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Generic Cymbalta is an effective medication with highly developed components which is taken in treatment of serious depression and all symptoms connected with depression. Generic Cymbalta is an antidepressant in a group of drugs called selective serotonin and norepinephrine reuptake inhibitors (SSNRIs). Generic Cymbalta affects chemicals in the brain that may become unbalanced and cause depression.

Other names for this medication:
Ariclaim, Delok, Deloxi, Duloxetin, Duloxetina, Duloxetinum, Duxetin, Duzela, Xeristar, Yentreve

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Also known as:  Duloxetine.


Generic Cymbalta is developed by medical scientists to treat major depressive disorder and general anxiety disorder. It is an antidepressant in a group of drugs called selective serotonin and norepinephrine reuptake inhibitors. Generic Cymbalta affects chemicals in the brain that may become unbalanced and cause depression.

Generic Cymbalta is also used to treat a chronic pain disorder called fibromyalgia, treat pain caused by nerve damage in people with diabetes (diabetic neuropathy) and to treat chronic musculoskeletal pain, including discomfort from osteoarthritis and chronic lower back pain.


Take Generic Cymbalta with a full glass of water with or without food.

It is recommended to take Generic Cymbalta at the same time each day.

Do not crush, chew, break, or open a delayed-release capsule. Swallow the tablet whole.

If you want to achieve most effective results do not stop using Generic Cymbalta suddenly.


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


Store at a room temperature between 4 and 30 degrees C (39 and 86 degrees F) away from moisture, light and heat. Throw away the after the expiration date. Keep out of the reach of children.

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The most common side effects associated with Cymbalta 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 Cymbalta if you are allergic to Generic Cymbalta components.

Do not take Generic Cymbalta if you're pregnant or you plan to have a baby, or you are a nursing mother. This medication can cause birth defects. Tell your doctor right away if you become pregnant during treatment.

Be very careful with Generic Cymbalta if you're pregnant or you plan to have a baby. Do not take Generic Cymbalta if you are breast-feeding.

Do not take Generic Cymbalta together with thioridazine (Mellaril), or an MAO inhibitor such as furazolidone (Furoxone), isocarboxazid (Marplan), phenelzine (Nardil), rasagiline (Azilect), selegiline (Eldepryl, Emsam, Zelapar), or tranylcypromine (Parnate). A dangerous drug interaction could occur, leading to serious side effects. You must wait at least 14 days after stopping an MAO inhibitor before you can take Generic Cymbalta. After you stop taking Generic Cymbalta, you must wait at least 5 days before you start taking an MAOI.

Generic Cymbalta can be not safety for children and people younger than 18 years old.

Do not take Generic Cymbalta if you have any of these conditions:liver or kidney disease, seizures or epilepsy, a bleeding or blood clotting disorder, glaucoma, bipolar disorder (manic depression), a history of drug abuse or suicidal thoughts.Be careful if you drive or do anything that requires you to be alert. Generic Cymbalta may impair your thinking or reactions.

Avoid alcohol.

It can be dangerous to stop Generic Cymbalta using suddenly.

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Baseline characteristics differed slightly between patient groups and studies. Duloxetine doses in most patients were lower than recommended. Overall, AE frequency with duloxetine was lower than in controlled studies (15.9% (95% CI 14.9, 16.9) and 9.1% (95% CI 8.2, 10.0) in the 12 and 24 week treatment groups, respectively), but exhibited a similar qualitative spectrum. In the logistic regression models, the following factors were associated with greater AE risk: investigator specialization (gynaecologist vs. urologist and primary care physician), initial duloxetine dose (80 vs. 20 mg day(-1) ) and use of any concomitant medication. Within the 24 week study, a positive screen for depressive disorder was surprisingly common, but no case of attempted suicide was reported in either study.

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Six hundred and fourteen patients were randomized. Mean changes in MADRS scores were -12.83 (±0.834), -14.30 (±0.890), -15.57 (±0.880), and -16.90 (±0.884) for placebo, vortioxetine 15 mg (P = .224), vortioxetine 20 mg (P = .023), and duloxetine 60 mg (P < .001) (P vs placebo), respectively. AEs reported by ≥5 % of vortioxetine patients included nausea, headache, diarrhea, dizziness, dry mouth, constipation, vomiting, insomnia, fatigue, and upper respiratory infection. Treatment-emergent sexual dysfunction, suicidal ideation or behavior, and discontinuation symptoms were not significantly different between vortioxetine and placebo.

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Duloxetine is indicated for patients with a variety of conditions, and some of these patients may have mild to moderate degrees of renal impairment. Renal impairment may affect the pharmacokinetics of a drug by causing changes in absorption, distribution, protein binding, renal excretion or nonrenal clearance. As duloxetine is highly bound to plasma proteins and its metabolites are renally excreted, it is prudent to evaluate the effect of renal insufficiency on exposure to duloxetine and its metabolites in the systemic circulation.

