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Antabuse (Disulfiram)
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Antabuse

Generic Antabuse is a high-quality medication which is taken in treatment of alcoholism. Generic Antabuse acts by blocking the breakdown of alcohol, causing unpleasant side effects (eg, vomiting, upset stomach) when even a small amount of alcohol is consumed. It is an alcohol-abuse deterrent.

Other names for this medication:
Alcophobin, Anticol, Aversan, Diabuse, Disulfiramo, Disulfiramum, Disulphiram, Esperal, Etabus, Etiltox, Refusal, Tenutex

Similar Products:
Camprall, Naltrexone, Vivitrol

 

Also known as:  Disulfiram.

Description

Generic Antabuse is a perfect remedy in struggle against alcoholism.

Generic Antabuse acts by blocking the breakdown of alcohol, causing unpleasant side effects (eg, vomiting, upset stomach) when even a small amount of alcohol is consumed. It is an alcohol-abuse deterrent.

Antabuse is also known as Disulfiram, Antabus.

Generic name of Generic Antabuse is Disulfiram.

Brand name of Generic Antabuse is Antabuse.

Dosage

Do not take the first dose of Generic Antabuse for at least 12 hours after drinking alcohol.

Take Generic Antabuse orally with or without food.

If you want to achieve most effective results do not stop taking Generic Antabuse suddenly.

Overdose

If you overdose Generic Antabuse and you don't feel good you should visit your doctor or health care provider immediately.

Storage

Store at room temperature between 20 and 25 degrees C (68 and 77 degrees F) away from moisture and heat. Keep in a tight light resistant container. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Antabuse are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

Do not take Generic Antabuse if you are allergic to Generic Antabuse components.

Do not take Generic Antabuse if you are pregnant, planning to become pregnant, or are breast-feeding.

Notify your doctor immediately if you experience yellowing of the skin or eyes, dark urine, weakness, tiredness, loss of appetite, or nausea and vomiting. These may be signs of a liver problem.

Before you have any medical or dental treatments, emergency care, or surgery, tell the health care provider or dentist that you are using Generic Antabuse.

Use Generic Antabuse with extreme caution in children.

Avoid all alcohol including alcohol found in sauces, vinegar, mouthwash, liquid medicines, lotions, after shave, or backrub products.

Avoid machine driving.

It can be dangerous to stop Generic Antabuse taking suddenly.

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The breath analyser can improve the assessment of the compliance status of patients receiving a daily dose regimen of disulfiram, but is less useful for this purpose if disulfiram is taken on a thrice-weekly regimen.

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The CT or TT MTHFR genotype group (N = 32) dropped from 73 to 52% cocaine-positive urines on disulfiram (p = 0.0001), while the placebo group showed no treatment effect. The CC MTHFR genotype group (N = 24) showed a smaller, but still significant, reduction in cocaine-positive urines on disulfiram compared to placebo; 81-69% (p = 0.007).

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For more than 55 years, disulfiram has been approved by the Food and Drug Administration for the treatment of alcohol dependence. It is a unique medication that relies on "psychological threat" to avoid disulfiram-ethanol reactions. This paper reviews the history of disulfiram treatment, the current status of disulfiram treatment, the ensuing developments in disulfiram use in treating various addictions, and future directions. Clinical trials using disulfiram for the treatment of alcohol, cocaine, or co-occurring alcohol + cocaine dependence were included in this review. Disulfiram efficacy studies focusing on supervised, implant, and combination pharmacotherapies were also examined. In clinical trials, disulfiram has demonstrated inconsistent results in helping patients to abstain from alcohol, and patients poorly adhere to a disulfiram-treatment regimen. This has raised questions about disulfiram's practicality in the treatment of alcohol dependence. Recently, however, disulfiram has gained attention as a complementary agent to newer pharmacological medications, such as an opiate antagonist that specifically reduces alcohol craving. One hypothesis is that disulfiram would assist patients in gaining psychological control over drinking when given in conjunction with an opiate antagonist that would act directly on reducing alcohol craving. Preliminary evidence also suggests that disulfiram treatment could be a viable treatment for cocaine dependence because it was shown to reduce cocaine use among nonalcoholic, cocaine-dependent patients.

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Alcohol-related diseases have multiple and varied associations with acetaldehyde, a highly toxic product of ethanol oxidation that accumulates in the absence of active aldehyde dehydrogenase (ALDH). This study was designed to clarify the role of acetaldehyde in liver injury, specifically in vivo and in vitro effects on Kupffer cell release of the inflammatory cytokine tumor necrosis factor-alpha (TNF-Alpha).

