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Serevent (Salmeterol)

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Serevent is used for long-term treatment of asthma. It may be used to prevent breathing problems in certain patients, including patients with nighttime asthma, or breathing problems caused by exercise. It may be used for long-term treatment of chronic obstructive pulmonary disease (COPD). It may also be used for other conditions as determined by your doctor.

Other names for this medication:

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Also known as:  Salmeterol.


Serevent is used to prevent asthma attacks. Its active ingredient Salmeterol is a bronchodilator. It works by relaxing muscles in the airways to improve breathing. It will not treat an asthma attack that has already begun.

Serevent is also used to treat chronic obstructive pulmonary disease (COPD) including emphysema and chronic bronchitis.

Generic name of Serevent is Salmeterol.

Brand name of Serevent is Serevent.


Follow the directions for using this medicine provided by your doctor. Use Serevent exactly as directed.

Do not change your doses or medication schedule without advice from your doctor.

The usual dose of Serevent for asthma and COPD is 1 inhalation twice a day. The 2 doses should be about 12 hours apart.


If you overdose Serevent and you don't feel good you should visit your doctor or health care provider immediately. Overdose symptoms may include nervousness, headache, tremor, dry mouth, chest pain or heavy feeling, rapid or uneven heart rate, pain spreading to the arm or shoulder, nausea, sweating, dizziness, seizure (convulsions), feeling light-headed or fainting.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture, light 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 Serevent 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 Serevent if you are allergic to Serevent components.

It is not known whether Serevent will harm an unborn baby. Do not use this medicine without your doctor's advice if you are pregnant or breast-feeding.

You shouldn't take Serevent if you have heart disease or high blood pressure; epilepsy or other seizure disorder; diabetes; a thyroid disorder; or liver disease.

Do not use a second form of salmeterol (such as Advair) or use a similar inhaled bronchodilator such as formoterol or arformoterol (Foradil, Perforomist, Symbicort, or Brovana) unless your doctor has told you to.

Do not give this medication to a child younger than 4 years old.

Do not use Serevent to treat an asthma attack that has already begun. Salmeterol may increase the risk of asthma-related death.

Avoid getting this medication in your eyes. If this does happen, rinse the eyes with water and seek medical attention.

Do not stop taking Serevent suddenly.

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Seventeen boys and three girls with mild-to-moderate asthma participated in the study. On two separate days either 50 micrograms salmeterol or placebo was inhaled. FEV1 and PD20 methacholine were determined before and 1, 4, 8, 12, and 24 hours after inhalation.

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A case-control study nested within a cohort of patients with asthma, identified in the year 2000, over a 2-year period was conducted. Cases were subjects who had a first-time hospitalization for asthma in the year 2001, and were matched with up to five controls by age (+/- 5 years), sex, and number of asthma-related outpatient visits.

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Although beta-agonists remain an important aspect of the treatment of asthma, their role has recently been questioned. Salmeterol has recently been developed as a beta-agonist with prolonged bronchodilator action. Using lucigenin-enhanced chemiluminescence, we have shown that salmeterol inhibits this aspect of phagocyte function in vitro in a concentration-dependent manner. However, salmeterol differs from classical beta 2-agonists in that at concentrations between 10(-5) and 10(-3) mol/L, its effects on phagocytes cannot be completely reversed by washing the cells or by propranolol. The effects on phagocytes may not therefore be explicable on the basis of beta-adrenergic mechanisms alone.

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The inhaled corticosteroid, fluticasone propionate (fluticasone), and the long-acting beta(2)-agonist, formoterol fumarate (formoterol), have been combined in a single aerosol inhaler (fluticasone/formoterol). In a randomized, open-label study, fluticasone/formoterol showed similar efficacy to fluticasone/salmeterol after 12 weeks of treatment. This post-hoc analysis compared the onset of bronchodilation with the two treatments.