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Duloxetine hydrochloride (1) is an important antidepressant that acts as a serotonin and noradrenaline reuptake inhibitor that has only recently been characterized by single-crystal X-ray diffraction. This study describes an investigation into polymorphism of duloxetine hydrochloride, discusses the challenges of characterizing new structures, and reports a new metastable solvate (1(acetone)) where acetone is trapped in a duloxetine hydrochloride host lattice. In view of the importance of formulation processing and bioavailability characteristics of the crystalline forms of 1, a comprehensive structural study of 1(acetone) was carried out using single-crystal and powder X-ray diffraction, infrared and Raman spectroscopies, and solid-state NMR spectroscopy. The rapid desolvation from 1(acetone) to the stable unsolvated form was investigated, and the structures of free and solvated forms are discussed in terms of the noncovalent intermolecular interactions.

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Though with limited power, these data provide preliminary support for the efficacy of duloxetine for GSAD, and suggest continued improvement but limited remission overall at 24 weeks for individuals remaining symptomatic at week 6. These observations warrant further controlled study.

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This was a post hoc analysis to determine whether baseline severity of depression influenced the efficacy of duloxetine in treating major depressive disorder (MDD) and to better characterise the symptom response profile for duloxetine in patients with mild, moderate or more severe depression.

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Little evidence is available relevant to the treatment of refractory neuropathic pain despite the clinical need. There is a notable lack of high-quality comparative studies. It is evident that there is a need for future, high quality trials, particularly "gold-standard" RCTs in this refractory patient population.

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There is limited evidence for efficacy of analgesics as monotherapy for neuropathic pain associated with HIV-associated polyneuropathies, in spite of demonstrated efficacy in other neuropathic pain conditions. We evaluated the tolerability and analgesic efficacy of duloxetine, methadone, and the combination of duloxetine-methadone compared with placebo.

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Seasonal affective disorder (SAD) is a seasonal pattern of recurrent depressive episodes that is often treated with second-generation antidepressants (SGAs), light therapy or psychotherapy.

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Treatment with SSRIs and duloxetine improved functional impairment in patients with major depressive disorder. Higher SDS or 17-item Hamilton Depression Rating Scale baseline scores predicted less probability of SDS improvement; female gender predicted better improvement in functional impairment at endpoint.

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Urine storage and micturition are controlled by a series of hard wired reflexes that are under the modulatory influence of serotonin and norepinephrine. Augmentation of the serotonergic and noradrenergic systems with duloxetine increases bladder capacity and urethral rhabdosphincter activity. The increase in sphincter activity is mediated by alpha1 adrenergic receptors and 5-hydroxytryptamine receptors.

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The authors report a case of treatment refractory bulimia nervosa successfully treated with duloxetine, a combined serotonin and norepinephrine reuptake inhibitor, with complete remission Xenical Hard Capsules of the patient's bingeing and purging behaviours. This case is discussed in the context of existing literature on the psychopharmacology of bulimia nervosa.

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Pooled data from 15 placebo-controlled clinical trials were used to compare the safety outcomes of duloxetine among patients of Caucasian, Hispanic, Asian, and Black race/ethnic origins. Patients were randomized to receive placebo (n = 2199) or duloxetine (n = 3148) for treatment of diabetic peripheral neuropathic pain, fibromyalgia, osteoarthritis pain, or chronic low back pain. For categorical outcomes such as study discontinuation, adverse events leading to discontinuation, and treatment-emergent adverse events, incidence rates were summarized by race/ethnic subgroups. The Breslow-Day test was used to assess the homogeneity of treatment odds ratios across the four subgroups. For continuous outcomes such as changes in vital signs, body weight, and laboratory measures, an analysis of covariance or analysis of variance model was used and Cymbalta 90 Mg duloxetine effects were compared among race/ethnic subgroups based on the test of treatment-by-subgroup interaction.

