Clorazepate Dipotassium
Nordazepam
Anti-Anxiety Agents
S-16924 [(R)-2-[1-[2-(2,3-dihydro-benzo[1,4]dioxin-5-yloxy)-ethyl]- pyrrolidin-3yl]-1-(4-fluorophenyl)-ethanone], a novel, potential antipsychotic with marked serotonin1A agonist properties: III. Anxiolytic actions in comparison with clozapine and haloperidol. (1/16)
S-16924 is a potential antipsychotic that displays agonist and antagonist properties at serotonin (5-HT)1A and 5-HT2A/2C receptors, respectively. In a pigeon conflict procedure, the benzodiazepine clorazepate (CLZ) increased punished responses, an action mimicked by S-16924, whereas the atypical antipsychotic clozapine and the neuroleptic haloperidol were inactive. Similarly, in a Vogel conflict paradigm in rats, CLZ increased punished responses, an action shared by S-16924 but not by clozapine or haloperidol. This action of S-16924 was abolished by the 5-HT1A antagonist WAY-100,635. Ultrasonic vocalizations in rats were inhibited by CLZ, S-16924, clozapine, and haloperidol. However, although WAY-100,635 abolished the action of S-16924, it did not affect clozapine and haloperidol. In a rat elevated plus-maze, CLZ, but not S-16924, clozapine, and haloperidol, increased open-arm entries. Like CLZ, S-16924 increased social interaction in rats, whereas clozapine and haloperidol were inactive. WAY-100,635 abolished this action of S-16924. CLZ, S-16924, clozapine, and haloperidol decreased aggressive interactions in isolated mice, but this effect of S-16924 was not blocked by WAY-100, 635. All drugs inhibited motor behavior, but the separation to anxiolytic doses was more pronounced for S-16924 than for CLZ. Finally, in freely moving rats, CLZ and S-16924, but not clozapine and haloperidol, decreased dialysis levels of 5-HT in the nucleus accumbens: this action of S-16924 was blocked by WAY-100,165. In conclusion, in contrast to haloperidol and clozapine, S-16924 possessed a broad-based profile of anxiolytic activity at doses lower than those provoking motor disruption. Its principal mechanism of action was activation of 5-HT1A (auto)receptors. (+info)Use of micellar mobile phases for the chromatographic determination of clorazepate, diazepam, and diltiazem in pharmaceuticals. (2/16)
An ODS-2 column, a micellar mobile phase of high elution strength containing 0.1M sodium dodecyl sulfate and 3% (v/v) butanol, and ultraviolet detection at 230 nm are used for the determination of either of two benzodiazepines (clorazepate and diazepam) and a benzothiazepine (diltiazem) in pharmaceuticals. The procedure is shown to be competitive against conventional chromatography with methanol-water mobile phases, especially for diltiazem. The composition of the micellar mobile phase is selected using a predictive strategy based on an accurate retention model and assisted by computer simulation. Calibration graphs are linear at least in the 2.5 to 20 microg/mL, 4 to 20 microg/mL, and 5 to 40 microg/mL ranges for clorazepate, diazepam, and diltiazem, respectively. The intra- and interday repeatabilities (%) are clorazepate (1.7, 5.2), diazepam (0.43, 3.7), and diltiazem (0.36, 3.1). Limits of detection are well below the concentrations of the drugs found in the commercial pharmaceutical preparations analyzed. The drug contents evaluated with the proposed procedure are compared with the declared contents given by the manufacturers. The achieved percentages of label claim are usually between 95 and 104%. (+info)Flumazenil-sensitive dose-related physical dependence in planarians produced by two benzodiazepine and one non-benzodiazepine benzodiazepine-receptor agonists. (3/16)
Two benzodiazepine (midazolam and clorazepate) and one non-benzodiazepine (zolpidem) benzodiazepine-receptor agonists produced dose-related physical dependence, as evidenced by abstinence-induced decrease in planarian locomotor velocity (pLMV) when drug-exposed planarians were placed into drug-free water, but not when they were placed into drug-containing water (i.e., an abstinence-induced withdrawal, since the effect was only obtained in the removal of drug and not in the continued presence of drug). We have previously shown that the decrease in pLMV is associated with specific and transient withdrawal signs. In the present study, the selective benzodiazepine-receptor antagonist flumazenil significantly antagonized (P<0.05), by co-application, the ability of each agonist to produce the withdrawal. These results: (1) suggest that benzodiazepine-receptor agonists, for two different chemical categories, produce dose-related physical dependence manifested as abstinence-induced withdrawal in this simple and convenient model, and (2) in the absence of cloning or radioligand binding literature, suggest a possible specific interaction site (receptor?) for these compounds in planarians. (+info)Generalized skin drug eruption to natalizumab in a patient with multiple sclerosis. (4/16)