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A randomized, double-blind, double-dummy, parallel-group, multicenter study was conducted in 539 adult asthma patients over 12 weeks. Patients were randomized to receive either salmeterol 42 microg via metered-dose inhaler twice daily or albuterol 180 microg four times daily. Upon entry into the study, 46% of patients were being treated with an inhaled corticosteroid and were allowed to continue treatment throughout the study. Pulmonary function and asthma symptoms were monitored daily, and patients completed the Asthma Quality of Life Questionnaire (AQLQ) at baseline and after 4, 8, and 12 weeks of treatment.

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Four hundred eight asthmatic patients > or = 12 years of age with baseline FEV1 of > or = 70% of predicted values. Patients were not using inhaled corticosteroids.

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The 1990 Omnibus Budget Reconciliation Act mandated drug utilization review in response to inappropriate drug use. In the Pennsylvania Medicaid program, pediatric asthma is associated with high healthcare utilization and cost.

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Long-term treatment studies with formoterol and salmeterol show that these inhaled long-acting beta 2-agonists compared to available beta 2-agonists produce better bronchodilation, decrease the need for additional doses, decrease asthma symptoms, and are strongly preferred by the patients. Development of tolerance has not been found. One case history indicates that these effective bronchodilators might mask deterioration of asthma.

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Chronic obstructive pulmonary disease (COPD) affects millions worldwide. Although many therapies exist and are being developed to relieve symptoms and reduce mortality, few data are available to understand which of the therapeutic alternatives is the most cost-effective for COPD patients in everyday clinical practice, especially for traditional Chinese medicine (TCM). Comparative effectiveness research can help patients, clinicians, and decision-makers make best informed treatment decisions where such evidence was previously lacking. This study aims to compare the effectiveness and economic evaluation of three treatments: (1) conventional Western medicine; (2) TCM treatments, which have been evaluated and have certain effect; and (3) a combination of both conventional Western medicine and TCM treatments, and then determine which treatment is the most suitable for COPD patients.

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To examine the relationship between number of prescriptions dispensed of salmeterol-containing products and inhaled corticosteroid (ICS)-containing products and the rates of asthma-related hospitalizations and mortality in the United States.

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There were no differences in beta2-adrenoceptor density (Bmax) between the three treatments prior to the first dose; whereas, after the last dose, Bmax was lower with both active treatments than with placebo, but was significant for salmeterol only--a 1.2-fold geometric mean fold difference (95% CI 1- to 1.4-fold), P = 0.04. Compared with placebo, there were n = 9 of 16 subjects with salmeterol and n = 6 of 16 with formoterol who had a greater than 15% fall in Bmax. Post-hoc trend analysis of polymorphism showed that the propensity for downregulation appeared to be related to the occurrence of an allelic substitution of glycine at codon 16-8 of 13 for salmeterol versus 5 of 13 for formoterol with a greater than 15% fall compared with placebo. There were no significant differences between salmeterol and formoterol in terms of mean or individual values for downregulation. There was evidence of persistent bronchodilator activity with both active treatments compared with placebo; this was significant for forced expiratory flow rate between 25% and 75% of vital capacity (FEF25-75)--the mean difference versus salmeterol was 0.39 1/s (95% CI 0.06-0.70), P = 0.02, and versus formoterol was 0.35 1/s (95% CI 0.16-0.53), P = 0.001. These effects were mirrored by significant improvements in morning peak flow rate compared with placebo--mean difference versus salmeterol was 24 1/min (95% CI 7-42), P = 0.01, and versus formoterol was 36 1/min (95% CI 25-48), P < 0.0001.

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Asthma is one of the most common chronic diseases in children. It is attributable to complicated coactions between various genetic factors and environmental allergens.