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The (+)-isomer of indeloxazine AS1069562 exerts multiple pharmacological actions including the inhibition of serotonin (5-HT) and norepinephrine reuptake and analgesia in experimental animal pain models. Here, we evaluated the antinociceptive effects of AS1069562 and the antidepressants duloxetine and amitriptyline in mouse models of prostaglandin-induced spinal hypersensitivity. Prostaglandin E2 (PGE2) and F2α (PGF2α) were intrathecally administered to induce spinal hypersensitivity, causing tactile allodynia in mice. Allodynia induced by PGF2α but not by PGE2 was suppressed by desensitization of C-fibers with systemic pretreatment with resiniferatoxin. C-fiber hyperexcitability might therefore play a role in allodynia induced by PGF2α but not PGE2. In the PGE2-induced allodynia model, AS1069562 and duloxetine significantly suppressed allodynia, whereas amitriptyline did not. In the PGF2α-induced allodynia model, AS1069562 and amitriptyline significantly ameliorated allodynia, whereas duloxetine did not. To demonstrate the broad effects of AS1069562 compared to duloxetine, additional studies were conducted to elucidate other target mechanisms of AS1069562 beyond 5-HT and norepinephrine reuptake inhibition. AS1069562 exhibited affinity for both 5-HT1A and 5-HT3 receptors, and the analgesic effect of AS1069562 on PGF2α-induced allodynia was significantly blocked by the 5- Prilosec 40mg Dosage HT1A receptor antagonist (S)-WAY100135 and the 5-HT3 receptor agonist SR57227. Taken together, these results indicate that AS1069562 inhibits both C-fiber- and non-C-fiber-dependent prostaglandin-induced allodynia, while duloxetine inhibits only non-C-fiber-triggered allodynia, and amitriptyline inhibits only C-fiber-triggered allodynia. These broad antinociceptive effects of AS1069562 may be due not only to 5-HT and norepinephrine reuptake inhibition but also to its effects on 5-HT receptors such as 5-HT1A and 5-HT3 receptors.

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Though premature ejaculation (PE) has been overshadowed by current attention given to erectile dysfunction, it is the Amaryl And Alcohol most widespread form of male sexual dysfunction. Delayed or inhibited ejaculation, a known side effect of selective serotonin reuptake inhibitors (SSRIs), has made SSRIs potentially useful in the treatment of this disorder. In the present study, we examined the efficacy of duloxetine, an SSRI, in the treatment of PE.

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To determine the effect Viagra Pill Splitter of duloxetine, 60 mg daily, on average pain severity.

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Elevations of alanine aminotransferase to three times the Prilosec Recommended Dosage upper limit of normal occurs in 0.9-1.7% of duloxetine-treated patients versus 0.0-0.3% of placebo-treated patients. Hepatocellular, cholestatic and mixed hepatocellular-cholestatic forms of hepatic injury have been described.

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Duloxetine is a selective serotonin-norepinephrine reuptake inhibitor (SNRI) approved to treat major depressive disorder and diabetic peripheral Amaryl Pill neuropathic pain. It is known to cause hepatotoxicity, in some cases leading to death. It has been reported that duloxetine causes time-dependent inhibition (TDI) of CYP1A2, CYP2B6, CYP2C19 and CYP3A4/5; but the nature of these TDI (whether reversible or irreversible) is not known. Irreversible TDI can cause clinically significant drug-drug interactions and also immune-mediated hepatotoxicity. Structurally, duloxetine possesses several toxicophores, i.e. the naphthyl and thiophene rings. It has been reported that the naphthyl ring undergoes epoxidation and was subsequently adducted to glutathione, but bioactivation related to the thiophene ring has not been completely elucidated. In this paper, the potential of duloxetine in causing irreversible TDI and generating reactive metabolites was investigated. Human liver microsomal assays demonstrated that duloxetine did not cause irreversible TDI of CYP1A2, CYP2B6, CYP2D6, CYP2C19 and CYP3A4/5. Subsequently, reactive metabolite trapping assays using soft nucleophiles (glutathione and glutathione ethyl ester) revealed a previously reported adduct at the naphthyl ring of duloxetine but not at the thiophene ring. Trapping assays utilizing a hard nucleophile (semicarbazide) did not demonstrate adducts with the thiophene ring, indicating an absence of thiophene ring opening. The hepatotoxicity of duloxetine is possibly not related to the irreversible TDI of CYP450 or the bioactivation of its thiophene moiety, but might be due to the epoxidation of its naphthyl ring.

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We selected all randomised or Buy Feldene Online quasi-randomised trials of any formulation of duloxetine, used for the treatment of painful peripheral neuropathy or chronic pain in adult participants.

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In depressed patients tricyclic antidepressants and selective serotonin and noradrenaline Dosage Bactrim reuptake inhibitors can reduce not only depressive, but also painful physical symptoms. We investigated whether under treatment with duloxetine pain improves earlier than mood.

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To study the effect of duloxetine (Cymbalta), a selective serotonin and norepinephrine reuptake inhibitor, on pain symptoms in Parkinson Disease (PD).

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We selected randomized, controlled trials of any formulation of SNRIs against placebo for the treatment of FMS in adults.

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Of 4517 patients enrolled, 4313 were included for TEAE evaluation. TEAEs occurred in 17.2% of patients, and SAEs occurred in 0.79% of patients, including one case of suicidal ideation. 1404 patients discontinued within 6 months (TEAEs: n = 119). Starting treatment with 30 mg/day DLX (72.7%) was favored in females, or after inadequate efficacy of previous antidepressant treatment; 60 mg/day DLX was favored in more severe depression and patients receiving concomitant pain medication.