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Moclobemide
Moclobemide (Ro 111163) · 4-chloro-N-(2-morpholinoethyl)benzamide · Manefix · CS-1682 · manerix · aurorix · Moclaime · Moclamine
Identifikatoren & physikalische Daten
| CAS No. | 71320-77-9 |
|---|---|
| Summenformel | C13H17ClN2O2 |
| Durchschnittliche Molmasse | 268,74 g/mol |
| Monoisotopische Masse | 268,09785546 g/mol |
| SMILES | O=C(NCCN1CCOCC1)c1ccc(Cl)cc1 |
| InChIKey | YHXISWVBGDMDLQ-UHFFFAOYSA-N |
| PubChem CID | 4235 |
| ChEMBL | CHEMBL86304 |
| ChEBI | CHEBI:83531 |
| EC No. | 636-108-5 |
| DTXSID | DTXSID9040554 |
Chemische & physikalische Eigenschaften
| XLogP | 1,5 |
|---|---|
| Polarare Oberfläche (TPSA) | 41,6 |
| H-Brücken-Donoren | 1 |
| H-Brücken-Akzeptoren | 3 |
| Frei drehbare Bindungen | 4 |
| Schwere Atome | 18 |
| Formalladung | 0 |
| Komplexität | 262 |
| Arzneimittel | Pharmaceuticals -> Synthetic Cannabinoids or Psychoactive CompoundsPharmaceuticals -> Listed in ZINC15Pharmaceuticals -> AntidepressantsPharmaceuticals -> Used in Switzerland |
| LogP (Verteilungskoeffizient) | 1.5 |
| Color/Form | Crystals from isopropanol |
| Löslichkeit | 1.12e+00 g/L>40.3 [ug/mL] (The mean of the results at pH 7.4)DMSO: >20mg/mL |
| Human Drugs | Breast FeedingLactationMilk, HumanAntidepressive AgentsMonoamine Oxidase Inhibitors |
| Schmelzpunkt | 137 °C137°C |
| Physical Description | Solid |
| Dissociation Constants | 10.6 (ethanol-air) |
| Collision Cross Section | 162.5 Ų [M+H]+ [CCS Type: TWMethod: Major Mix IMS/Tof Calibration Kit (Waters)]162.9 Ų [M+H]+ [CCS Type: DTMethod: single field calibrated] |
| Other Experimental Properties | Crystals from isopropanolmp 208 /Hydrochloride/ |
| Siedepunkt | 447.7±40.0 °C(Predicted) |
| Dichte | 1.206±0.06 g/cm3(Predicted) |
| Lagerbedingungen | room temp |
| pKa (Säurekonstante) | 14.26±0.46(Predicted) |
| Aggregatzustand | solid |
| Farbe | white |
| Merck | 14,6226 |
| InChI | InChI=1S/C13H17ClN2O2/c14-12-3-1-11(2-4-12)13(17)15-5-6-16-7-9-18-10-8-16/h1-4H,5-10H2,(H,15,17) |
| InChIKey | YHXISWVBGDMDLQ-UHFFFAOYSA-N |
| SMILES | C(NCCN1CCOCC1)(=O)C1=CC=C(Cl)C=C1 |
| CAS Datenbank | 71320-77-9(CAS DataBase Reference) |
| NIST chemische Informationen | Moclobemide(71320-77-9) |
Sicherheit & Vorschriften
| GHS-Einstufung | DangerH302 (100%): Harmful if swallowed [Warning Acute toxicity, oral]P261, P264, P264+P265, P270, P271, P280, P301+P317, P302+P352, P304+P340, P305+P354+P338, P317, P319, P321, P330, P332+P317, P362+P364, P403+P233, P405, and P501 (click each P-code to see the statement)Aggregated GHS information provided per 48 reports by companies from 7 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies. |
|---|---|
| Hazard Classes and Categories | Acute Tox. 4 (100%) |
| Lagerbedingungen | Store between 15 and 30 °C (59 and 86 °F) |
| Entsorgungsverfahren | SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air qualitypotential migration in soil or watereffects on animal, aquatic, and plant lifeand conformance with environmental and public health regulations. |
| Körperbelastung | /Toxicological/ results obtained /post-mortem from a 41-yr-old Caucasian male, with a history of depression and suicide attempts showed/ blood and urine /levels/, respectively, were as follows: Ro 12-5637 (moclobemide N'-oxide) not detected and 424 ug/mLRo 12-8095 (3-keto-moclobemide) 2.26 ug/mL and 49.7 ug/mLmoclobemide 5.62 ug/mL and 204 ug/mLAutopsy findings /for a young man was found shivering and incoherent at home/ were unremarkable, but toxicology testing revealed the following: moclobemide (subclavian blood, 18.5 mg/Lliver, 28.5 mg/kggastric contents, 77 mg/69 g) and paroxetine (subclavian blood, 1.58 mg/Lliver, 15.3 mg/kggastric contents, 0.7 mg/69 g). |
| Wechselwirkungen | Moclobemide has been shown to potentiate the effects of opiates. Co-administration of moclobemide with meperidine is contraindicated /SRP:due to the risk of serotonin syndrome/. Other opioid analgesics should be used with caution and a dose adjustment for these agents may be necessary.Increased moclobemide plasma concentrations may occur50% reduction of moclobemide doses may be needed when coadministered with cimetidine.Concomitant use of moclobemide and a tricyclic antidepressant (TCA) is contraindicated. Treatment with a TCA may be initiated following discontinuation of moclobemide and a wash-out period of no less than 2 days. Moclobemide should not be administered