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Fifty-nine couples with an alcoholic husband, after receiving weekly BMT couples sessions for 5-6 months, were assigned randomly to get or not get 15 additional couples relapse prevention (RP) sessions over the next 12 months. Outcome measures were collected before and after BMT and at quarterly intervals for the 30 months after BMT.

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Acetaldehyde has been proposed as one of the mediators of liver injury in alcoholic liver disease. We investigated whether increased acetaldehyde levels affected the development of alcoholic liver injury. Male Wistar rats were fed a liquid diet containing fish oil and ethanol by intragastric infusion. Sustained elevations of acetaldehyde were achieved by daily treatment with two inhibitors of aldehyde dehydrogenase (ALDH): disulfiram and benzcoprine. Pathologic changes, plasma and liver acetaldehyde, nuclear factor-kappa B (NF-kappaB) and I kappa B alpha (I kappaB alpha) protein, tumor necrosis factor-alpha (TNF-alpha) and cyclooxygenase 2 (COX-2) mRNA were evaluated. Treatment with the ALDH inhibitors led to increased acetaldehyde in liver and plasma but prevented necrosis and inflammation. Steatosis was not affected. Both inhibitors decreased activation of NF-kappaB and down-regulated TNF-alpha and COX-2 expression. Decreased activation of NF-kappaB was accompanied by I kappaB alpha preservation. Acetaldehyde probably inhibits NF-kappaB activation through I kappaB alpha preservation. Down-regulation of TNF-alpha and COX-2 occur secondary to inhibition of NF-kappaB and account for the absence of necrosis and inflammation in the ALDH inhibitor-treated groups.

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Little is known about the occurrence and course of alcohol problems in patients with affective syndromes treated in psychiatric facilities. We have shown previously that a high proportion of such patients abused alcohol. In a 5-year follow-up of patients in the initial study, a large majority had a remission of their alcohol problems lasting at least 6 months, although many of these patients had subsequent relapses. Using survival analyses, we found that alcohol dependence indicators, previous chronicity of alcohol problems, and a diagnosis of schizoaffective disorder predicted poor outcome (specifically, longer time to remission of the alcohol problems). However, these factors were unrelated to receiving alcohol-specific treatment during the 5 years. Severity of social/occupational alcohol problems did not predict poor outcome, but did predict alcohol-specific treatment (detoxification, rehabilitation, Alcoholics Anonymous [AA], or Antabuse).

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Human aldehyde dehydrogenase (ALDH) consists of two main isozymes with low and high Km for aldehyde. ALDH isozymes in hair sheats were tested from 40 Japanese using isoelectric focusing and blood acetaldehyde determination with gas chromatography. About 43% of Japanese, who lacked the low Km enzyme (ALDH I) showed an elevated acetaldehyde concentration due to their inability to metabolize acetaldehyde quickly and effectively. Studies regarding the inhibitory reaction of disulfiram and its metabolites have been performed. Among the metabolites, diethylamine inhibited the low Km enzyme strongly. It is presumed that vasomotor symptoms and high acetaldehyde concentration in blood after alcohol intake in patients who are treated with disulfiram might be mainly due to a decrease in activity of the low Km enzyme caused by diethylamine which is produced in vivo as one of the metabolites from disulfiram, rather than to an inhibitory reaction of disulfiram only. Thus, alcohol sensitivity in Mongoloids and disulfiram-ethanol reaction may have a common mechanism.

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This study was designed to investigate the effects of four compounds that are shown to influence the cytochrome P450 system, on the metabolism of and DNA adduct formation by benzo[alpha]pyrene (BaP) in human skin epithelial cells in culture. Radiolabeled BaP was used in the metabolism studies, and the levels of metabolites in the ethylacetate extracts of the intracellular and extracellular fractions were determined by HPLC. Among the various metabolites detected BaP-7,8-diol was the only one that was an intermediate on the activation pathway of BaP to the ultimate carcinogen, BPDE I. Both BHA and 7,8-BF pretreatment significantly decreased intracellular production of BaP-7,8-diol compared to cultures treated with only radiolabeled BaP. MeBHA pretreatment greatly increased intracellular BaP-7,8-diol formation compared to BaP treated controls, while disulfiram pretreatment had no effect on the intracellular concentration. Cultures pretreated with BHA, 7,8-BF or disulfiram formed 30-40% less BPDE I-dG adducts than nonpretreated cultures, while cultures pretreated with MeBHA exhibited approximately 200% increase in the BPDE I-dG adduct formation. Thus, BHA and 7,8-BF act similarly in reducing BaP activation and adduct formation. Alternatively, MeBHA increased BaP activation and adduct formation in human keratinocyte cultures in vitro. Disulfiram pretreatment did not reduce BaP-7,8-diol formation, but decreased BPDE I-dG adducts. These studies indicate that modulators of the P450 system act in different fashions at the level of production of an oxygenated procarcinogen metabolite, altering the amount of specific carcinogen-dG adducts that lead to the expression of a transformed phenotype.