We report a generalized skin eruption in a young man being treated with natalizumab, a new drug used in patients with multiple sclerosis. (+info)Differential behavioral profile induced by the injection of dipotassium chlorazepate within brain areas that project to the nucleus accumbens septi. (5/16)
BACKGROUND: The effect of the agonism on gamma-aminobutyric acid (GABA) receptors was studied within medial prefrontal cortex (mPFC), amygdala (AMY) and ventral hipocampus (VH) in the plus-maze test in male rats bilaterally cannulated. These structures send glutamatergic projections to the nucleus accumbens septi (NAS), in which interaction and integration between these afferent pathways has been described. In a previous study of our group, blockade of glutamatergic transmission within NAS induced an anxiolytic like effect. METHODS: Three rat groups received either saline or dipotassium chlorazepate (1 or 2 mug/1 mul solution) 15 min before testing. Time spent in the open arms (TSOA), time per entry (TPE), extreme arrivals (EA), open and closed arms entries (OAE, CAE) and relationship between open- and closed-arms quotient (OCAQ) were recorded. RESULTS: In the AMY injected group TSOA, OAE and EA were increased by the higher doses of dipotassium chlorazepate (p < 0.01). In the mPFC, TPE was decreased by both doses (p < 0.05). Injection within ventral hippocampus (VH) decreased TSOA, OAE and OCAQ with lower doses (p < 0.05). When the three studied saline groups were compared, TSOA, OAE, EA and OCAQ were enhanced in the VH group when compared to mPFC and AMY (p < 0.001). Insertion of inner canula (p < 0.001, p < 0.01, p < 0.01) and saline injection showed an increasing significant difference (p < 0.001 in all cases) with the action of guide cannula alone within VH in TSOA, OAE and EA. CONCLUSION: We conclude that the injection of dipotassium chlorazepate has a differential effect depending of the brain area, leading to facilitatory and inhibitory effects on anxiety processing. (+info)Allosteric modulation by benzodiazepine receptor ligands of the GABAA receptor channel expressed in Xenopus oocytes. (6/16)
Chick brain mRNA was isolated and injected into Xenopus oocytes. This led to the expression in the surface membrane of functional GABA-activated channels with properties reminiscent of vertebrate GABAA channels. The GABA-induced current was analyzed quantitatively under voltage-clamp conditions. Picrotoxin inhibited this current in a concentration-dependent manner with IC50 = 0.6 microM. The allosteric modulation of GABA currents by a number of drugs acting at the benzodiazepine binding site was characterized quantitatively. In the presence of the benzodiazepine receptor ligands diazepam and clorazepate, GABA responses were enhanced, and in the presence of the convulsant beta-carboline compound methyl 6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate (DMCM), they were depressed. Maximal stimulation of the response elicited by 10 microM GABA was 160% with diazepam and 90% with clorazepate, and maximal inhibition was 42% with DMCM, 30% with methyl beta-carboline-3-carboxylate (beta-CCM), 15% with ethyl-8-fluoro-5,6-dihydro-5-methyl-6-oxo-4H-imidazo [1,5a][1,4]benzodiazepine-3-carboxylate (Ro 15-1788), and 12% with ethyl beta-carboline-3-carboxylate (beta-CCE). Half-maximal stimulation was observed with 20 nM diazepam and 390 nM clorazepate, respectively, and half-maximal inhibition with 6 nM DMCM. beta-CCM had a similar effect to DMCM, whereas beta-CCE and Ro 15-1788 showed only small inhibition at low concentrations (less than 1 microM). All the tested carboline compounds and Ro 15-1788 showed a biphasic action and stimulated GABA current at concentrations higher than 1 microM.(ABSTRACT TRUNCATED AT 250 WORDS) (+info)Clorazepate use may prevent alcohol withdrawal convulsions. (7/16)
Clorazepate dipotassium was administered orally for the five-day prophylactic treatment of potential, incipient and overt withdrawal signs and symptoms in 226 patients on admission to an inpatient alcohol treatment unit. Conservative estimates based on these patients' histories and on literature reports predicted that between 7 and 40 (3% to 18%) of these persons would be expected to have a withdrawal convulsion. No patients experienced convulsions. This complete absence of seizures suggests that clorazepate is effective in counteracting convulsive and other manifestations of the alcohol withdrawal syndrome. (+info)Single daily dose treatment of anxiety with clobazam or dipotassium clorazepate. (8/16)
