Generic Requip is an anti-Pakirson medication. Generic Requip is also used to treat restless legs syndrome (RLS).
Other names for this medication:
Generic Requip is an anti-Pakirson medication. Generic Requip is also used to treat restless legs syndrome (RLS).
Other names for this medication:
Also known as: Ropinirole.
Generic Requip is an anti-Pakirson medication.
Generic Requip is used to treat symptoms of Parkinson's disease such as stiffness, tremors, muscle spasms, poor muscle control.
Requip is also known as Ropinirole, Ropidon, Adartrel, Ropark.
Generic Requip is also used to treat restless legs syndrome (RLS).
Generic Requip has some of the same effects as a chemical called dopamine, which occurs naturally in your body. Low levels of dopamine in the brain are associated with Parkinson's disease.
Generic name of Generic Requip is Ropinirole.
Brand names of Generic Requip are Requip, Requip XL.
Take Generic Requip orally.
Take Generic Requip with or without food.
The dose and timing of Generic Requip in treating Parkinson's disease is different from the dose and timing in treating RLS.
If you want to achieve most effective results do not stop taking Generic Requip suddenly.
If you overdose Generic Requip and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Generic Requip overdosage: nausea, vomiting, weakness, fainting, agitation, confusion, hallucinations, muscle twitching, tingly feeling, chest pain.
Store at room temperature between 20 and 25 degrees C (68 and 77 degrees F) away from moisture, light and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.
The most common side effects associated with Requip are:
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 Requip if you are allergic to Generic Requip components.
Be very careful with Generic Requip if you are pregnant, planning to become pregnant, or are breast-feeding.
Be very careful with Generic Requip if you have heart disease, high or low blood pressure, mental illness or compulsive behaviors, kidney or liver disease.
Be very careful with Generic Requip if you are taking levodopa, ciprofloxacin (Cipro), fluvoxamine (Luvox), metoclopramide (Reglan), omeprazole (Prilosec); medication used to treat nausea and vomiting or mental illness, such as chlorpromazine (Thorazine), fluphenazine (Prolixin), mesoridazine (Serentil), perphenazine (Trilafon), thioridazine (Mellaril), promazine (Sparine), trifluoperazine (Stelazine), thiothixene (Navane), or haloperidol (Haldol); estrogen such as Premarin, Prempro, Estratest, Ogen, Estraderm, Climara, Vivelle, estradiol and others.
Avoid getting up too fast from a sitting or lying position. Get up slowly and steady yourself to prevent a fall.
Avoid alcohol and smoking.
Avoid machine driving.
It can be dangerous to stop Generic Requip taking suddenly.
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Among the neurodegenerative diseases (ND), Parkinson's disease affects 6.3 million people worldwide characterized by the progressive loss of dopaminergic neurons in substantia nigra. The mitochondrial permeability transition pore (mtPTP) is a non-selective voltage-dependent mitochondrial channel whose opening modifies the permeability properties of the mitochondrial inner membrane. It is recognized as a potent pharmacological target for diseases associated with mitochondrial dysfunction and excessive cell death including ND such as Parkinson's disease (PD). Imbalance in Ca(2+) concentration, change in mitochondrial membrane potential, overproduction of reactive oxygen species (ROS), or mutation in mitochondrial genome has been implicated in the pathophysiology of the opening of the mtPTP. Different proteins are released by permeability transition including cytochrome c which is responsible for apoptosis. This review aims to discuss the importance of PTP in the pathophysiology of PD and puts together different positive as well as negative aspects of drugs such as pramipexole, ropinirole, minocyclin, rasagilin, and safinamide which act as a blocker or modifier for mtPTP. Some of them may be detrimental in their neuroprotective nature.
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A cost-minimisation analysis was performed from both the societal and Ministry of Health (MoH) of Ontario, Canada perspectives, using 5-year data from a study of dyskinesia outcomes comparing ropinirole with levodopa plus benserazide. A predictive model was developed to capture resource utilisation over 5 years, such as medication costs, medical consultations, hospital admissions, nursing home admissions, caregiver time and productivity loss. The model was based on a previously reported clinical trial which determined dyskinesia rates to be 20% for ropinirole and 45% for levodopa. Standard costing lists were used, and costs were discounted at various rates. Constant 1999 Canadian dollars ($Can) were applied, and no increases were assumed over the time horizon of the analysis. A multivariate sensitivity analysis with changes in key parameters was also performed.
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Ropinirole is a non-ergot dopaminergic agonist with a high affinity for D2 dopaminergic receptors which improves the symptoms of Parkinson's disease (PD) and delays the appearance of motor complications. It is different to the first generation of dopaminergic agonists in that, because it lacks an ergolinic structure, it does not have the side effects that usually appear with the use of this pharmacological group.
