Amoxapine

313.78

313.78

237-867-1

R63VQ857OT

759559

DTXSID7022598

C47397

N - Nervous system

2934990002

36.9

2.6

Solid

1.2613 (rough estimate)

175.5 °C

469.9±55.0 °C(Predicted)

9℃

1.5800 (estimate)

methanol: soluble

-20°C Freezer

5.32E-09mmHg at 25°C

Oral-rat LD50: 313 mg/kg;Oral-Mouse LD50: 122 mg/kg

Flammable; heat produces toxic nitrogen oxides and chloride fumes

170.2 Ų [M+H]+ [CCS Type: TW, Method: Major Mix IMS/Tof Calibration Kit (Waters)]|171.2 Ų [M+H]+ [CCS Type: TW, Method: calibrated with polyalanine and drug standards]

III

6.1(b)

3249

3

22

36

HQ4025500

Xn

Warehouse ventilated, low temperature and dry

Stable at normal temperatures and pressures.

P301 + P312 + P330

H302

|Warning|H302 (100%): Harmful if swallowed [Warning Acute toxicity, oral]|P264, P270, P301+P312, P330, and P501|Aggregated GHS information provided by 45 companies from 2 notifications to the ECHA C&L Inventory.

highly toxic

Toxic manifestations of amoxapine overdosage differ significantly from those of other tricyclic antidepressants. Serious cardiovascular effects are seldom if ever observed. However, CNS effects, particularly grand mal convulsions, occur frequently, and treatment should be directed primarily toward prevention or control of seizures. Status epilepticus may develop and constitutes a neurologic emergency. Coma and acidosis are other serious complications of substantial amoxapine overdosage in some cases. Renal failure may develop two to five days after toxic overdose in patients who may appear otherwise recovered. Acute tubular necrosis with rhabdomuolysis and myolobinurla is the most common renal complication in such cases. This reaction probably occurs in less than 5% of overdose cases, and typically in those who have experienced multiple seizures.

Liver test abnormalities occur in a small proportion of patients on long term therapy with amoxapine, but elevations are usually mild, asymptomatic and transient, reversing even with continuation of medication. Instances of clinically apparent acute liver injury without jaundice have been reported due to amoxapine, but have been quite rare. Published cases have been mild, anicteric and asymptomatic. The onset of injury was within 1 to 4 weeks of starting, and the pattern of serum enzyme elevations was hepatocellular. Immunoallergic features and autoantibody formation were not present.

In vitro tests show that amoxapine binding to human plasma proteins is approximately 90%.

For the relief of symptoms of depression in patients with neurotic or reactive depressive disorders as well as endogenous and psychotic depressions. May also be used to treat depression accompanied by anxiety or agitation.

Amoxapine is a tetracyclic antidepressant used for relief of symptoms of depression caused by either reactive or psychotic depression. Amoxapine has been associated with a low rate of minor serum aminotransferase elevations during treatment and to very rare instances of clinically apparent acute liver injury.

Antidepressant Agents

Amoxapine is a tricyclic antidepressant of the dibenzoxazepine class, chemically distinct from the dibenzodiazepines, dibenzocycloheptenes, and dibenzoxepines. It has a mild sedative component to its action. The mechanism of its clinical action in man is not well understood. In animals, amoxapine reduced the uptake of nor-epinephirine and serotonin and blocked the response of dopamine receptors to dopamine. Amoxapine is not a monoamine oxidase inhibitor. Clinical studies have demonstrated that amoxapine has a more rapid onset of action than either amitriptyline or imipramine

Drugs that block the transport of adrenergic transmitters into axon terminals or into storage vesicles within terminals. The tricyclic antidepressants (ANTIDEPRESSIVE AGENTS, TRICYCLIC) and amphetamines are among the therapeutically important drugs that may act via inhibition of adrenergic transport. Many of these drugs also block transport of serotonin. (See all compounds classified as Adrenergic Uptake Inhibitors.)|Compounds that specifically inhibit the reuptake of serotonin in the brain. (See all compounds classified as Serotonin Uptake Inhibitors.)|Substances that contain a fused three-ring moiety and are used in the treatment of depression. These drugs block the uptake of norepinephrine and serotonin into axon terminals and may block some subtypes of serotonin, adrenergic, and histamine receptors. However the mechanism of their antidepressant effects is not clear because the therapeutic effects usually take weeks to develop and may reflect compensatory changes in the central nervous system. (See all compounds classified as Antidepressive Agents, Tricyclic.)|Drugs that bind to but do not activate DOPAMINE RECEPTORS, thereby blocking the actions of dopamine or exogenous agonists. Many drugs used in the treatment of psychotic disorders (ANTIPSYCHOTIC AGENTS) are dopamine antagonists, although their therapeutic effects may be due to long-term adjustments of the brain rather than to the acute effects of blocking dopamine receptors. Dopamine antagonists have been used for several other clinical purposes including as ANTIEMETICS, in the treatment of Tourette syndrome, and for hiccup. Dopamine receptor blockade is associated with NEUROLEPTIC MALIGNANT SYNDROME. (See all compounds classified as Dopamine Antagonists.)|Drugs that inhibit the transport of neurotransmitters into axon terminals or into storage vesicles within terminals. For many transmitters, uptake determines the time course of transmitter action so inhibiting uptake prolongs the activity of the transmitter. Blocking uptake may also deplete available transmitter stores. Many clinically important drugs are uptake inhibitors although the indirect reactions of the brain rather than the acute block of uptake itself is often responsible for the therapeutic effects. (See all compounds classified as Neurotransmitter Uptake Inhibitors.)

Rapidly and almost completely absorbed from the GI tract. Peak plasma concentrations occur within 1-2 hours of oral administration of a single dose.|60-69% of a single orally administered dose of amoxapine is excreted in urine, principally as conjugated metabolites. 7-18% of the dose is excrete feces mainly as unconjugated metabolites. Less than 5% of the dose is excreted as unchanged drug in urine.|Widely distributed in body tissues with highest concentrations found in lungs, spleen, kidneys, heart, and brain. Lower concentrations can be detected in testes and muscle.

Amoxapine is almost completely metabolized in the liver to its major metabolite, 8-hydroxyamoxapine, and a minor metabolite, 7-hydroxyamoxapine. Both metabolites are phamacologically inactive and have half-lives of approximately 30 and 6.5 hours, respectively.

8 hours

Amoxapine acts by decreasing the reuptake of norepinephrine and serotonin (5-HT).

2-Chloro-11-(1-piperazinyl)dibenz(b,f)(1,4)oxazepine

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