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Effexor (Venlafaxine)

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Generic Effexor is a qualitative medication which is taken in treatment of panic disorder, anxiety and depression. Generic Effexor effectiveness is in balancing the brain. It is a SSNRIs (selective serotonin and norepinephrine reuptake inhibitors).

Other names for this medication:
Agrofan, Alventa, Anapresin, Argofan, Axyven, Benolaxe, Depant prolong, Deprevix, Deprexor, Depurol, Desinax, Dobupal, Efaxil, Efaxin, Efectin, Efectin er, Efetrin, Efevelone, Efexiva, Efexor, Efexor exel, Effexor, Elafax, Elify, Faxine, Faxiprol, Flavix, Ganavax, Idoxen, Ireven, Jarvis, Lafax, Lanvexin, Laroxin, Melocin, Memomax, Mezine, Mollome, Nervix, Nopekar, Norafexine, Norpilen, Odven, Olwexya, Prefaxine, Quilarex, Ranfaxiran, Senexon, Sentidol, Sesaren, Subelan, Tavex, Tifaxin, Trevilor, Valax, Valosine, Vandral, Vedixal, Velafax, Velaxin, Venax, Venaxibene, Venex, Venexor, Veniz, Venla, Venlaf, Venlafab, Venlafaxina, Venlafaxinum, Venlagamma, Venlalek, Venlalic, Venlasan, Venlax, Venlax er, Venlaxor, Venlectine, Venlift, Venlix, Venlofex, Vennaxa, Vensir, Viepax, Voxatin

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Also known as:  Venlafaxine.


Generic Effexor is a perfect remedy in struggle against panic disorder, anxiety. Its target is to treat depression. Generic Effexor effectiveness is in balancing the brain. It is a SSNRIs (selective serotonin and norepinephrine reuptake inhibitors).

Generic name of Generic Effexor is Venlafaxine.

Effexor is also known as Venlafaxine, Ventab, Efexor, Venlor, Venla, Venlift.

Brand names of Generic Effexor are Effexor, Effexor XR.


Generic Effexor is available in tablets and capsules. Generic Effexor is taken orally with food.

Do not crush or chew it.

Take Generic Effexor at the same time every day with water.

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


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


Store at a controlled temperature between 20 and 25 degrees C (68 degrees and 77 degrees F) away from moisture and heat. 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 Effexor 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.


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

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

Do not take it if you are under 18.

Be careful with Generic Effexor if you take ketoconazole (such as Nizoral); other antidepressants (fluoxetine (such as Prozac), sertraline (such as Zoloft), amoxapine (such as Ascendin), paroxetine (such as Paxil), citalopram (such as Celexa), protriptyline (such as Vivactil), clomipramine (such as Anafranil), trimipramine (such as Surmontil), desipramine (such as Norpramin), escitalopram (such as Lexapro), fluvoxamine (such as Luvox), imipramine (such as Tofranil), amitriptyline (such as Elavil), nortriptyline (such as Pamelor)); imetidine ( such as Tagamet HB, Tagamet); tryptophan; zolmitriptan (such as Zomig); rizatriptan (such as Maxalt), almotriptan (such as Axert), frovatriptan (such as Frova), naratriptan (such as Amerge), sumatriptan (such as Imitrex); warfarin (such as Coumadin); risperidone (such as Risperdal) or haloperidol (such as Haldol), monoamine oxidase inhibitors (MAOIs).

Avoid alcohol.

Be careful when you are driving or operating machinery.

It can be dangerous to stop Generic Effexor taking suddenly.

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Neural activity, as measured using functional magnetic resonance imaging during performance of an emotion regulation paradigm, as well as regular assessments of symptom severity using the Hamilton Depression Rating Scale. For use of all data points, slope trajectories were calculated for rate of change in depression severity and for rate of change in neural engagement.

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The national pharmacy database was used to select patients using venlafaxine for at least 6 months. Switchers and nonswitchers were identified, and switch behavior was compared for a 12-month follow-up period. Change in health service use following switching was also compared between switchers and nonswitchers including use of the emergency department, hospital, and specialist outpatient services over the same period.

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Outpatients (n = 232) with major depressive disorder were randomly assigned to 8 weeks of treatment with either "standard" (n = 119; mean dose = 148 mg/d) or "higher" (n = 113; mean dose = 309 mg/d) dosage therapies. Between weeks 8 and 12, nonresponders in the standard dose group could receive higher dose therapy.