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On average, the 59 patients completing the study (mean age ± SD 51 ± 12 years, 38 women) had significant improvement in VAS and QLQ scores at the end of the treatment period (49.1 ± 2.4 vs. 73.1 ± 2.05 and 146.1 ± 2.7 vs. 176.7.1 ± 3.4 respectively, P < 0.001), but not in the inflammatory indicators (EBT, CRP and Eos). However, when comparing the "top responders" with the "poor responders", significant improvement in these inflammatory indicators was observed: EBT significantly decreased from 34.04/mean/± 0.30/s.e.m./[°C] to 33.57 ± 0.33, P = 0.003, Eos in blood fell from 381.7 ± 91.2 [cells/μL] to 244.2 ± 43.2, P = 0.02. Before/after treatment differences in hsCRP decreased significantly in the top responders compared with the poor responders (Mann-Whitney test, P = 0.04).

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Randomised, double blind, placebo controlled crossover study.

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For the primary outcome there was significant protection after single and long-term dosing with fluticasone alone and fluticasone-salmeterol combination, whereas salmeterol alone only afforded protection after the first dose. Fluticasone-salmeterol combination and fluticasone but not salmeterol conferred significant chronic dosing effects on secondary outcomes of nasal symptoms and disease-specific quality of life. There was no potentiation of the response to fluticasone by salmeterol on any outcomes when given in combination.

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Indacaterol monotherapy is expected to be at least as good as FOR/BUD (9/320 and 9/160 μg) and comparable to SAL/FP (50/250 and 50/500 μg) in terms of lung function. Indacaterol is also expected to be comparable to FOR/BUD (9/320 and 9/160 μg) and SAL/FP 50/500 μg in terms of health status and to SAL/FP (50/250 and 50/500 μg) in terms of breathlessness.

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Earlier use of FSC following an asthma exacerbation was associated with reduced risk of future asthma-related exacerbation and lower use of rescue medications.

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The clinical development of salmeterol xinafoate, the 1-hydroxy-2-naphthoic acid salt of salmeterol, a potent long acting beta 2 agonist bronchodilator, has required the development of a method for the determination of 1-hydroxy-2-naphthoic acid (HNA), in human plasma. A sensitive, accurate and precise method was, therefore, required to enable the pharmacokinetic profile to be established. HNA was determined in human plasma using a semi-automated procedure with solid-phase extraction using an automated analytical sample processor (AASP) and high-performance liquid chromatography (HPLC) with fluorescence detection. The method was sensitive to 10 ng ml-1. The method is specific for HNA with respect to endogenous plasma components and has been shown to be robust, accurate and precise. Over four independent assay runs, the relative standard deviations (RSD) of the quality control samples (QC) were 1.6, 2.4 and 5.5% at 180, 100 and 40 ng ml-1, respectively. A pharmacokinetic profile of HNA in man has been established from a single dose kinetic study in healthy volunteers following an oral dose of 500 micrograms salmeterol xinafoate, equivalent to 225 micrograms HNA. Maximum plasma concentrations attained at 1 h after dosing ranged between 35.3 and 66.8 ng ml-1 and were within the calibration range of the assay.

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To compare the effects of salmeterol, an adrenergic drug, and ipratropium bromide, an anticholinergic drug, on breathlessness and gas exchange during exercise in patients with chronic obstructive lung disease (COPD), we performed a progressive treadmill exercise test on 15 patients on 3 days (24 h apart), after inhalation placebo, ipratropium bromide (120 micrograms) or salmeterol (50 micrograms) in a randomized fashion. Dyspnoea during exercise was evaluated from the regression slope between Borg scale (BS) scores and distance walked each minute on the treadmill. The regression was expressed as the distance walked at BS score 5, the threshold load of dyspnoea (TLD) and breakpoint load of dyspnoea. During and after the exercise, oxygen saturation was monitored by pulse oxymeter and we measured the lower SaO2 during exercise and the recovery time of SaO2 after exercise. In comparison to placebo inhalation we found the same small but significant improvement in airflow limitation after salmeterol or ipratropium inhalation, also the distance walked on treadmill increased after bronchodilators. After bronchodilators the magnitude of oxyhaemoglobin desaturation with exercise was similar to that observed after placebo but the duration of the recovery from sustained SaO2 desaturation after exercise was shorter to the same extent as after ipratropium or salmeterol. Dyspnoeic sensation, when assessed by the TLD and by the distance walked at BS score 5, was decreased after salmeterol and after ipratropium bromide to a similar extent. We conclude that the salmeterol, when given in conventional doses, produces significant improvement in the airway obstruction in the recovery of postexercise HbO2 desaturation and in dyspnoeic sensation in patients with COPD, effects which were similar to those observed after inhalation of the anticholinergic agent ipratropium bromide.