1 Forty-four clinically anxious patients entered a comparative double-blind trial of clobazam 20 mg, clobazam 30 mg and dipotassium clorazepate 15 mg, all drugs given as a single dose at night. 2 Assessment by the Hamilton Anxiety Scale, Morbid Anxiety Inventory (Salkind) and a Visual Analogue Scale showed a statistically significant improvement for all treatment groups after 2 weeks, with continued improvement after a further 2 weeks. 3 Daytime drowsiness was the commonest side-effect in all treatment groups but there was a tendency for a lower incidence in patients on clobazam. There was no evidence of a dose-related incidence of drowsiness in the clobazam 20 mg and 30 mg groups. Other side-effects were few and nonspecific. 4 Clobazam is a 1,5-benzodiazepine with an elimination half-life of 18 hours. When given in single doses of 20-30 mg at night it has an equivalent effect to dipotassium clorazepate 15 mg. (+info)Types of Alcoholic Psychoses:
1. Alcohol-related psychosis (ARP): This type of psychosis can occur in people who are intoxicated or experiencing withdrawal symptoms after stopping alcohol use. Symptoms include hallucinations, delusions, and disorganized thinking and behavior.
2. Korsakoff's syndrome: This is a memory disorder that occurs as a result of vitamin B1 (thiamine) deficiency caused by heavy drinking. People with Korsakoff's syndrome may experience confusion, amnesia, and psychotic symptoms such as hallucinations and delusions.
3. Wernicke-Korsakoff syndrome: This is a disorder that affects the brain and nervous system, caused by a combination of thiamine deficiency and chronic alcohol consumption. Symptoms include confusion, memory loss, and psychotic symptoms such as hallucinations and delusions.
Causes and Risk Factors:
1. Alcohol use: The primary cause of alcoholic psychosis is excessive and long-term alcohol consumption.
2. Genetics: People with a family history of mental health issues may be more susceptible to developing alcoholic psychosis.
3. Nutritional deficiencies: Poor nutrition, especially a lack of vitamin B1 (thiamine), can contribute to the development of alcoholic psychosis.
4. Brain changes: Long-term heavy drinking can cause changes in brain structure and function, which may increase the risk of developing psychotic symptoms.
5. Other factors: Trauma, stress, and social isolation may also contribute to the development of alcoholic psychosis.
Symptoms:
1. Hallucinations: People with alcoholic psychosis may experience hallucinations that can be visual, auditory, or both. These can range from simple sounds or voices to complex visions or conversations.
2. Delusions: Delusions are false beliefs that are not based in reality and cannot be explained by a person's cultural or religious beliefs. In alcoholic psychosis, delusions can range from paranoid thoughts to grandiose ideas.
3. Confusion: People with alcoholic psychosis may experience confusion about their surroundings, events, or people in their lives.
4. Memory loss: Alcoholic psychosis can cause short-term memory loss, difficulty with concentration, and difficulty learning new information.
5. Psychomotor agitation: People with alcoholic psychosis may exhibit agitated behavior, such as pacing, restlessness, or irritability.
6. Catatonia: In severe cases of alcoholic psychosis, people may exhibit catatonic symptoms, such as immobility, mutism, or negativism (resisting instructions or commands).
Diagnosis:
1. Physical examination: A healthcare professional will perform a physical examination to rule out other medical conditions that may cause similar symptoms.
2. Medical history: The healthcare professional will ask questions about the person's medical history, including their alcohol use and any previous psychotic episodes.
3. Mental status evaluation: The healthcare professional will evaluate the person's mental status, including their cognitive function, memory, and thought processes.
4. Laboratory tests: The healthcare professional may order laboratory tests to rule out other medical conditions that may cause similar symptoms.
5. Imaging studies: The healthcare professional may order imaging studies, such as a CT or MRI scan, to rule out other medical conditions that may cause similar symptoms.
Treatment:
1. Hospitalization: People with alcoholic psychosis are often hospitalized for their own safety and the safety of others.
2. Detoxification: The person will undergo detoxification to remove alcohol from their body.
3. Antipsychotic medications: The healthcare professional may prescribe antipsychotic medications to reduce the severity of symptoms.
4. Antidepressant medications: The healthcare professional may prescribe antidepressant medications to help manage depressive symptoms.