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Desvenlafaxine succinate (DVS) is one of several serotonin-norepinephrine reuptake inhibitors (SNRIs). Others are venlafaxine hydrochloride, milnacipran, and duloxetine. Desvenlafaxine has been approved by the US Food and Drug Administration (FDA) for the treatment of major depressive disorder (MDD) based on a number of randomized, placebo-controlled clinical trials. Clinical studies have investigated the efficacy of DVS in doses ranging from 50 to 400 mg/day for the treatment of MDD in adult outpatients. The effects of DVS 50 mg/day have been clearly distinguished from placebo in the reduction of MDD symptoms in such clinical trials. No additional therapeutic benefits were found at doses > 50 mg/day. The recommended dose of DVS ranges from 50 to 100 mg. Desvenlafaxine is currently the third SNRI approved by the FDA for this indication. Preliminary evidence also suggests the clinical usefulness of DVS in the treatment of vasomotor symptoms of menopause, anxiety symptoms, and painful physical symptoms. The modified pharmacokinetic and pharmacodynamic profiles of DVS differentiate this drug from the original product, venlafaxine. Significant points of difference, compared with venlafaxine, are once-daily dosing and the achievement of steady-state plasma concentrations within 4 to 5 days. To summarize, current evidence indicates that DVS has proven efficacy, acceptable safety and tolerability profiles, convenient dosing, and minimal impact on the cytochrome P450 enzyme system. A reduced risk for pharmacokinetic drug interactions is a potential advantage over other selective serotonin noradrenaline reuptake inhibitors. Desvenlafaxine succinate has demonstrated its efficacy for treating MDD but its variable efficacy, as shown in individual studies, limited long-term data, and its different risk-to-benefit ratio compared with earlier antidepressants, means that further investigation of this drug is necessary.

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A double-blind, randomized, parallel study in 167 hospitalized patients with major depression and melancholia was conducted to determine if rapidly escalated doses of venlafaxine produced an earlier response, compared with rapidly escalated doses of imipramine. The daily dose of venlafaxine was rapidly increased to 375 mg/day over a five-day period, was maintained at this level for 10 days, and then was reduced to 150 mg/day for the remainder of the study. The imipramine dose was rapidly increased to 200 mg/day over five days and was maintained at this level to the end of the study. The primary efficacy variables were time to response and time to sustained response on the HAM-D and MADRS. No differences in the response rates on the HAM-D or MADRS were observed between treatments. However, among patients who demonstrated a response on the HAM-D, there was a significantly faster onset of response (p = 0.036) and sustained response (p = 0.018) in the venlafaxine group. The median time to response on the HAM-D among responders was 14 days with venlafaxine and 21 days with imipramine. However, no differences between treatments were observed among responders on the MADRS (median time to response: 15 days for venlafaxine, 18 days for imipramine). Study events were reported in 69% of venlafaxine-treated patients and 76% of imipramine-treated patients. In severely depressed patients with melancholia, a faster onset of response was observed with venlafaxine on the HAM-D, but not the MADRS, and maximal tolerated doses of venlafaxine and imipramine were comparable for overall efficacy. These results confirm and extend previous observations and suggest that venlafaxine may have an early onset of action and may produce a rapid response in hospitalized patients with severe depression complicated by melancholia.

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Antidepressants have been associated with increased bone loss and fractures in older adults in observational studies, but the mechanism is unclear. We examined the effects of a serotonin-norepinephrine reuptake inhibitor, venlafaxine, on biomarkers of bone turnover in a prospective treatment study of late-life depression.

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In a pragmatic randomized controlled trial, patients diagnosed with a major depressive disorder according to the DSM-IV and aged 60 years or older will be recruited from psychiatric centers across the Netherlands. After CYP2D6 genotyping determined in peripheral blood obtained by finger-prick, patients will be grouped into poor, intermediate, extensive, or ultrarapid metabolizers. Patients with deviant genotype (that is poor, intermediate or ultrarapid genotype) will be randomly allocated to an intervention group in which the genotype and dosing advice is communicated to the treating physician, or to a control group in which patients receive care as usual. Additionally, an external reference group of patients with the extensive metabolizer genotype is included. Primary outcome in all groups is time needed to obtain an adequate blood level of the antidepressant drug. Secondary outcomes include adverse drug reactions measured by a shortened Antidepressant Side-Effects Checklist (ASEC), and cost-effectiveness of the screening.

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We used a retrospective chart review from 22 inpatients who underwent ECT and 22 patients treated with venlafaxine due to resistant unipolar or bipolar depression. We used bilateral ECT in a median of 8 (IQR 7-9.7) sessions and venlafaxine therapy with a median daily dosage of 225 mg (IQR 150-225 mg) for a median of 4 (IQR 4-5) weeks. The main outcome was change in a self-evaluation scale - Short Form of the Beck Depression Inventory (BDI-SF). The response was defined as the decreasing of the BDI-SF score by >or=50%, remission as decreasing of BDI-SF score

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Despite some limitations associated with the system of data collection in the GPRD (need to apply proxies for severity assessment and external unit costs to resource consumption), the results of this real-life study brings additional evidence of escitalopram appearing to be a cost-effective treatment for patients suffering from severe depression as diagnosed in routine practice and could be considered for first-line treatment in these patients.

