Pronunciation: dye-AZ-e-pam
Chemical Abstracts Service Registry Number: 439-14-5
Formal Names: Alupram, Atensine, Diastat, Diazemuls, Evacalm, Solis, Stesolid, Tensium, Valium, Valrelease, Vival
Informal Names: Blues, Drunk Pills, Ludes, Mother’s Little Helper, V, Val
Type: Depressant (benzodiazepine class).
Federal Schedule Listing: Schedule IV (DEA no. 2765)
USA Availability: Prescription
Pregnancy Category: D

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Pronunciation: al-PRAY-zoh-lam (also pronounced al-PRAZ-oh-lam)
Chemical Abstracts Service Registry Number: 28981-97-7
Formal Names: Alplax, Frontal, Solanax, Tafil, Trankimazin, Xanax, Xanor, Zotran
Type: Depressant (benzodiazepine class).
Federal Schedule Listing: Schedule IV (DEA no. 2882)
USA Availability: Prescription
Pregnancy Category: D

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Most polular benzodiapines drugs:

Xanax - generic name Alprazolam

Valium - generic name Diazepam

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Diazepam is a widely used sedative anti-anxiety medication. Trade names are: Ansiolin, Apaurin, Apozepam, Atilen, Bensedin, Diapam, Diazepam, Eridan, Lembrol, Pacitrian, Quetinil, Relanium, Saromet, Seduxen, Serenamin, Serensin, Sonacon, Stesolin, Ushamir, Valitran, Valium, Valium Roche, Vatran, Vival and others. Read the rest of this entry »

Buspirone, marketed as Buspar, a nonbenzodiazepine and generally nonsedating anxiolytic, was the first prominent anxiolytic introduced after the benzodiazepines. Its antianxiety effects are believed to be secondary to its acting as a partial agonist of the 5-HT1A receptor. Buspirone is as effective as diazepam and superior to placebo in double-blind trials involving anxious outpatients (Schatzberg et al. 2003). The parent drug is metabolized by CYP3A4 while its metabolite is metabolized by CYP2D6. Important drug–drug interactions with buspirone include agents that may inhibit CYP3A4 and 2D6. Read the rest of this entry »

Investigations into the use of noradrenergic agents as anxiolytics were first directed toward their use in anxious musical performers. B-Blockers such as propranolol were found to be useful in alleviating symptoms of anxiety (e.g., palpitations, sweating). Years later, clonidine was shown by Gold et al. (1978) to be effective in blocking physiological symptoms associated with opioid withdrawal. Although not found to be effective in blocking panic, agents such as propranolol, atenolol, and nadolol have been found to be useful when used adjunctively with other agents in reducing symptoms of autonomic arousal associated with panic and social anxiety (Rosenbaum et al. 1998). Importantly, propranolol is metabolized primarily by CYP2D6 and should probably be used in lower dosages in Asians who are slower metabolizers of CYP2D6 substrates.

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Monoamine oxidase inhibitors (MAOIs) have been shown to be effective in the treatment of anxiety disorders such as social anxiety and panic disorder. In a 12-week, placebo-controlled trial of patients with panic disorder, Sheehan and colleagues reported that phenelzine (45 mg/day) was better than placebo; however, higher doses of the MAOI (e.g., 60–90 mg/day) may be more effective (Sheehan 1980; Buiges1987). Because of the potential risk of a hypertensive crisis with a tyramine-containing diet, the MAOIs have grown less in favor with clinicians, especially since the advent of the SSRIs. MAOIs, however, remain clinically effective agents in the treatment of atypical depression and anxiety disorders, and therefore their metabolism by patients of different ethnic origin remains an important topic of research. MAOIs are predominantly metabolized by CYP2C19 (Bezchlibnzyk-Buler and Jeffries 1999). Its pharmacokinetic properties are significant for auto-inhibition or metabolite-induced inhibition. Thus, clearance at higher dosages is decreased and caution should be exercised when prescribing these agents at higher dosages. Pharmacogenetic findings suggest a higher percentage of Asian Americans and African Americans are poor metabolizers of CYP2C19 substrates. Pharmacokinetics and pharmacodynamics studies with MAOIs are scarce with respect to potential variations in ethnic groups and may offer further information on the use of these agents in safer and clinically more effective fashions.

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Several SSRIs have been FDA approved for one or more specific anxiety diagnoses [e.g., paroxetine for social anxiety, generalized anxiety disorder (GAD) and posttraumatic stress disorder (PTSD); sertraline for obsessive–compulsive disorder (OCD) and PTSD]. In clinical practice, the SSRIs have become the “first-line” treatment for panic disorder because of their overall safety and tolerability, their safety in overdose, and their low potential for addiction and withdrawal.

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Benzodiazepines comprise the most frequently prescribed subclass of antianxiety agents. These agents, first introduced in the early 1960s, quickly replaced the use of barbiturates as the pharmacological approach to anxiety. The popularity of these agents can be attributed to their generally quick onset of action and wider safety margin in overdose compared to the barbiturates. However, the potential of these agents to elicit physical dependence also quickly became apparent. In addition to the frequent use of these agents as anxiolytics, benzodiazepines are also commonly used for muscle tension, insomnia, status epilepticus (diazepam), myoclonic epilepsy (clonazepam), preoperative anesthesia, and alcohol withdrawal. Importantly, Ativan (lorazepam) is often used in the emergency room and inpatient setting to manage acute agitation in patients. Controlled studies involving Asians and Caucasians demonstrated significant pharmacokinetic differences involving use of the benzodiazepines (Ghoneim et al. 1981; Kumana et al. 1987). The volume of distribution of diazepam in these studies was found to be lower, and both serum diazepam and desmethyldiazepam levels were higher in Asian than in white physically and psychiatrically healthy volunteers. These differences became statistically insignificant, however, after controlling for ethnic differences in skinfold thickness and the ratio of actual to ideal body weight, suggesting that ethnic differences may be secondary to differences in the percentage of body fat.

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The focus of pharmacogenetic studies has largely been on those genes that encode enzymes responsible for the metabolism of medications. However, ethnic differences may also be affected by genes controlling the function and response of therapeutic targets. A well-established example of the difference that exists between different ethnic groups is the metabolism of alcohol. One of the enzymes responsible for the metabolism of alcohol is acetaldehyde dehydrogenase (ALDH), and 40%–50% of Asian subjects have a mutation that renders this enzyme inactive. The result is an uncomfortable “flushing” response, well known among many Asians even with a very small amount of alcohol (Agarwal and Goedde 1992; Yoshida 1993). It is now known that a mutation in a single nucleotide is responsible for the production of the inactive form of ALDH (Novoradovsky et al. 1995; Goedde et al. 1986).

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