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Many drugs have been found to increase or decrease the clearance of theophylline, probably by interaction with one or more of the variants of the cytochrome P450 drug-metabolising system. Theophylline may be particularly susceptible to alteration of its clearance because of the particular form(s) of the P450 system involved, because its metabolism is saturable, and/or because 90% of its elimination is via metabolism. Its clearance has been found to be decreased (typically by around 25%, but often by far more) by erythromycin, troleandomycin (triacetyloleandomycin), roxithromycin, enoxacin, ciprofloxacin, pefloxacin, norfloxacin, ofloxacin, fluoroquinolone T-3262, pipemidic acid, cimetidine, etintidine, propranolol, verapamil, diltiazem, nifedipine, furosemide (frusemide), at least some anovulent agents, viloxazine, allopurinol, ticlopidine, idrocilamide, thiabendazole, disulfiram, influenza- and BCG-vaccination, interferon, and caffeine (half-life increase). In contrast, theophylline clearance (clearance/bioavailability) was found to be increased by isoprenaline (isoproterenol), terbutaline, some corticosteroids, phenytoin, phenobarbital, activated charcoal, felodipine moricizine, benzodiazepines and sulfinpyrazone - typically by about 25%, but sometimes by as much as 80% or more. For several of these concomitant medications, however, only some of the published studies can substantiate an influence, which may highlight the sensitivity of some interactions to particular experimental and/or clinical conditions, e.g. with terbutaline, erythromycin, ciprofloxacin, norfloxacin, ofloxacin, phenobarbital, cimetidine, verapamil, diltiazem, nifedipine, anovulents, allopurinol and influenza vaccination. Moreover, reports both of inhibition and of induction of theophylline clearance by each of rifampicin and isoniazid have appeared. Nevertheless, under investigation many medications have not been found to perceptibly influence theophylline disposition kinetics, e.g. ephedrine, orciprenaline (metaproterenol), prednisone, prednisolone, temelastine, terfenadine, mequitazine, picumast, repirinast, josamycin, midecamycin, miocamycin, spiramycin, amoxicillin, ampicillin, cefalexin, cefaclor, ceftibuten, cotrimoxazole (trimethoprim plus sulfamethoxazole), tetracycline, doxycycline, lomefloxacin, fluoroquinolones NY-198 and AM-833, nalidixic acid, lincomycin, metronidazole, certain antacids, ranitidine, roxatidine, pirenzepine, rioprostil, metoclopramide, metoprolol, atenolol, nadolol, medroxyprogesterone, dextropropoxyphene (propoxyphene), piroxicam, ozagrel, mebendazole and ascorbic acid.(ABSTRACT TRUNCATED AT 400 WORDS)

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A functional screen in yeast has expanded the list of genes required for Cu-dependent fitness, revealing a complex cellular system with implications for human health. Respiratory fitness defects arising from perturbations in this Buy Cialis 200mg system can be corrected with pharmacological agents that increase intracellular copper concentrations.

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Using PUBMED and the list of references from key publications, this review article covered the epidemiology, neurobiology and pharmacotherapy of PTSD with comorbid alcohol, opiate, and cannabis use disorders. These SUD represent two with and Buy Topamax Mexico one without FDA approved pharmacotherapies.

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1-(4,5-Dimethylthiazol-2-yl)-3,5-diphenylformazan (MTT), combination index (CI)-isobologram, western blot, luciferase reporter gene Buy Valtrex Online India assay, electrophoretic mobility-shift assay and ALDH analysis were used in this study.

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The effect of disulfiram on egg shell morphology in the parasitic nematode Trichuris muris was studied in vitro and in vivo. Daily disulfiram treatment of mice infected with T. muris beginning 25 days after infection and continuing for 26 days resulted in the production of malformed eggs by adult female worms in all treated groups. In addition, significantly fewer adult worms were found at necropsy in mice treated with 5.0 or 7.5 mg/kg/day of disulfiram as Buy Sildenafil Dapoxetine compared with mice treated with 2.5 mg/kg/day or control mice. Adult worms collected from infected, untreated mice and placed in aerobic culture for 5 days in media containing 4 or 8 micrograms/ml of disulfiram released malformed eggs into the culture medium after 30 hr in culture. Oral inoculation of naive mice with malformed eggs did not result in T. muris infections in the mice. The results of these studies suggest that inhibition of phenol oxidase results in disruption of normal egg production by T. muris females and that the enzyme might be a useful target in the development of control strategies aimed at nematode parasites that rely on phenol oxidase for egg shell hardening.