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Seventy-seven studies met the entry criteria and randomised 21,248 participants (4625 children and 16,623 adults). Participants were generally symptomatic at baseline with moderate airway obstruction despite their current ICS regimen. Formoterol or salmeterol were most frequently added to low-dose ICS (200 to 400 microg/day of beclomethasone (BDP) or equivalent) in 49% of the studies. The addition of a daily LABA to ICS reduced the risk of exacerbations requiring oral steroids by 23% from 15% to 11% (RR 0.77, 95% CI 0.68 to 0.87, 28 studies, 6808 participants). The number needed to treat with the addition of LABA to prevent one use of rescue oral corticosteroids is 41 (29, 72), although the event rates in the ICS groups varied between 0% and 38%. Studies recruiting adults dominated the analysis (6203 adult participants versus 605 children). The subgroup estimate for paediatric studies was not statistically significant (RR 0.89, 95% CI 0.58 to 1.39) and includes the possibility of the superiority of ICS alone in children.Higher than usual dose of LABA was associated with significantly less benefit. The difference in the relative risk of serious adverse events with LABA was not statistically significant from that of ICS alone (RR 1.06, 95% CI 0.87 to 1.30). The addition of LABA led to a significantly greater improvement in FEV(1) (0.11 litres, 95% 0.09 to 0.13) and in the proportion of symptom-free days (11.88%, 95% CI 8.25 to 15.50) compared to ICS monotherapy. It was also associated with a reduction in the use of rescue short-acting ss(2)-agonists (-0.58 puffs/day, 95% CI -0.80 to -0.35), fewer withdrawals due to poor asthma control (RR 0.50, 95% CI 0.41 to 0.61), and fewer withdrawals due to any reason (RR 0.80, 95% CI 0.75 to 0.87). There was no statistically significant group difference in the risk of overall adverse effects (RR 1.00, 95% 0.97 to 1.04), withdrawals due to adverse health events (RR 1.04, 95% CI 0.86 to 1.26) or any of the specific adverse health events.

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Sixty patients were enrolled in this study, and the scores of the asthma control test (ACT) and asthma control questionnaire-5 item version (ACQ5) were significantly improved 4 and 8 weeks after the switch to ICS/LABA treatments, and well-controlled asthma (ACQ5 score <0.75) and good control (ACT score >20) was achieved in 54 (90%) and 40 (66.7%) patients, respectively, at 8 weeks. The spirometric analysis revealed significant improvements of the values of the peak expiratory flow (PEF) and forced expiratory volume in one second (FEV1) after switching from FP/SM to BUD/FM, and significantly improved small airway impairments ([Formula: see text]50 and [Formula: see text]25) were observed in patients treated with high-dose ICS/LABA. These subjective and objective improvements were also seen in patients aged over 65 years old.

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Patients with physician-diagnosed COPD and a record of postdiagnosis treatment with a fixed combination of budesonide/formoterol or fluticasone/salmeterol were included. Data from primary care medical records were linked to those from Swedish national hospital, drug and cause of death registers. Pairwise (1 : 1) propensity score matching was carried out at the index date (first prescription) by prescribed fixed ICS/LABA combination. Exacerbations were defined as hospitalizations, emergency visits and collection of oral steroids or antibiotics for COPD. Yearly event rates were compared using Poisson regression.

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Evidence suggests that systemic inflammation may play an important role in the progression and morbidity of chronic obstructive pulmonary disease. It remains controversial whether inhaled corticosteroid in combination with a long-acting beta(2)-adrenoceptor agonist can attenuate systemic inflammation. We evaluated the effect of salmeterol/fluticasone propionate on circulating C-reactive protein level in stable chronic obstructive pulmonary disease patients.

