. /Norepinephrine bitartrate/|In the event of on overdose, supportive and symptomatic measures should be used. If blood pressure fails to lower, a short-acting alpha adrenergic blocking agent may be administered. /Norepinephrine bitartrate/|/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

/SIGNS AND SYMPTOMS/ Overdosage with norepinephrine may result in headache, severe hypertension, reflex bradycardia, marked increase in peripheral resistance, and decreased cardiac output. In case of accidental overdosage, as evidenced by excessive blood pressure elevation, discontinue norepinephrine until the condition of the patient stabilizes.|/SIGNS AND SYMPTOMS/ Overdoses or conventional doses in hypersensitive persons (e.g., hyperthyroid patients) cause severe hypertension with violent headache, photophobia, stabbing retrosternal pain, pallor, intense sweating, and vomiting.|/SIGNS AND SYMPTOMS/ Possible allergic reaction to material if inhaled, ingested or in contact with skin. /Norepinephrine bitartrate/|/CASE REPORTS/ The syndrome of symmetrical peripheral gangrene is characterised by distal ischaemic damage in two or more extremities, without large vessel obstruction. Four patients with bilateral pedal ischaemia are described and their haemodynamic profiles presented. In all four cases the syndrome developed in association with noradrenaline administration, sepsis and DIC, despite a high cardiac output and a low calculated systemic vascular resistance index. Early treatment with epoprostenol was instituted in the final case and was successful.|/OTHER TOXICITY INFORMATION/ A rare case of cardiac failure due to hypertensive crisis in pheochromocytoma in a 25-year-old young man is presented. In the Emergency Department the patient complained of persisting headache and vomiting; he was distressed but fully alert, his heart rate was 110 b/min and blood pressure 180/80 mmHg. Few hours after admission, the clinical course suddenly got worse with signs and symptoms of fatal cardiac shock (dyspnea, cyanosis, pulmonary edema, hypocontractility of left ventricle). Autopsy revealed a large tumor of the left adrenal gland. Histological examination confirmed macroscopic suspicion of pheochromocytoma. Catecholamine serum levels were analysed by high pressure liquid chromatography (HPLC) with electrochemical detection. The urine contained 35 ug/24 hr norepinephrine and 184 ug/24 hr epinephrine (normal range < or = 64 and < or = 36 ug/24 hr respectively). These laboratory findings impressively demonstrate that the tumor was active, secreting high levels of epinephrine. Cardiac failure due to an acute catecholamine-related hypertensive crisis was established as the cause of death.

Arterenol

Adrenor|Aktamin|Arterenol|1-Arterenol|For more Formulations/Preparations (Complete) data for Norepinephrine (10 total), please visit the HSDB record page.

Analyte: norepinephrine bitartrate; matrix: chemical identification; procedure: infrared absorption spectrophotometry with comparison to standards /Norepinephrine bitartrate/|Analyte: norepinephrine bitartrate; matrix: chemical identification; procedure: dissolution in water; addition of ferric chloride; development of intense green color /Norepinephrine bitartrate/|Analyte: norepinephrine bitartrate; matrix: chemical identification; procedure: addition of iodine; addition of sodium thiosulfate; development of colorless or slightly pink or slightly violet color /Norepinephrine bitartrate/|Analyte: norepinephrine bitartrate; matrix: chemical purity; procedure: dissolution in acetic acid; addition of crystal violet indicator; titration with perchloric acid /Norepinephrine bitartrate/|For more Analytic Laboratory Methods (Complete) data for Norepinephrine (7 total), please visit the HSDB record page.

Analyte: norepinephrine bitartrate; matrix: pharmaceutical preparation (injection solution); procedure: dissolution in water; addition of ferric chloride; development of intense green color (chemical identification) /Norepinephrine bitartrate/|Analyte: norepinephrine bitartrate; matrix: pharmaceutical preparation (injection solution); procedure: addition of iodine; addition of sodium thiosulfate; development of colorless or slightly pink or slightly violet color (chemical identification) /Norepinephrine bitartrate/|Analyte: norepinephrine bitartrate; matrix: pharmaceutical preparation (injection solution); procedure: liquid chromatography with ultraviolet detection at 280 nm and comparison to standards (chemical purity) /Norepinephrine bitartrate/|Analyte: norepinephrine; matrix: blood (whole), urine; procedure: high-performance liquid chromatography with ultraviolent detection at 220 nm|For more Clinical Laboratory Methods (Complete) data for Norepinephrine (8 total), please visit the HSDB record page.

Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients