Clortermine

183.67786

183.68

4FA88HM3IX

1647

DTXSID0022850

26

2.5

1.074±0.06 g/cm3(Predicted)

245-246

116-118 °C @ Press: 16 Torr

Manufacturers, packers, and distributors of drug and drug products for human use are responsible for complying with the labeling, certification, and usage requirements as prescribed by the Federal Food, Drug, and Cosmetic Act, as amended (secs 201-902, 52 Stat. 1040 et seq., as amended; 21 U.S.C. 321-392).|Schedules of controlled substances are established by section 202 of the Controlled Substances Act (21 U.S.C. 812). Schedule III includes clortermine, DEA Code #1647; Drug class: Stimulant.|Drugs; statement of required warning. The label of any drug listed as a "controlled substance" in schedule II, III, or IV of the Federal Controlled Substances Act shall, when dispensed to or for a patient, contain the following warning: "Caution: Federal law prohibits the transfer of this drug to any person other than the patient for whom it was prescribed." This statement is not required to appear on the label of a controlled substance for use in clinical investigations which are "blind".

IDENTIFICATION: Clortermine hydrochloride is a centrally acting antiobesity drug. It is an amphetamine derivative and misused for performance enhancement and relief of fatigue. Its abuse is either orally or by injection. HUMAN EXPOSURE: Main risks and target organs: Acute central nervous system stimulation, cardiotoxicity causing tachycardia, arrhythmias, hypertension and cardiovascular collapse. High risk of dependency and abuse. Summary of clinical effects: Cardiovascular: Palpitation, chest pain, tachycardia, arrhythmias and hypertension are common; cardiovascular collapse can occur in severe poisoning. Myocardial ischaemia, infarction and ventricular dysfunction are described. Central Nervous System (CNS): Stimulation of CNS, tremor, restlessness, agitation, insomnia, increased motor activity, headache, convulsions, coma and hyperreflexia are described. Stroke and cerebral vasculitis have been observed. Gastrointestinal: Vomiting, diarrhea and cramps may occur. Genitourinary: Increased bladder sphincter tone may cause dysuria, hesitancy and acute urinary retention. Renal failure can occur secondary to dehydration or rhabdomyolysis. Renal ischemia may be noted. Dermatologic: Skin is usually pale and diaphoretic, but mucous membranes appear dry. Endocrine: Transient hyperthyroxinemia may be noted. Metabolism: Increased metabolic and muscular activity may result in hyperventilation and hyperthermia. Weight loss is common with chronic use. Fluid/Electrolyte: Hypo- and hyperkalemia have been reported. Dehydration is common. Musculoskeletal: Fasciculations and rigidity may be noted. Rhabdomyolysis is an important consequence of severe poisoning. Psychiatric: Agitation, confusion, mood elevation, increased wakefulness, talkativeness, irritability and panic attacks are typical. Chronic abuse can cause delusions and paranoia. A withdrawal syndrome occurs after abrupt cessation following chronic use. Contraindications: Anorexia, insomnia, psychopathic personality disorders, suicidal tendencies, Tourette syndrome and other disorders, hyperthyroidism, narrow angle glaucoma, diabetes mellitis and cardiovascular diseases such as angina, hypertension and arrythmias.Interacts with several other CNS stimulant drugs. Routes of exposure: Oral: Readily absorbed from the gastro-intestinal tract and buccal mucosa. It is resistant to metabolism by monoamine oxidase. Inhalation: Rapidly absorbed by inhalation and is abused by this route. Parenteral: Frequent route of entry in abuse situations. Absorption by route of exposure: Rapidly absorbed after oral ingestion. Peak plasma levels occur within 1 to 3 hours, varying with the degree of physical activity and the amount of food in the stomach. Absorption is usually complete by 4 to 6 hours. Sustained release preparations are available as resin bound, rather than soluble, salts. These compounds display reduced peak blood levels compared with standard preparations, but total amount absorbed and time to peak levels remain similar. Distribution by route of exposure: Concentrated in the kidney, lungs, cerebrospinal fluid and brain. Highly lipid soluble and readily cross the blood-brain barrier. Protein binding and volume of distribution varies widely, but the average volume of distribution is 5 L/kg body weight. Biological half-life by route of exposure: Under normal conditions, about 30% is excreted unchanged in the urine but this excretion is highly variable and is dependent on urinary pH. When the urinary pH is acidic (pH 5.5 to 6.0), elimination is predominantly by urinary excretion with approximately 60% of a dose being excreted unchanged by the kidney within 48 hours. When the urinary pH is alkaline (pH 7.5 to 8.0), elimination is predominantly by deamination (less than 7% excreted unchanged in the urine); the half-life ranging from 16 to 31 hours. Metabolism: The major metabolic pathway involves deamination by cytochrome P450 to the para-hydroxy compound and its congener phenylacetone; this latter compound is subsequently oxidized to chloro benzoic acid and excreted as glucuronide or glycine (hippuric acid) conjugate. Smaller amounts are converted to chloronorephedrine by oxidation. Hydroxylation produces an active metabolite, O-hyroxynorephedrine, which acts as a false neurotransmitter and may account for some drug effect, especially in chronic users. Elimination and excretion: Normally 5 to 30% of a therapeutic dose is excreted unchanged in the urine by 24 hours, but the actual amount of urinary excretion and metabolism is highly pH dependent. Mode of action: Toxicodynamics: Appears to exert most or all of its effect in the CNS by causing release of biogenic amines, especialy norepinephrine and dopamine, from storage sites in nerve terminals. It may also slow down catecholamine metabolism by inhibiting monoamine oxidase. Teratogenicity: Use of the compound for medical indications does not pose a significant risk to the fetus for congenital anomalies. Mild withdrawal symptoms may be observed in the newborn, but the few studies of infant follow-up have not shown long-term sequele, although more studies of this nature are needed. Illicit maternal use or abuse presents a significant risk to the fetus and newborn, including intrauterine growth retardation, premature delivery and the potential for increased maternal, fetal and neonatal morbidity. These poor outcomes are probably multifactorial in origin, involving multiple drug use, life-styles and poor maternal health. However, cerebral injuries occurring in newborns exposed in utero appear to be directly related to the vasoconstrictive properties of the compound. Those children exposed throughout pregnancy tended to be more aggressive. Interactions: Acetazolamide: administration may increase serum concentration. Alcohol: may increase serum concentration. Ascorbic acid: lowering urinary pH, may enhance excretion. Furazolidone: May induce a hypertensive response in patients taking furazolidone. Guanethidine: Inhibits the antihypertensive response to guanethidine. Haloperidol: limited evidence indicates that haloperidol may inhibit the effects but the clinical importance of this interaction is not established. Lithium carbonate: isolated case reports indicate that lithium may inhibit the effects. Monoamine oxidase inhibitor: severe hypertensive reactions have followed the administration to patients taking monoamine oxidase inhibitors. Norepinephrine: Abuse may enhance the pressor response to norepinephrine. Phenothiazines: May inhibit the antipsychotic effect of phenothiazines, and phenothiazines may inhibit the anorectic effect. Sodium bicarbonate: large doses of sodium bicarbonate inhibit its elimination, thus increasing the effect. Tricyclic antidepressants: theoretically increases the effect, but clinical evidence is lacking. /Clortermine hydrochloride/

AN ANORECTIC DRUG SIMILAR TO CHLORPHENTERMINE. ALTHOUGH IT IS A SYMPATHOMIMETIC, CARDIOVASCULAR ACTIONS ARE USUALLY MINIMAL IN THERAPEUTIC DOSES. LIKE OTHER DRUGS IN THIS CLASS, CONTROL OF APPETITE IS MAINTAINED FOR ONLY A FEW WEEKS & ... IS NO SUBSTITUTE FOR RETRAINING IN EATING HABITS. /CLORTERMINE HYDROCHLORIDE/|IT SHOULD BE PRESCRIBED ONLY AS A SHORT-TERM ADJUNCT (FOUR TO SIX WEEKS) IN A PROGRAM THAT ALSO INCLUDES CALORIC RESTRICTION, APPROPRIATE EXERCISE, & PSYCHOLOGIC SUPPORT. /CLORTERMINE HYDROCHLORIDE/|CONTROLLED STUDIES IN PT WITH CARDIOVASCULAR DISEASES HAVE FAILED TO DEMONSTRATE THAT ... /CLORTERMINE/ HAS A SIGNIFICANT EFFECT ON BLOOD PRESSURE, PULSE, OR ELECTROCARDIOGRAPHIC READINGS. ... THERE IS EVIDENCE TO SUGGEST THAT CONTROL OF DIABETES MELLITUS IS NOT ADVERSELY AFFECTED BY CLORTERMINE. /CLORTERMINE HYDROCHLORIDE/

THE DRUG HAS A POTENTIAL FOR ABUSE. ... CLORTERMINE IS CONTRAINDICATED IN AGITATED STATES, HYPERTHYROIDISM, GLAUCOMA, HYPERSENSITIVITY, OR IDIOSYNCRASY TO OTHER SYMPATHOMIMETIC DRUGS. IT SHOULD BE USED CAUTIOUSLY IN PT WITH HYPERTENSION OR CARDIOVASCULAR DISEASE. /CLORTERMINE HYDROCHLORIDE/|THE DRUG MAY ALTER INSULIN REQUIREMENTS IN DIABETES MELLITUS. IT SHOULD NOT BE USED WHEN THERE IS A HISTORY OF DRUG ABUSE. ... DRUG IS NOT ADVISED FOR USE IN CHILDREN. /CLORTERMINE HYDROCHLORIDE/|... CLORTERMINE SHOULD NOT BE USED IN PT WHO ARE RECEIVING ... /GUANETHIDINE OR MONOAMINE OXIDASE INHIBITORS/. /CLORTERMINE HYDROCHLORIDE/|THE MANIFESTATIONS OF CHRONIC INTOXICATION & OVERDOSAGE WITH CLORTERMINE MAY CLOSELY RESEMBLE THOSE ASSOCIATED WITH ABUSE & OVERUSE OF AMPHETAMINES. /CLORTERMINE HYDROCHLORIDE/|For more Drug Warnings (Complete) data for CLORTERMINE (7 total), please visit the HSDB record page.

9 to 24 hr /Clortermine hydrochloride/

/CLORTERMINE/ ... IS THE ORTHO-CHLORO ISOMER OF CHLORPHENTERMINE HYDROCHLORIDE, TO WHICH IT IS COMPARABLE IN SUPPRESSING APPETITE. /CLORTERMINE HYDROCHLORIDE/

Diazepam may be given to control central nervous system stimulation and convulsions. For marked excitement or hallucinations chlorpromazine may be necessary and, in addition, its alpha-adrenoceptor blocking properties may be useful for the management of hypertension. Severe hypertension may call for the administration of an alpha-adrenoceptor blocking agent, such as phentolamine. Measures should be taken to control increased body temperature.

CARDIOVASCULAR SIDE EFFECTS INCL TACHYCARDIA, PALPITATION, & HYPERTENSION. UNTOWARD EFFECTS ON NERVOUS SYSTEM INCL RESTLESSNESS, EXCITEMENT, INSOMNIA, EUPHORIA, DYSPHORIA, DIZZINESS, TREMOR, HEADACHE, & RARE PSYCHOTIC EPISODES. /CLORTERMINE HYDROCHLORIDE/|OTHER SIDE EFFECTS INCL XEROSTOMIA, UNPLEASANT TASTE, CONSTIPATION, DIARRHEA, GI UPSETS, URTICARIA, IMPOTENCE, & DIMINISHED LIBIDO. /CLORTERMINE HYDROCHLORIDE/|WHEN AMT SUBSTANTIALLY LARGER THAN CLINICAL DOSAGE WERE ADMIN TO VOLUNTEERS, CHILLS, DIZZINESS, NAUSEA, & TREMORS (BUT NO CARDIOVASCULAR EFFECTS) OBSERVED. /CHLORTERMINE HYDROCHLORIDE/|Excessive use may lead to tolerance and physical dependence.

Clortermine|Voranil|1647|Schedule III - Substances in the DEA Schedule III have a potential for abuse less than substances in Schedules I or II and abuse may lead to moderate or low physical dependence or high psychological dependence.|No

CHLOROPHENETHYLAMINE HYDROCHLORIDE; S 77 /CLORTERMINE HYDROCHLORIDE/

Applications of capillary gas chromatography in routine toxicological analyses. /Clortermine is one of the substances identified/.