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In 15 patients with chronic airflow obstruction 0.2 mg salbutamol was administered to determine reversibility within 15 minutes ("test effect"). Subsequently, maximum 24-hour effects of three beta 2-agonists (fenoterol 0.2 mg, salbutamol 0.2 mg, salmeterol 0.05 mg, each by MDI) were determined in random order ("best effect"). Airways obstruction was measured by FEV1, MEF50, MEF25, airway resistance Raw and thoracic gas volume TGV. "Best effects" were compared with "test effects". As a whole test effects were significantly smaller than best effects, often not reaching a 15% change, normally achieved during the 24-hour observation. Significant correlations existed between FEV1 and the corresponding values of Raw, MEF50 and MEF25, although there were considerable individual differences between test results. The reduction of TGV after a beta 2-agonist was significantly related to TGV-baseline values. We conclude in line with other authors that tests of acute reversibility of airways obstruction cannot reliably differentiate between "responders" and "non-responders" and that such tests may mislead if used for the differentiation of asthma and COPD.

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Bronchodilator therapy is central to the symptomatic management of chronic obstructive pulmonary disease (COPD), and treatment with short-acting bronchodilators is recommended in patients with mild COPD.

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serevent drug class 2015-04-24

Six hundred eighty patients buy serevent with asthma previously uncontrolled with low-dose inhaled corticosteroids.

serevent mdi dosage 2015-04-14

In severe chronic asthma, long-term oral steroids may be necessary to control symptoms. In patients in whom such treatment was under consideration, the efficacy and safety of salmeterol xinafoate 100 micrograms b.i.d. was investigated in a randomized, double-blind, placebo-controlled parallel-group, multicentre study. One hundred and nineteen chronic symptomatic asthmatics were randomized to receive either salmeterol, 100 micrograms b.i.d. (n = 55; baseline % predicted morning peak expiratory flow (PEF) 59%; forced expiratory volume in one second (FEV1) 66%) or placebo (n = 64; baseline % predicted morning PEF 63%; FEV1 66%) both via the Diskhaler. Morning and evening PEF and asthma symptoms were recorded in daily record booklets by the patient over a 12 week period. A significant improvement in morning PEF was achieved after 1 month in the salmeterol treated group; this persisted throughout the treatment period (estimated treatment difference 22 L.min-1). There was a significant increase in the proportion of symptom-free nights experienced by the salmeterol treated group (33 (SD 32) %) compared with placebo (13 (26) %), and a significant buy serevent decrease in daily use of relief medication (mean decrease 5.1 (4.7) doses per day with salmeterol, 2.5 (4.0) doses with placebo). Both treatments were well-tolerated, with no evidence of any difference in the side-effects associated with beta 2-agonists. In conclusion, the addition of salmeterol (100 micrograms daily) to the existing treatment of chronic asthmatics under consideration for maintenance oral corticosteroid therapy is well-tolerated, improves lung function and provides additional symptom control.

serevent mdi dose 2017-05-19

Baseline Quality Control (QC): Actuation log buy serevent accuracy and device functionality tests were undertaken. Simulated Patient Use: Salmeterol/fluticasone inhalers with STs were actuated two times twice daily for 48 h. Accuracy of reminders, data logging, and uploads was tested. Patient Field Testing: Devices were quality tested before dispensing. Asthma patients each field-tested one ST for 7 days and recorded actuations in a diary. Uploaded data were compared to pMDI dose counter and patient diaries. Patient-reported ease of use for the ST was recorded.

serevent diskus cost 2016-06-05

A randomized, double-blind, double-dummy, multicenter study was conducted. Adult patients with moderate-to-severe persistent asthma (ages 14-73 years) receiving inhaled fluticasone (220 microg/d) who buy serevent remained symptomatic during a 4-week run-in period were randomized to the addition of salmeterol (84 microg/d) or montelukast (10 mg/d) for 48 weeks.