5. Counseling and therapy: The person will receive counseling and therapy to address their alcohol use disorder and any co-occurring mental health conditions.
6. Family support: The healthcare professional may involve the person's family in their treatment, as they can provide valuable support and help with recovery.
7. Follow-up care: The healthcare professional will follow up with the person to monitor their progress and make any necessary adjustments to their treatment plan.
Prognosis:
The prognosis for alcoholic psychosis is generally good if the person receives prompt and appropriate treatment. However, the condition can be challenging to treat, and recovery may take time. It is essential for the person to stay in treatment and follow their healthcare professional's recommendations to achieve the best possible outcome.
Complications:
Alcoholic psychosis can have several complications, including:
1. Suicide: People with alcoholic psychosis are at a higher risk of suicide due to their underlying mental health conditions and the stress of dealing with the condition.
2. Seizures: Alcohol withdrawal seizures can occur in people who suddenly stop drinking alcohol.
3. Dementia: Chronic alcohol consumption can cause permanent damage to the brain, leading to dementia.
4. Liver disease: Long-term heavy drinking can lead to liver disease, which can be life-threatening.
5. Heart disease: Excessive alcohol consumption can increase the risk of heart disease and stroke.
6. Nutritional deficiencies: Alcohol can interfere with the body's ability to absorb nutrients, leading to deficiencies in vitamins and minerals.
7. Social problems: Alcoholic psychosis can cause significant social problems, including strained relationships, financial difficulties, and legal issues.
Prevention:
Preventing alcoholic psychosis is essential, as it can be challenging to treat once it has developed. Some ways to prevent the condition include:
1. Avoiding excessive alcohol consumption: Limiting alcohol intake to moderate levels (up to one drink per day for women and up to two drinks per day for men) can reduce the risk of developing alcoholic psychosis.
2. Seeking professional help: If you or someone you know is struggling with alcohol addiction, seeking professional help from a mental health professional or a substance abuse treatment center can be beneficial.
3. Maintaining a healthy lifestyle: Engaging in regular exercise, eating a balanced diet, and getting enough sleep can help reduce the risk of developing alcoholic psychosis.
4. Avoiding triggers: Identifying and avoiding triggers that may cause you to drink excessively can help prevent the development of alcoholic psychosis.
5. Support groups: Joining a support group, such as Alcoholics Anonymous (AA), can provide a supportive community and resources for individuals struggling with alcohol addiction.
Treatment:
If you or someone you know is experiencing symptoms of alcoholic psychosis, it is essential to seek professional help immediately. Treatment options may include:
1. Hospitalization: In severe cases of alcoholic psychosis, hospitalization may be necessary to ensure the individual's safety and provide appropriate care.
2. Medications: Antipsychotic medications, such as risperidone or olanzapine, may be prescribed to manage symptoms of alcoholic psychosis.
3. Therapy: Cognitive-behavioral therapy (CBT) and other forms of talk therapy can help individuals understand the underlying causes of their addiction and develop strategies for maintaining sobriety.
4. Support groups: Joining a support group, such as Alcoholics Anonymous (AA), can provide a supportive community and resources for individuals recovering from alcoholic psychosis.
5. Lifestyle changes: Making lifestyle changes, such as avoiding triggers, engaging in regular exercise, and maintaining a healthy diet, can help individuals recovering from alcoholic psychosis maintain their sobriety and reduce the risk of relapse.
Clorazepate
Canine epileptoid cramping syndrome
Midazolam
List of MeSH codes (D03)
List of drugs: Df-Di
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Clorazepate (Clorazepate Dipotassium) Lederle
75 WATSON 364 Pill Beige Round - Pill Identifier
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DeCS
2023 Drugs Underdosing ICD-10-CM Codes
Formulary Clear Spring Health Premier Rx (PDP) S6946-040.