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Mean M/PAUC values of 2.5 (range 2.0-3.2) and 2.7 (range 2.3-3.2) were calculated for V and ODV, respectively. The mean maximum concentrations (95% CI) of V and ODV in milk were 1161 (95% CI, 588, 1734) microg l(-1) and 796 (362, 1230) microg l(-1). Mean infant exposure was 3.2% (1.7, 4.7%) for V and 3.2% (1.9, 4.9%) for ODV (as V equivalents). V was detected in the plasma of one out of seven infants studied (5 microg l(-1)), while ODV was detected in four of the infants, at concentrations ranging from 3 to 38 microg l(-1). All of the infants in the study were healthy, as reported by their mothers and/or by clinical examination on the study day.

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A MEDLINE search was used to identify pertinent literature, including reviews.

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effexor user reviews 2015-12-30

The objective of this work was to study the effect of various barrier layer formulation compositions, its orientations and manufacturing Crestor Normal Dosage technology on release profile of highly soluble VH.

effexor drug class 2016-11-21

Depression in the elderly and very elderly, especially those in long-term care facilities, often is more difficult to treat than depression in young or middle-aged adults. Because this population may be more sensitive to the common adverse effects of many antidepressant drugs Diovan 180 Mg , particularly the anticholinergic side effects, administration of pharmacologic therapy for depression in the elderly requires careful consideration of the side effect profiles of the various classes of antidepressant medication.

effexor common dose 2016-08-23

In this paper the experimental and the computational studies of the morphology of three polymorphs of the free base of Venlafaxine ((N,N-dimethyl)-2-(1-hydroxy cyclohex-1-yl)-2-(4-methoxyphenyl) ethylamine) are reported. The morphology of all polymorphs has been predicted using the Bravais-Friedel-Donnay-Harker method, the attachment energy method and kinetic Monte Carlo growth simulations and these predictions have been compared with experimental observations. The Monte Carlo simulations allow for a detailed simulation of the growth process, including driving force and growth mechanism, which leads to a semi-quantitative prediction of the growth morphologies of all three phases. For phase I two distinct growth habits are found experimentally under the same conditions. This is explained by the occurrence of a spiral growth mechanism in one of the two, which was observed using AFM and which is also supported by the Monte Carlo simulations. The habit of phase II could only be explained from simulations when a spiral growth mechanism is assumed; the shape of phase III could not be modeled accurately from the Monte Carlo simulations. Although the shape of the crystal is reproduced accurately, Diovan Hct Dose some of the indices of the faces predicted are not in agreement with the indices measured. The deviations are interpreted to be due to the presence of domains in the crystals as a result of the layered structure.

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This meta-analysis aimed to identify all studies that have assessed treatment response for pathological hoarding treated with pharmacological agents. Seven Prevacid Dosage Child studies were identified with a total of 92 participants. Most participants had a diagnosis of obsessive-compulsive disorder. Studies assessed response to serotonin-reuptake inhibitors (SRIs); venlafaxine; methylphenidate; and augmentation of SRIs with quetiapine, minocycline and naltrexone. More than half (ER=0.58, 95% CI=0.37-0.76) of the participants treated with pharmacotherapy responded. This study encourages us to consider the use of SRIs in patients with hoarding disorder. The study also encourages more studies of pharmacotherapy for pathological hoarding, noting that these studies should use validated outcome measures that specifically assess pathological hoarding and novel agents that target the unique neurobiological correlates of pathological hoarding.

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The increase in resting pupil diameter could be indicative of parasympathetic inhibition and/or sympathetic activation. The shortening of the recovery time of the light reflex response is consistent with sympathetic potentiation resulting from noradrenaline uptake blockade in the iris. The prolongation of the latency and decrease of the amplitude of the light reflex response are indicative of a parasympatholytic effect of venlafaxine. However, as venlafaxine has negligible affinity for muscarinic cholinoceptors, this effect cannot be attributed to the blockade of cholinoceptors in the iris. A possible explanation for this finding is that it reflects a central rather than a peripheral effect of the drug: the blockade of noradrenaline uptake in the brain could lead to the potentiation of the noradrenergic inhibition of central parasympathetic (Edinger-Westphal) neurones. These results demonstrate the ability of therapeutically relevant single doses of venlafaxine to potentiate noradrenergic responses Priligy With Alcohol in man, consistent with the blockade of noradrenaline uptake.