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Forty-four consecutive PD patients with or without motor complications (MC+ group and MC- group, respectively); 6-month prospective study; scales administered in the "on" motor state: Unified Parkinson's Disease Rating Scale, Hamilton Anxiety Scale (HAMA), Montgomery-Asberg Depression Rating Scale (MADRS), Parkinson's Disease Sleep Scale, Epworth Sleep Scale, International Index of Erectile Function, and Female Sexual Function Index; serum sexual hormones collected.
We contacted 929 patients with PD and administered a 45- to 60-minute interview addressing medication use, adverse events, and the patient's clinical status in the preceding 6 months. Their physicians completed record reviews detailing their clinical histories and drug regimens. The outcome of interest in this case-control study was an episode of somnolence that was uncontrollable, severe, and inappropriate, such as while driving or engaged in social activity. For multiple events, the first was chosen as the index event. For each case, we sampled control time from all respondents who had no event as of the index time for that case. Multiple logistic regression was used to adjust for potential confounders.
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The consumption of levodopa in Sweden continues to increase in spite of a dramatic increase in the utilisation of dopamine agonists and the introduction of COMT-inhibitors.
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Behavioral measures are often used to distinguish subgroups of patients with stroke (eg, to predict treatment gains, stratify clinical trial enrollees, or select rehabilitation therapy). In studies of the upper extremity, measures of brain function using functional magnetic resonance imaging (fMRI) have also been found useful, but this approach has not been examined for the lower extremity. The current study hypothesized that an fMRI-based measure of cortical function would significantly improve prediction of treatment-induced lower extremity behavioral gains. Biomarkers of treatment gains were also explored.
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Long-term levodopa therapy for Parkinson's disease is complicated by the development of motor fluctuations and abnormal involuntary movements. One approach is to add a dopamine agonist at this stage of the disease to reduce the time the patient spends immobile or off and to reduce the dose of levodopa in the hope of reducing such problems in the future.
In bivariate analysis, 8 baseline measures belonging to 4 categories (medical history, impairment, disability, and brain function) significantly predicted change in gait velocity. Prediction was strongest, however, using a multivariate model containing 2 measures (leg Fugl-Meyer score and fMRI activation volume within ipsilesional foot sensorimotor cortex). Increased activation volume within bilateral foot primary sensorimotor cortex correlated positively with treatment-induced leg motor gains.
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Apomorphine and certain ergot alkaloids (bromocriptine, lisuride and pergolide) have been available for several decades; for the last few years, they were joined by newer dopamine agonists (cabergoline, pramipexole and ropinirole) most of them are non-ergolines. Each of these dopamine agonists has its own pharmacological characteristics and occupies a place in the pharmacotherapy of Parkinsons disease. In this evidence-based review, emphasis is put on the clinical efficacy of dopamine agonists in early and advanced Parkinsons disease, and where possible comparative evidence regarding their efficacy and safety is provided. In addition, their clinical pharmacokinetics, adverse effect profiles and most relevant interactions will be summarized.
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Chaotropic agents recently gained popularity as interesting and useful mobile phase additives in liquid chromatography due to their effect on analytes retention, peak symmetry and separation efficiency. They mimic the role of classical ion-pairing agents, but with less drawbacks, so their use becomes attractive in the field of pharmaceutical analysis. In this paper, the influence of sodium trifluoroacetate and sodium perchlorate on the chromatographic behavior of ropinirole and its impurities is examined. By the extended thermodynamic approach, it was shown that the separation in the given system was predominantly governed by electrostatic interactions between the protonated analytes and the charged surface of the stationary phase, but the ion-pair complex formation in the eluent also proved to be significant. Further, the employment of face-centered central composite design enabled the understanding of the effect of chaotropic agent concentration and its interactions with other factors (acetonitrile content and pH of the water phase) that influence the given chromatographic system. Finally, the same data was used for multi-objective optimization based on the grid point search method. After the method validation, the adequacy of the suggested approach in development of methods for routine pharmaceutical analysis was proven.