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Patients with chronic obstructive pulmonary disease (COPD) have few options for treatment. The efficacy and safety of the phosphodiesterase buy serevent -4 inhibitor roflumilast have been investigated in studies of patients with moderate-to-severe COPD, but not in those concomitantly treated with longacting inhaled bronchodilators. The effect of roflumilast on lung function in patients with COPD that is moderate to severe who are already being treated with salmeterol or tiotropium was investigated.

serevent pediatric dose 2017-06-06

In the treatment of bronchial asthma, salmeterol is believed to have a greater anti-inflammatory activity than buy serevent salbutamol. To determine whether the comparative effects of these drugs on eosinophil function are the basis of their differential anti-inflammatory properties, we studied the effect of the two drugs on interleukin-5 (IL-5) and 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine (PAF)-induced O2- release and adherence to fibronectin-coated plates, as well as the C5a- and N-formylmethionyl-leucyl-phenylalanine (FMLP)-induced degranulation of purified human blood eosinophils in vitro. Salmeterol significantly inhibited IL-5-induced O2- release in a concentration-dependent manner with an IC50 of 2.2 X 10(-6) M (95% CI, 1.6-2.7 X 10(-6) M) and a maximal inhibition of about 70%. In contrast, salbutamol had no significant effect even at 10(-5) M. Both drugs significantly inhibited PAF-induced O2- generation, but salmeterol was approximately 20 times more potent than salbutamol. Salmeterol also significantly inhibited adherence induced by both IL-5 and PAF, whereas salbutamol had no significant effect on adherence induced by both agents. Both drugs failed to block C5a-induced eosinophil peroxidase release, whereas for FMLP-induced release, salbutamol, but not salmeterol, produced significant inhibition. Unlike salbutamol, all the actions of salmeterol were independent of beta-2 adrenoceptors. These results confirm that human eosinophils can be modulated directly by beta-2 adrenoceptor agonists, but that salmeterol and salbutamol have differential effects which depend on both the stimulus used and the response being measured and that the reportedly greater in vivo anti-inflammatory effect of salmeterol may reflect its superior ability to inhibit eosinophil O2- release and adherence, rather than degranulation.

serevent inhaler cost 2016-03-04

1. Mechanical and electrophysiological studies of guinea-pig isolated trachealis have been made with the objectives of: (a) identifying which of the beta-adrenoceptor subtypes mediates the opening of plasmalemmal K(+)-channels, (b) gaining further insight into the properties of the novel, long-acting beta-adrenoceptor agonist, salmeterol and (c) clarifying the role of K(+)-channel opening in mediating the relaxant actions of agonists at beta-adrenoceptors. 2. Noradrenaline (10 nM-100 microM) caused a concentration-dependent increase in the rate of beating of guinea-pig isolated atria. The selective beta 1-adrenoceptor blocking drug, CGP 20712A (100 nM-10 microM) caused concentration-dependent antagonism of noradrenaline. The selective beta 2-adrenoceptor blocking drug, ICI 118551, also produced concentration-dependent antagonism of noradrenaline, but only when used in concentrations greater than 300 nM. 3. Cromakalim (100 nM-10 microM), isoprenaline (1-100 nM), procaterol (0.1-30 nM), salbutamol (1 nM-1 microM), salmeterol (1-100 nM) and theophylline (1 microM-1 mM) each caused concentration-dependent suppression of the spontaneous tone of guinea-pig isolated trachealis. 4. ICI 118551 (10 nM-1 microM) antagonized isoprenaline, procaterol and salmeterol in suppressing the spontaneous tone of the isolated trachea. The antagonism was concentration-dependent. In contrast, ICI 118551 (1 microM) antagonized neither cromakalim nor theophylline. CGP 20712A (up to 1 microM) failed to antagonize cromakalim, isoprenaline, procaterol, salmeterol or theophylline. In trachea treated with indomethacin (2.8 microM) and carbachol (10 microM), salmeterol (1 microM) antagonized the effects of isoprenaline but not aminophylline. 5. Intracellular electrophysiological recording from guinea-pig isolated trachealis showed that the relaxant effects of cromakalim (10 microM), isoprenaline (100 nM), procaterol (10 nM) and salbutamol(10 nM- 1 microM) were accompanied by the suppression of spontaneous electrical slow waves and by cellular hyperpolarization. In contrast, the relaxant effects of salmeterol (10 nM- 1 microM) were not accompanied by significant cellular hyperpolarization.6. CGP 20712A (1 microM) inhibited the hyperpolarization but not the relaxation induced by isoprenaline(100 nM). In contrast ICI 118551 (100 nM) inhibited both the hyperpolarization and the relaxation induced by isoprenaline (100 nM). Neither CGP 20712A (1 microM) nor ICI 118551 (100 nM) inhibited the hyperpolarization induced by cromakalim (10 buy serevent microM). Salmeterol (1 microM) inhibited the hyperpolarization induced by isoprenaline (100 nM) but not that induced by cromakalim (10 microM).7. It is concluded that activation of either beta l- or beta 2-adrenoceptors can promote the opening of K+-channels in the trachealis plasmalemma. The poor ability of salmeterol to hyperpolarize trachealis muscle reflects neither its selectivity in activating beta 2-adrenoceptors as opposed to beta 1-adrenoceptors nor a non-specific action in stabilizing the cell membrane. Instead, it may reflect low intrinsic efficacy of the drug at beta 2-adrenoceptors. The opening of plasmalemmal K+-channels plays a supportive rather than a crucial role in mediating the tracheal relaxant actions of agonists at beta-adrenoceptors.