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T-helper 17 (Th17) cells play an important role in the pathogenesis of multiple sclerosis (MS), an autoimmune demyelinating disease that affects the CNS. In the present study, MicroRNA sequencing (miRNA-seq) was performed in mouse Th0 and Th17 cells to determine the critical miRNAs that are related to Th17 differentiation. We found that miR-30a was significantly downregulated during mouse Th17 differentiation. In addition, the level of miR-30a in CD4(+) T cells from peripheral blood of MS patients and experimental autoimmune encephalomyelitis (EAE) animal models was also decreased and inversely correlated with the expression of interleukin 17a, the Buy Omeprazole Liquid canonical cytokine of Th17 cells. Moreover, overexpression of miR-30a inhibited Th17 differentiation and prevented the full development of EAE, whereas interference of miR-30a promoted Th17 differentiation. Mechanism studies showed that miR-30a reduced IRF4 expression by specifically binding with the 3'-untranslated region. Through screening of 640 different Food and Drug Administration (FDA)-approved drugs, we found that disulfiram and diphenhydramine hydrochloride were effective candidates for inhibiting Th17 differentiation and ameliorating EAE development through upregulating miR-30a. To our knowledge, the present work is not only the first miRNA-seq study focusing on Th17 differentiation, but also the first chemical screening for FDA-approved drugs that inhibit Th17 differentiation through regulating miRNA expression.

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4-methylpyrazole (4-MP), an inhibitor of alcohol dehydrogenase, rapidly abolished the accumulation of Buy Flagyl 2g Online acetaldehyde following alcohol ingestion both in volunteers pretreated with the Antabuse analog calcium carbimide and in an antabuse-treated alcoholic. 4-MP also attenuated other typical symptoms, including facial flushing and tachycardia, thus suggesting its usefulness in the acute treatment of severe disulfiram-alcohol reactions.

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A genetic association study of the unique tag single nucleotide polymorphism (SNP) rs11915160 of the SOX2 gene was Buy Metformin Tablets conducted in patients with type 1 diabetes mellitus (T1DM), with or without DN, who were identified from the Genetics of Kidneys in Diabetes (GoKinD) study.

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Hypotensive action of a new dopamine beta-hydroxylase (DBH) inhibitor, 5-(4'-chlorobutyl)picolinic acid (FD-008) was investigated in dogs and rats. FD-008, which is one of the most potent inhibitors among fusaric acid derivatives, decreased blood pressure in spontaneously hypertensive rats relatively parallel to DBH inhibition in vitro. The effect of FD-008 on blood pressure was stronger in hypertensive rats than in normotensive rats. No cumulative effect was observed in rats by repeated administration, On Buy Sumatriptan 50mg the other hand, repeated administration was required to lower blood pressure in normotensive dogs. The acute effect of FD-008 on blood pressure of anesthetized dogs was somewhat different from that of its mother compound, fusaric acid.

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Acetaldehyde has been proposed as one of the mediators of liver injury in alcoholic liver disease. We investigated whether increased acetaldehyde levels affected the development of alcoholic liver injury. Male Wistar rats were fed a liquid diet containing fish oil and ethanol by intragastric infusion. Sustained elevations of acetaldehyde were achieved by daily treatment with two inhibitors of aldehyde dehydrogenase (ALDH): disulfiram and benzcoprine. Pathologic changes, plasma and Buy Prednisone liver acetaldehyde, nuclear factor-kappa B (NF-kappaB) and I kappa B alpha (I kappaB alpha) protein, tumor necrosis factor-alpha (TNF-alpha) and cyclooxygenase 2 (COX-2) mRNA were evaluated. Treatment with the ALDH inhibitors led to increased acetaldehyde in liver and plasma but prevented necrosis and inflammation. Steatosis was not affected. Both inhibitors decreased activation of NF-kappaB and down-regulated TNF-alpha and COX-2 expression. Decreased activation of NF-kappaB was accompanied by I kappaB alpha preservation. Acetaldehyde probably inhibits NF-kappaB activation through I kappaB alpha preservation. Down-regulation of TNF-alpha and COX-2 occur secondary to inhibition of NF-kappaB and account for the absence of necrosis and inflammation in the ALDH inhibitor-treated groups.