The absorption, protein binding, blood-to-plasma ratio, renal excretion, and pharmacokinetics of the dopamine-2 agonists (D2-agonists) 4-(2-di-n-propylaminoethyl)-7-hydroxy-2-(3H)-indolone (1), N-(2'-hydroxy-5'-[N,N-di-n-propylaminoethylphenyl])methanesulfonamide (2), and 4-(2-di-n-propylaminoethyl)-2-(3H)-indolone (3) were examined in dogs and rats. On the basis of relative cumulative urinary recoveries of radiolabeled drug, all three compounds are well absorbed in rats and dogs. In dogs, the free fractions in plasma of unchanged 1, 2, and 3, determined by in vitro studies, were 74, 86, and 63%, respectively, and the protein binding was constant with increasing concentration. The blood-to-plasma partition ratios of the respective compounds were 1.22, 1.14, and 1.16 in dogs, and the ratios were constant with increasing concentration. Large differences between species (dogs, rats, and humans) in protein binding and blood-to-plasma ratios were not seen. The clearances (blood or plasma) of 1 and 2 in dogs were significantly greater than the clearance of 3. The clearance of 3 was almost exclusively nonrenal, whereas 13% of 1 and 2 were recovered unchanged in urine. The steady-state volumes of distribution and the distribution and elimination half-lives of the three compounds were not significantly different. Importantly, the mean residence time of 3 (147 min) in dogs was significantly longer than those of 1 (90 min) and 2 (96 min). The results of analogous studies in rats indicate that 1 and 2 are more rapidly metabolized than 3.
Sensory nerves regulate central and local reflexes such as airway plasma leakage, and cough and their function may be enhanced during inflammation. Evidence suggests that dopamine receptor agonists may inhibit sensory nerve-mediated responses. In this study dopamine inhibited vagal sensory nerve induced microvascular leakage in the rat. In order to characterize the receptor involved rat vagus preparations were utilized. Quinagolide (D(2/3) agonist), ropinirole (D(2/3/4) agonist), SKF 38393 (D(1/5) agonist), AR-C68397AA (Viozan) (dual D(2)/B(2) agonist) and dopamine inhibited hypertonic saline induced depolarization by approximately 50%. Data suggests that AR-C68397AA and quinagolide also inhibited depolarization of the human vagus. The quinagolide response was blocked by sulpiride (D(2/3) antagonist) but not SCH 23390 (D(1/5) antagonist); ropinirole was partially blocked by sulpiride, totally blocked by spiperone (at a concentration that blocks all dopamine receptors) but not by SCH 23390. The response to SKF 38393 was not blocked by sulpiride but was by SCH 23390. The inhibition evoked by AR-C68397AA was only partially blocked by SCH 23390 but not by sulpiride or spiperone whereas dopamine was blocked by spiperone. The effect of dopamine was not stimulus-specific as it inhibited capsaicin-induced depolarization of the rat vagus in a spiperone sensitive manner. In conclusion, dopamine receptor ligands inhibit depolarization of the rat and human vagus. These data suggest that dopamine receptor agonists may be of therapeutic benefit in the treatment of symptoms such as cough and mucus secretion which are evident in respiratory diseases such as asthma and chronic obstructive pulmonary disease.
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1. SK&F 101468, a non phenolic indolone derivative, has been characterised preclinically as a novel, potent and specific dopamine D2-receptor agonist. 2. Its tolerability and effects on serum prolactin were investigated in 14 healthy male volunteers in a study of the first administration of SK&F 101468 to man. 3. Doses between 80 micrograms and 2.5 mg caused statistically significant (P less than 0.05) lowering of basal and food stimulated serum prolactin, relative to placebo, over a 6 h post treatment period. 4. SK&F 101468 was well tolerated up to 1 mg with symptoms of nausea and postural hypotension at higher doses.
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In contrast to transcranial direct current stimulation (tDCS), aftereffects of tRNS are seem to be not NMDA receptor dependent and can be suppressed by benzodiazepines suggesting that tDCS and tRNS depend upon different mechanisms.
A Task Force was established by the International Restless Legs Syndrome Study Group (IRLSSG) to develop evidence-based and consensus-based recommendations for the long-term pharmacologic treatment of restless legs syndrome/Willis-Ekbom disease (RLS/WED). The Task Force reviewed the results of all studies of RLS/WED treatments with durations of 6 months or longer presented at meetings over the past 2 years, posted on Web sites of pharmaceutical companies, or published in peer-reviewed journals, asking the questions, "What is the efficacy of this treatment in patients with RLS/WED?" and "What is the safety of this treatment in patients with RLS/WED?" The Task Force developed guidelines based on their review of 61 papers meeting inclusion criteria, and using a modified evidence-grading scheme. Pregabalin has been established as effective for up to 1 year in treating RLS/WED (Level A evidence). Pramipexole, ropinirole, and rotigotine have been established as effective for up to 6 months in treating RLS/WED (Level A). The following drugs have been established as probably effective (Level B) in treating RLS/WED for durations ranging from 1 to 5 years: gabapentin enacarbil, pramipexole, and ropinirole (1 year); levodopa (2 years); and rotigotine (5 years). Because of associated safety concerns, pergolide and cabergoline should not be used in the treatment of RLS/WED unless the benefits clearly outweigh the risks. Other pharmacologic therapies have insufficient evidence to support their long-term use in treating RLS/WED. The IRLSSG Task Force also developed consensus-based strategies for the prevention and treatment of complications (such as augmentation, loss of efficacy, excessive daytime sleepiness, and impulse control disorders) that may develop with the long-term pharmacologic treatment of RLS/WED. The use of either a dopamine-receptor agonist or α2δ calcium-channel ligand is recommended as the first-line treatment of RLS/WED for most patients, with the choice of agent dependent on the patient's severity of RLS/WED symptoms, cognitive status, history, and comorbid conditions.