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A total of buy serevent 2011 differentially expressed genes were obtained by comparing asthmatic sample treated with Seretide and healthy controls. A total of 403 differentially expressed genes were collected between asthma samples untreated by Seretide and healthy sample controls. The enriched pathway of differentially expressed genes included signal transduction disorder (such as TGF-beta signaling pathway) and metabolism disorder (such as Phenylalanine metabolism). There were 27 pathway crosstalk pairs among 13 pathways.

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Pharmacy and Therapeutics committees of managed care organizations have traditionally developed formularies by limiting the numbers and kinds of pharmaceuticals they purchase, with the goal of cutting costs. These attempts to manage pharmaceutical costs do not take into account the interrelationship of the costs of various components of care; thus, drug costs may decrease, but expenditures for utilization of other resources may increase. Cost-minimization and basic cost-effectiveness studies, on which many prior- authorization and formulary programs are based, only evaluate only the cost of the drug and its effectiveness. However, with the heightened competition in the healthcare market, emphasis is increasingly being laid on patient satisfaction and outcomes. Cost-utility analysis is a potentially superior pharmacoeconomic tool because it evaluate the effect of drug therapy on quality of life; however, data from such analyses are seldom readily available to the committees that evaluate a drug's potential effects on the entire healthcare system. The purpose of this buy serevent review is to stress the importance of approaching formulary management from a wider perspective and to emphasize that the results of cost-utility studies should be proactively evaluated and incorporated into decisions regarding formularies. This is especially important for symptom-intensive diseases, such as asthma, in which the quality of life can be notably impaired. Cost-utility analyses should be conducted for all newer therapies, such as salmeterol, which are highly effective and which have a positive impact on quality of life, to determine the overall effect on the managed care plan's budget.