in combination with a conventional monamine oxidase inhibitor (MAOI) (phenelzine, tranylcypromine) or a selective serotonin reuptake inhibitor (SSRI). When switching patients from MAOI or serotonergic antidepressants to moclobemide, a wash-out period of 4 to 5 half-lives of the previous administrated drug (and any active metabolites) should intervene. At least 5 weeks should elapse between withdrawal of fluoxetine and initiation of moclobemide.A potentially lethal hyperserotonergic state known as the serotonin syndrome may occur as the result of combining serotonergic agents (such as amitriptyline, clomipramine, doxepin, or imipramine, fluvoxamine, fluoxetine, paroxetine, sertraline /SRP: and meperidine) with monoamine oxidase inhibitors. The syndrome may be manifested by mental status changes (confusion, hypomania), restlessness, myoclonus, hyperreflexia, diaphoresis, shivering, tremor, diarrhea, incoordination, and/or fever.For more Interactions (Complete) data for MOCLOBEMIDE (11 total), please visit the HSDB record page. |
| Expositionspfade | Well absorbed from the gastrointestinal tract (> 95%). The presence of food reduces the rate but not the extent of absorption. Hepatic first pass metabolism reduces bioavailability to 45-70% following administration of a single dose, but increases to 80% with multiple dosing as a result of saturation of the first pass effect. Peak plasma concentrations are reached within 1 - 2 hours following oral administration. |
| Milk Concentrations | Small quantities of moclobemide are distributed into human breast milk.The concentrations of moclobemide and /3-keto-meclobemide/ (Ro-12-8095) in milk were highest at 3 hr after moclobemide administration and the drug and metabolite were not detectable after 12 hr. |
| Toxizitätsübersicht | IDENTIFICATION: Moclobemide is a monoamine oxidase inhibitor drug. Moclobemide is a white to red crystalline substance with a weak odor. It is soluble in chloroform, methanol and water. Indications: Accepted: Major mental depression and dysthymia. Investigational: Menopausal flushing, prophylactic treatment of migraine, smoking cessation and abstinence in heavy dependent smokers. HUMAN EXPOSURE: Main risks and target organs: Moclobemide is a short-acting, selective and reversible monoamine oxidase type A inhibitor (MAO-AI). It is generally well tolerated in overdose when taken alone. The serotonergic effects of moclobemide may be enhanced by combination with tricyclic antidepressants, other monoamine oxidase inhibitors, selective serotonin reuptake inhibitors (SSRIs), lithium or serotonergic substances. A life-threatening serotonin syndrome consisting of hyperthermia, tremor and convulsions can develop when moclobemide is ingested with these drugs. The concomitant consumption of large amounts of tyramine-rich foodstuff may result in a moderate increase of systolic blood pressure (cheese reaction). Summary of clinical effects: Agitation, drowsiness, disorientation, slow-reacting pupils, myoclonic jerks in upper extremitieshypo or Hypertension, tachycardianausea, vomiting, abdominal pain. Contraindications: Absolute: Hypersensitivity to moclobemide, children less than 15 years old, breast feeding (in the absence of available data on potential toxic effects to suckling infants): less than 3 % of the administered dose of moclobemide is excreted in breast milk. Coadministration of sumatriptan: hypertensive crises, severe coronary vasoconstriction may occur. Co-administration of pethidine (meperidine), dextromethorphan: the serotonin syndrome may occur. Moclobemide is contraindicated in patients with acute confusional states and in those with pheochromocytoma. It should be avoided in excited or agitated patients and in those with severe hepatic impairment. Relative: Co-administration of drugs which increase the levels of monoamines such as serotonin and norepinephrine: tricyclic antidepressants, selective serotonin re-uptake inhibitor antidepressants: a serotonin syndrome may occur. Alcohol (as for other psychoactive drugs). Routes of exposure: Oral: Moclobemide is available as tablets, thus ingestion is the most common route of exposure. Kinetics: Absorption by route of exposure: Readily absorbed from the gastro-intestinal tract. Food delays absorption. Peak plasma concentration: 1 to 2 hours after ingestion. Oral bioavailability was reported as 60 % after a single dose and 80 % after repeated doses, due to an important and saturable hepatic first-pass effect. Distribution by route of exposure: Widely distributed throughout the body. Plasma protein binding is 50 %. After oral administration to 6 healthy subjects, the mean volume of distribution was about 1 L/kg. Biological half-life by route of exposure: After single oral doses, plasma half-life is 1 to 2 hourswith long term treatment, the half-life is reported to increase to 2 to 4 hours. Metabolism: Moclobemide undergoes extensive metabolism, mainly carbon and nitrogen oxidation in the liver, deamination and aromatic hydroxylation. Metabolites are inactive. Elimination and excretion: Metabolites of moclobemide and a small amount of unchanged drug (less than 1 %) are excreted in the urineafter an oral dose of radio-labelled moclobemide, 92% of the dose was excreted in the urine within 12 hours.Mode of action: Toxicodynamics: Moclobemide selectively and reversibly inhibits the activity of the intracellular enzyme monoamine oxidase A (MAO-A), thus preventing the normal metabolism of biogenic amines (noradrenaline, adrenaline, serotonin, dopamine). Mono amine oxidase inhibitors (MAOIs) exert their toxic effects by inhibiting the metabolism of sympathomimetic amines and serotonin, and by decreasing noradrenaline stores in post-ganglionic sympathetic neurons. They do not inhibit MAO synthesis. MAOIs also inhibit enzymes other than MAO, including dopamine-beta-oxidase, diamine-oxidase, amino-acid decarboxylase and choline dehydrogenase. Inhibition of these enzymes occurs only with very high doses of MAOIs and may be responsible for some of the toxic effects of MAOIs. Drugs that enhance serotonin release or reuptake (tricyclic antidepressants, selective serotonin reuptake inhibitors) may cause the serotonin syndrome when they are administered concurrently with the MAOIs, even at therapeutic doses. A toxic reaction to MAOIs may be caused by pressor amines such as tyramine, resulting in hypertensive crisis. When the protective role of intestinal and hepatic MAO is eliminated, increased absorption of tyramine from certain foods occurs and can cause a significant increase in blood pressure (cheese reaction) through the release of noradrenaline from pre-synaptic vesicles. Two isoforms of the MAO enzyme have been discovered: MAO-A and MAO-B. These isoforms differ in anatomical distribution and preferred substrates. The new MAOIs such as moclobemide are isoform selective and reversibly inhibit MAO-A. Thus having a lower potential for interactions than non selective MAOIs at therapeutic doses. Selectivity is lost in overdoses and in extreme situations such as high-dose combination therapies and mixed drug overdoses, and severe toxic reactions may occur. Pharmacodynamics: The MAOs are a group of enzymes that metabolize, and therefore inactivate endogenous pressor amines (such as norepinephrine, dopamine, serotonin) as well as ingested indogenous amines (such as tyramine). MAOIs inhibit the degradation of these amines by MAO. The increased availability of biogenic amines (such as norepinephrine and serotonin) is thought to be linked with the improvement in depression accounted for by MAIO treatment. Two isoforms of the MAO enzyme have been discovered: MAO-A and MAO-B, which differ in anatomical distribution and preferred substrates. The MAO type A enzymes preferentially metabolize serotonin and noradrenaline and are located primarily in the placenta, gut and liver. The MAO type B enzymes are predominant in brain, liver and platelets, and phenylethylamine, methylhistamine and tryptamine are their primary substrates. Both MAO-A and MAO-B metabolize tyramine. New MAOIs such as moclobemide, which are isoform selective and have reversible inhibition of the enzyme are called Reversible Inhibitors of MAO-A. The duration of MAO-A inhibition by moclobemide is shorter (16 to 24 hours) than the inhibition induced by conventional MAOIs (> 10 days). The interaction of the newer MAO-AI with hepatic cytochrome P450 appears to be much weaker than with the irreversible and nonspecific MAOIs. However, several studies in humans have suggested there is some involvement of cytochtome P450 in the metabolism of moclobemide, and also a weak inhibitory effect of moclobemide for its isoenzyme CYP2D6. The clinical relevance of this weak interaction is not clear and is probably of little consequence. Like tricyclic antidepressants, SSRIs and other MAOIs, moclobemide significantly reduces REM (rapid eye movement) sleep density, REM time and the REM percentage of total sleep time in patients with major depression. Interactions: Drug-food interactions: the dietary restrictions that need to be followed with irreversible MAOIs are less stringent with selective reversible inhibitors of monoamine oxidase type A such as moclobemide. However, the manufacturer of moclobemide recommends that since some patients may be more sensitive to tyramine, the consumption of large amounts of tyramine-rich foodstuffs should still be avoidedthese foods include chocolate, aged cheeses, beer, chianti, vermouth, pickled fish and concentrated yeast extracts. Drug-drug interactions: Sympathomimetics and anorectic drugs should not be taken with moclobemide. Opioid analgesics: Central Nervous System (CNS) excitation or depression may occur. Drugs used in anesthesia: anesthesia may be performed 24 hours after discontinuation of moclobemide with little potential for significant interactionwhen the washout period is not feasible, the use of meperidine and parenteral sympathomimetics should be avoided. Levodopa: a hypertensive crisis may be precipitated. Sumatriptan: the manufacturer recommends to not prescribe moclobemide concominantiantly with sumatriptan which is a selective agonist at serotonin type 1D receptors, because of possible hypertensive crises and severe coronary vasoconstriction, and advises a washout period of 24 hours after discontinuation of moclobemidehowever a clinical study involving 103 episodes of migraine, did not show evidence of significant adverse effects. The metabolism of moclobemide is inhibited by cimetidine, leading to a prolonged half-life and increased plasma concentrationsthe manufacturer recommends that the dose of moclobemide be reduced to half strength in patients who are also given cimetidine. The co-administration of drugs that increase the levels of monoamines such as serotonin and norepinephrine, including tricyclic antidepressants (mainly clomipramine), selective serotonin re-uptake inhibitor antidepressants, and potentially other antidepressants may cause a serotonin syndrome. Lithium: Care should be taken when co-prescribing MAO-AI with lithium, since it increases serotonin levels, although no interactions have been reported to date. Therapy with moclobemide should not be started until at least 7 days following the discontinuation of tricyclic or serotonin reuptake inhibitor antidepressant treatment (2 weeks in the case of paroxetine5 weeks in the case of fluoxetine) or for at least a week after stopping treatment with other monoamine oxidase inhibitors. Conversely, a washout period of 24 hours is advised when switching from moclobemide to other antidepressants. Antipsychotics, benzodiazepines, nifedipine and hydrochlorothiazide may be coprescribed without major interaction. Main adverse effects: They include sleep disturbances, dizziness, nausea, and headache. Confusional states, restlessness or agitation may occur. Mild elevations in liver enzyme values have been reported. Care is required in patients with thyrotoxicosis as moclobemide may theoretically precipitate a hypertensive reaction. Mental alertness may be impaired, patients under treatment should not drive or operate machinery. Manic episodes may be provoked in patients with bipolar disorders, moclobemide should be discontinued and antipsychotic therapy should be initiated. Less common adverse effects include: hypertension, although the role of concomitant administration of clomipramine, buspirone, and thyroxin in the case series reported may have contributed and cannot be disregarded, alopecia. Acute poisoning: Ingestion: Patients may display minimal or no symptoms following pure moclobemide overdose. However, the ingestion of moclobemide may cause nausea, vomiting, gastric painagitation, disorientation, drowsiness, impaired reflexes, myoclonic jerks in upper extremities, slow reacting pupilsslight rise in blood pressure or moderate hypotension and tachycardia. Co-ingestion of tricyclic antidepressants (primarily clomipramine), opioids, or selective serotonin reuptake inibitors can result in more varied and severe symptoms appearing within 2 to 3 hours after ingestion, even with lower doses of moclobemide. Symptoms include: both CNS depression (confusion, drowsiness) and excitation (seizure), tremor, mydriasis, hyperthermia with muscle rigidity, hypertension and metabolic acidosis. Several fatal cases have been reported after a combination of moclobemide with citalopram, clomipramine and fluoxetine and moclobemide with citalopram and fluoxetine. Course, prognosis, cause of death: Pure moclobemide overdoses usually have a fairly benign course. Several fatalities are reported in the literature, all involving a co-ingestion. The clinical course consisted of euphoria, agitation, then extreme tremor, followed by convulsions and hyperthermia. Death occurred within 3 to 16 hours after ingestion, after intractable seizure and/or hyperthermia and its subsequent complications: disseminated intravascular coagulation and multiple organ failure. Systematic description of clinical effects: Cardiovascular: Mild to moderate hypertension, moderate hypotension and sinus tachycardia. Neurological: Central nervous system: Mild disorientation, agitation, slurred speech, anxiety, dizzinessdrowsiness, coma. Autonomic nervous system: Slow-reacting pupils, mydriasis. Skeletal and smooth muscle: Myoclonic jerks in upper extremitiesrhabdomyolysis. Gastrointestinal: Dry mouthnausea, vomiting, gastric paindiarrhea. Hepatic: Mild increases in liver enzymes values. Urinary: Renal Metabolic: Acid-base disturbances: Acidosis is expected in association with coma and/or convulsions. Fluid and electrolyte disturbances: Hyperkalemia. Others: Creatine phosphokinase may be elevated in patients with muscular hyperactivity or rigidity. ANIMAL STUDIES: In mice: (after oral and ip injection) Symptomatology: sedation, muscle twitching, respiratory depression, death. In rats: (after oral and ip injection) Symptomatology: sedation, respiratory depression, death. In rabbits (after oral and ip injection): Symptomatology: ataxia, decrease in motor activity, respiratory depression, tremor, seizures, salivation and death. Carcinogenicity: Animal studies: moclobemide was not carcinogenic in rats at oral doses for 2 years. In mice given the drug orally over 80 weeks, no carcinogenic effect was observed. Teratogenicity: Animal studies: doses up to 100 mg/kg/day did not affect fertility in rats. In rabbits and rats oral doses of up to 100 and 200 mg/kg/day respectively did not have embryotoxic or teratogenic effects. Mutagenicity: In vitro and in vivo: moclobemide did not show mutagenicity.The mechanism of action of moclobemide involves the selective, reversible inhibition of MAO-A. This inhibition leads to a decrease in the metabolism and destruction of monoamines in the neurotransmitters. This results in an increase in the monoamines, relieving depressive symptoms. |
| Human Toxicity Excerpts | /SIGNS AND SYMPTOMS/ Patients ingesting up to 2000 mg of moclobemide have shown only mild gastrointestinal symptoms or no symptoms at all. At 3000 to 4000 mg, depressed consciousness and a slight increase in blood pressure have been observed. At 7000 to 8000 mg, patients show fatigue, agitation, tachycardia, increased blood pressure, and dilated slow-reacting pupils. Both central nervous system depression and excitation (Seizures) have been observed. Tremor, mydriasis, hyperthermia, hypertension, and acidosis may be seen. There may be an additive effect with tricyclic antidepressants. In massive overdoses (>2000 to 6000 mg), seizures, hyperthermia, muscle rigidity, and pain, together with rhabdomyolysis, resemble classical MAOI intoxication as well as the unusual neuroleptic malignant syndrome./CASE REPORTS/ A 41-yr-old Caucasian male, with a history of depression and suicide attempts, was found deceased at home. Multiple containers of medication, the MAO-inhibitor moclobemide (Aurorix), the SSRI citalopram (Cipramil), and the benzodiazepine lormetazepam (Noctamid) as active substance, as well as a bottle of whiskey were present at the scene. The autopsy findings were unremarkable, but systematic toxicological analysis (EMIT, radioimmunoassay, high-performance liquid chromatography-diode-array detection [HPLC-DAD], gas chromatography-nitrogen-phosphorus detection, and gas chromatography-mass spectrometry) revealed the following: ethanol (0.23 g/L blood, 0.67 g/L urine), lormetazepam (1.65 ug/mL urine), cotinine (0.63 ug/mL blood, 5.08 ug/mL urine), caffeine (1.20 ug/mL urine), moclobemide (and metabolites), and citalopram (and metabolite). There upon, we developed a new liquid chromatographic separation with optimized DAD, preceded by an automated solid-phase extraction, for the quantitation of the previously mentioned antidepressive drugs. The results obtained for blood and urine, respectively, were as follows: Ro 12-5637 (moclobemide N'-oxide) not detected and 424 ug/mLRo 12-8095 (3-keto-moclobemide) 2.26 ug/mL and 49.7 ug/mLmoclobemide 5.62 ug/mL and 204 ug/mLdesmethylcitalopram 0.42 ug/mL and 1.22 ug/mLand citalopram 4.47 ug/mL and 19.7 ug/mL. The cause of death was attributed to the synergistic toxicity of moclobemide and citalopram, both antidepressants, which, by intentional or accidental combined ingestion, can produce a potentially lethal hyperserotoninergic state. Based on the history of the case and pharmacology of the drugs involved, the forensic pathologists ruled that the cause of death was multiple drug intoxication, resulting in a fatal "serotonin syndrome," and that the manner of death was suicide./CASE REPORTS/ The cases of 5 patients (ages 19-41 yr) who developed fatal serotonin syndrome following overdoses of 1000-1500 mg moclobemide (Aurorix) and 225-500 mg clomipramine hydrochloride (Anafranil Retard) or moclobemide and citalopram hydrobromide (Cipramil) are described. The patients were initially euphoric, but then developed tremor, followed by convulsions and loss of consciousness. The patients died 3-16 hr after ingesting the drugs. Blood levels for the drugs at admission and at necropsy are reported. |
| Carcinogen Classification | No indication of carcinogenicity to humans (not listed by IARC). |
| Non-Human Toxicity Excerpts | /GENOTOXICITY/ Moclobemide did not exhibit mutagenicity in laboratory evaluations, including the Ames test and Micronucleus test (mouse bone marrow) and assays of Chinese hamster V79 cells, rat hepatocytes, or human lymphocytes. |
| Antidote and Emergency Treatment | With symptomatic and supportive treatment in a hospital, moclobemide overdose patients ... appeared to recover usually within 24 hours and, in two cases, within 5 to 7 days. Seizures may require diazepam, thiopental, and mechanical ventilation. Dantrolene may be useful for hyperthermia. Blood pressure must be monitored in all moclobemide overdose patients.Monitoring: Monitor closely for signs of potentially fatal serotonergic syndrome, which has been reported after overdose of moclobemide with other antidepressants. /SRP: Serotonin syndrome/Basic treatment: Establish a patent airway. 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 normal saline 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 ... . /Poison A and B/Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in respiratory arrest. Positive pressure ventilation techniques with a bag valve mask device may be beneficial. Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start an IV with D5W /SRP: "To keep open", minimal flow rate/. Use lactated Ringer's if signs of hypovolemia are present. Watch for signs of fluid overload. Consider drug therapy for pulmonary edema ... . For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam (Valium) ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poison A and B/For more Antidote and Emergency Treatment (Complete) data for MOCLOBEMIDE (9 total), please visit the HSDB record page. |
| Effects During Pregnancy and Lactation | ◉ Summary of Use during Lactation |
| Toxicity Data | LD50: 730mg/kg (Mouse) (A308) LD50: 1300mg/kg (Rat) (A308) |
| Non-Human Toxicity Values | LD50 Rat oral 707 mg/kg |
| Wassergefährdungsklasse (WGK) | 2 |
| UN-Transportnummer | 3249 |
| Zollcode | 29349990 |
| RTECS-Nr. | CV2462000 |
| R-Sätze (R) | 22-37/38-41-26/27/28 |
| Toxizität | LD50 in rats (mg/kg): 707 orally (Burkard, Wyss) |
| Gefahrensymbole | Xn,T+ |
| Sicherheitshinweise (S) | 26-39-45-36/37/39-22 |
| Gefahrenklasse | 6.1(b)Acute Tox. 4 OralEye Dam. 1Skin Irrit. 2STOT SE 3 |
| Verpackungsgruppe | III |
| Lagerklasse | 11 - Combustible Solids |
| Gefahrstoffdaten | 71320-77-9(Hazardous Substances Data) |
Anwendungen & Verwendung
Beschreibung
Moclobemide is the first of a new generation of non-hydrazine, reversible MAO-A inhibitors useful in the treatment of depression. Moclobemide is a selective inhibitor of MAO-A, allowing tyramine to be metabolized by MAO-B. In controlled studies, moclobemide was clinically superior to desipramine and showed no cholinergic or cardiovascular side-effects. A metabolite is currently under investigation for treatment of Parkinson’s disease,.