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Approximately one third of patients in each group withdrew prematurely, mostly because of adverse experiences; 61/102 (60%) of ropinirole-treated and 59/112 (53%) of bromocriptine-treated patients completed the study on the dopamine agonist alone. Mean doses for all patients at completion were 12 mg (SD 6) ropinirole and 24 mg (SD 8) bromocriptine. Occurrence of adverse experiences in both groups was similar. Emergence of dyskinesias was low. Both treatments induced marked improvements in Unified Parkinson's Disease Rating Scale activities of daily living (ADL, Part II) and motor (Part III) scores over the first 12 weeks, which were maintained during the study. After 3 years, patients in the ropinirole group had a mean improvement in motor score of 31% compared with 22% in the bromocriptine group (p = 0.086) and a significantly better ADL score (treatment difference 1.46 points, p = 0.009) [corrected].
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4-[2-(Di-n-propylamino)ethyl]-2(3H)-indolone (1c) (SK&F 101468) is a potent and selective prejunctional dopamine receptor agonist. It caused a dose-related inhibition of the constrictor response to electrical stimulation in the isolated perfused rabbit ear artery (EC50 = 100 nM), and this response was antagonized by (S)-sulpiride (KB = 7 nM). Compound 1c did not stimulate or block dopamine-sensitive adenylate cyclase and did not produce stimulation of the central nervous system in rats. It was prepared from (2-methyl-3-nitrophenyl)acetic acid in a multistep sequence based on the Reissert indole synthesis.
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1. The human urinary excretory amounts of total drug (parent + metabolites) were predicted for nine drugs with diverse chemical structures using simple allometry. The drugs used for scaling were cephapirin, olanzapine, labetolol, carisbamate, voriconazole, tofacitinib, nevirapine, ropinirole, and cyclindole. 2. The traditional allometric scaling was attempted using Y = aW(b) relationship. The corresponding predicted urinary amounts were converted into % recovery by using appropriate human dose. Appropriate statistical tests comprising of fold-difference (predicted/observed values) and error calculations (MAE and RMSE) were performed. 3. The interspecies scaling of all nine drugs tested showed excellent correlation (r > 0.9672). The predictions for eight out of nine drugs (exception was cephaphirin) were contained within 0.80-1.25 fold-differences. The MAE and RMSE were within ± 18% and 14.64%, respectively. 4. The present work supported the potential application of prospective allometry scaling to predict the urinary excretory amounts of the total drug and gauge any issues for the renal handling of the total drug.
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Ropinirole is a specific non-ergoline dopamine D2-receptor agonist with antiparkinsonian properties. The pharmacokinetic parameters of ropinirole taken in the fasted condition were compared with those when it was co-administered with food.
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Dopamine agonists (DAs) represent the first-line treatment in restless legs syndrome (RLS); however, in the long term, a substantial proportion of patients will develop augmentation, which is a severe drug-related exacerbation of symptoms and the main reason for late DA withdrawal. Polysomnographic features and mechanisms underlining augmentation are unknown. No practice guidelines for management of augmentation are available.
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Primary end points were AUC0-8 and Cmax for ropinirole, and AUC0-8, AUC0-infinity and Cmax for L-dopa. Secondary end points were Tmax for ropinirole, and Tmax and half-life for L-dopa. Coadministration with L-dopa at steady state did not affect rate or extent of availability of ropinirole: point estimates of the geometric mean ratio for ropinirole plus L-dopa compared with ropinirole alone for both Cmax and AUC0-8 approximated to unity. The small (16%) increase in peak concentrations of L-dopa on administration with ropinirole is unlikely to be of clinical consequence, as peak concentrations of L-dopa are typically highly variable.
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Six-month data were gathered from three trials of monotherapy in patients with PD.
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