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We performed a single-blind placebo run-in trial of 150-225 mg of venlafaxine in 18 subjects with activity-limiting osteoarthritis pain. Each subject received 2 weeks of placebo followed by 10 weeks of venlafaxine. The primary outcome was reduction in average pain intensity between 2 and 12 weeks. For subjects not completing the trial, their last observation was carried forward Stromectol With Alcohol as an imputed outcome.

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The studies were Celebrex 200mg Generic performed on male rats. The changes in nociceptive thresholds were determined by using mechanical stimuli (the Randall-Selitto and the von Frey tests). Diabetes was induced by intramuscular administration of streptozotocin. In order to investigate the mechanism of interaction, animals were also pretreated with naloxone (NLX), a nonselective opioid antagonist, yohimbine (YOH), a nonselective α2-adrenergic antagonist, and p-chloroamphetamine (PCA), a neurotoxin that destroys serotonergic neurons. The μ-opioid receptors' density was determined with the use of radioligand binding assay.

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A body of evidence indicates that the therapeutic activity of antidepressants is connected with their modulatory effect on the inflammatory response system and cell-mediated immunity. The present study was carried out to examine the effects of antidepressant agents, such as Mestinon Tablets imipramne, venlafaxine, l-5-hydroxytryptophan, fluoxetine and a combination of l-5-hydroxytryptophan and fluoxetine, on the production of the pleotrophic cytokines TNF-alpha and IL-6. Diluted whole blood from fluoxetine-treated patients with treatment-resistant depression (TRD) (mean age: 50.6+/-3.9 years), age-matched healthy controls (mean age: 51.6+/-1.7 years) and younger healthy volunteers (mean age: 35.4+/-1.7 years) was stimulated with phytohemagglutinin (PHA) and lipopolysaccharide (LPS) for 48 h with or without incubation with the antidepressants at 10(-6) and 10(-5) M. The major findings of this study are: (1). imipramine and venlafaxine (at the higher concentration), 5-HTP (at lower and higher concentrations) and a combination of 5-HTP and fluoxetine (both at the lower concentration) increased the production of IL-6; (2). all drugs used did not affect TNF-alpha production. IL-6 production was significantly higher in depressed patients than in age-matched volunteers, whereas TNF-alpha production was significantly higher in older volunteers than in younger ones. We speculate that the therapeutic activity of these antidepressants is at least partly connected with their effect on the cytokine network and IL-6 production.

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Some authors have described the combined use of ECT and psychotropic drugs, emphasizing possible interactions and synergisms of this combined therapy. We are unaware of reports of the concurrent use of the new antidepressant venlafaxine with ECT. The goals of our study were to assess the possible effects of venlafaxine on seizure length during ECT and the possible cardiovascular effects of this combined treatment. Nine severely ill, depressed patients were treated simultaneously with bilateral ECT and venlafaxine 150 mg/day and were compared with nine control, depressed subjects taking tricyclic antidepressants (TCA) and ECT. No patients had prolonged seizures and no spontaneous/tardive seizures outside ECT were observed. With regard to mean seizure length, no statistically significant differences were observed between the control group and the venlafaxine group. Neither significant increases in arterial blood pressure nor electrocardiographic recording abnormalities were found in venlafaxine patients when compared with the tricyclic group. Even though the small number of patients used is a significant limitation of this study, we found that combined venlafaxine and ECT appears to be safe when used in depression.

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Compounds that block both serotonin (5-HT) and norepinephrine (NE) transporters have been proposed to have improved antidepressant efficacy. We compared the ability of four dual transporter inhibitors-chlorimipramine, duloxetine, milnacipran and venlafaxine-to block monoamine transporters in vitro and in vivo and increase extracellular monoamines in rat brain. Inhibition of radioligand binding to clonal human monoamine transporters in vitro and in vivo in rats was determined. Extracellular concentrations of 5-HT and NE in rat prefrontal cortex (PFC) were quantified using the microdialysis technique. All compounds blocked binding to human 5-HT and NE transporters, although chlorimipramine and venlafaxine had markedly greater affinity for 5-HT than NE transporters. In vivo, chlorimipramine and duloxetine potently blocked both transporters, milnacipran blocked both with lower potency and venlafaxine only blocked the 5-HT transporter. Chlorimipramine and duloxetine increased robustly and approximately equally monoamine extracellular concentrations. Milnacipran produced only small increases in NE, whereas venlafaxine increased 5-HT markedly at the lower doses and both monoamines at high doses. Thus, the dual transporter inhibitors blocked 5-HT and NE transporters in vitro and in vivo with varying potency. Chlorimipramine, duloxetine, and high dose venlafaxine acted as dual transporter inhibitors in rat PFC and increased extracellular concentrations of the monoamines, indicating functional dual transporter inhibition.