Antianginal Drugs Nursing Consideration & Management - RNpedia
Concrete Bullfloat - 6 x 48 Inch Aluminum - Ox Tools - Carbour Tools
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DailyMed - CLORAZEPATE DIPOTASSIUM tablet
Drug Treatment, Definition and Diagnosis for Insomnia
Review of the side-effect profile of buspirone - PubMed
Review of the side-effect profile of buspirone - PubMed
Betaxolol Hydrochloride|N0000004400
Code System Concept
MeSH Browser
MeSH Browser
Tranxene SD, Tranxene T-Tab (clorazepate) dosing, indications, interactions, adverse effects, and more
E0000163|Adriamycin|doxorubicin
Ponceau de Xylidine
(3761-53-3)
- Chemical Safety, Models, Suppliers, Regulation, and Patents - Chemchart
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ABORTIFACIENT AGENTS ABORTIFACIENT AGENTS
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3.75 mg2
- Each Clorazepate Dipotassium Tablet, USP 3.75 mg contains clorazepate equivalent to 2.9 mg. (nih.gov)
- Inactive ingredients for Clorazepate Dipotassium Tablets, USP: Colloidal Silicon Dioxide, FD&C Blue No.2 Aluminum Lake (3.75 mg), FD&C Yellow No.6 Aluminum Lake (7.5 mg), Magnesium Oxide, Potassium Chloride, Potassium Carbonate, Microcrystalline Cellulose, Croscarmellose Sodium and Magnesium Stearate. (nih.gov)
Potassium Clorazepate2
Chlorazepate1
- Esophageal burn due to chlorazepate dipotassium (Tranxene). (nih.gov)
Benzodiazepine2
- Chemically, clorazepate dipotassium is a benzodiazepine. (nih.gov)
- Risk of withdrawal was investigated in a prospective, double-blind comparison of clorazepate dipotassium, a benzodiazepine with a long half-life, and the nonbenzodiazepine buspirone hydrochloride in the long-term treatment of anxious outpatients. (nih.gov)
Doses1
- Patients were treated with therapeutic doses of clorazepate dipotassium (15 to 60 mg/d) or buspirone hydrochloride (10 to 40 mg/d) for six continuous months before their tranquilizer therapy was blindly and abruptly stopped. (nih.gov)
Withdrawal4
- Abrupt discontinuation or rapid dosage reduction of clorazepate dipotassium after continued use may precipitate acute withdrawal reactions, which can be life-threatening. (nih.gov)
- To reduce the risk of withdrawal reactions, use a gradual taper to discontinue clorazepate dipotassium or reduce the dosage (See DOSAGE AND ADMINISTRATION and WARNINGS). (nih.gov)
- There was a significant increase in symptom severity consistent with a withdrawal reaction for the clorazepate group but not the buspirone group. (nih.gov)
- For the clorazepate group, there was a suggestion that previous discontinuous exposure to benzodiazepines might sensitize patients to subsequent withdrawal effects. (nih.gov)
Lorazepam1
- Clorazepate and lorazepam: clinical improvement and rebound anxiety. (nih.gov)
Treatment1
- Before prescribing clorazepate dipotassium and throughout out treatment, assess each patient's risk for abuse, misuse, and addiction (See WARNINGS). (nih.gov)
Respiratory depression and sedation1
- If a decision is made to prescribe clorazepate dipotassium tablets concomitantly with opioids, prescribe the lowest effective dosages and minimum durations of concomitant use, and follow patients closely for signs and symptoms of respiratory depression and sedation. (nih.gov)
Magnesium2
- Inactive ingredients for clorazepate dipotassium tablets: croscarmellose sodium, magnesium oxide, magnesium stearate, microcrystalline cellulose, potassium carbonate, sodium chloride and sodium lauryl sulfate. (nih.gov)
- clorazepate, calcium/magnesium/potassium/sodium oxybates. (medscape.com)
Increase4
- Plasma levels of nordiazepam increase proportionally with clorazepate dipotassium dose and show moderate accumulation with repeated administration. (nih.gov)
- abametapir will increase the level or effect of clorazepate by affecting hepatic/intestinal enzyme CYP3A4 metabolism. (medscape.com)
- conivaptan will increase the level or effect of clorazepate by affecting hepatic/intestinal enzyme CYP3A4 metabolism. (medscape.com)
- idelalisib will increase the level or effect of clorazepate by affecting hepatic/intestinal enzyme CYP3A4 metabolism. (medscape.com)
Patients5
- The incidence of drowsiness in buspirone-treated patients was significantly less than that in each of the groups receiving diazepam (32 percent), clorazepate (26 percent), lorazepam (58 percent), or alprazolam (43 percent). (nih.gov)
- Depression occurred less frequently in buspirone-treated patients than in those receiving clorazepate, diazepam, or lorazepam. (nih.gov)
- Impotence occurred only in clorazepate- and lorazepam-treated patients. (nih.gov)
- Decreased libido occurred more frequently in diazepam-treated patients, whereas increased libido was more frequent in clorazepate-treated patients. (nih.gov)
- Clorazepate dipotassium tablets are contraindicated in patients with a known hypersensitivity to the drug and in those with acute narrow angle glaucoma. (nih.gov)