serevent inhaler dosage 2017-09-28

We investigated the effect and mechanism(s) of PDE-4 treatment with concurrent beta2-adrenoceptor stimulation on human eosinophil adhesion mediated by beta2-integrin buy serevent in vitro. Eosinophils were pretreated with either rolipram, a PDE-4 inhibitor, alone or combined with salmeterol, a beta2-adrenoceptor agonist, before activation with either eotaxin or IL-5. Beta2-integrin mediated adhesion was assessed as adherence to BSA, an established surrogate for ICAM-1. Rolipram caused progressive blockade (77.7 +/- 6.2%) of adhesion elicited by eotaxin. Maximal blockade of IL-5-activated adhesion by rolipram was substantially less (29.9 +/- 5.2%). Salmeterol + rolipram synergistically enhanced the blockade of eotaxin-activated adhesion. Eotaxin also caused approximately 50% increase in surface CD11b expression, which was blocked additively by rolipram + salmeterol. By contrast, CD11b upregulation caused by IL-5 was not blocked by rolipram + salmeterol. Rolipram also attenuated cPLA2 phosphorylation caused by eotaxin but did not block IL-5-induced phosphorylation. We conclude that rolipram blocks expression of CD11b and inhibits cPLA2 phosphorylation in human eosinophils, thus blocking eotaxin-induced adhesion of beta2-integrin. IL-5-induced adhesion likely utilizes a different upstream mechanism in regulation of integrin adhesion.

serevent evohaler dosage 2017-02-23

A study was done to compare the efficacy and safety of the coprescription of salmeterol 50 microgram twice daily or 100 microgram twice daily with beclomethasone dipropionate (BDP) 500 micrograms twice daily (SALM 50 and SALM 100) with BDP 1,000 microgram twice daily (BDP 1,000) in patients with asthma not controlled by BDP 500 microgram twice daily (or the equivalent). Following a run-in period, 738 patients at 72 centers were randomized to treatment for 24 wk in a double-blind, parallel-group study during which they maintained a daily record of peak expiratory flow rates (PEFRs) and symptom scores. At about 40 of the centers, bronchial hyperresponsiveness (BHR) to histamine was measured during and at 3 and 14 d after stopping treatment. Both groups taking salmeterol showed an improvement of more than 45 L/min in their morning PEFR and 30 L/min in their evening PEFR, compared with respective improvements of 16 L/min and 6 L/min in the group taking BDP 1,000. Both the SALM 50 and SALM 100 groups had a significantly increased percentage of symptom-free and rescue-free days and nights compared with the BDP 1,000 group, and there was no difference between the two salmeterol groups. None of the treatments altered BHR. Exacerbation rates did not differ among the three groups. We conclude that in this selected group of symptomatic buy serevent patients taking BDP 500 micrograms twice daily, the addition of salmeterol provides better improvement in lung function and symptom control, without altering BHR or increasing exacerbation rates, than does doubling the dose of BDP.

serevent 200 mg 2016-03-09

Concentration response experiments were conducted with isolated tracheal preparations (n = 4-6 in all experiments), precontracted by carbachol to cause either 40% (60 nmol/l), 80% (0.3 mumol/l) or 100% (3 mumol/l, supramaximal) of the maximum contraction. Each beta agonist was added cumulatively at each level of precontraction. Additional cumulative concentration response experiments were conducted for salmeterol alone at the highest level of precontraction, with and without beta blockade by sotalol (1 mmol/l). With the drug concentrations which produced the maximum response and the highest level of precontraction, the relaxation of formoterol (10 nmol/l) and salmeterol (1 mumol/l) was also compared non-cumulatively. Finally, with the corresponding drug concentrations and precontraction, the relaxant effect was compared for formoterol (10 nmol/l) in salmeterol relaxed airways with that of salmeterol ( buy serevent 1 mumol/l) in formoterol relaxed airways.

serevent inhaler dose 2015-06-10

In response to the Montreal Protocol, a salmeterol (Serevent) metered dose inhaler (MDI) has been developed containing the non-chlorofluorocarbon propellant, hydrofluoroalkane 134a (HFA), to replace the marketed buy serevent Serevent chlorofluorocarbon (CFC) propellant MDI. This paper details the pharmaceutical assessment of salmeterol HFA MDI and confirms that this product meets the current Committee for Proprietary Medicinal Products regulatory requirements, and is comparable to the CFC MDI in product performance. Criteria investigated included fine particle mass (FPM), dose delivery and uniformity, priming requirements and simulated-use-testing. Dose delivery was unaffected by changing product orientation during storage. The mean dose delivered per actuation ranged from 21.3 to 22.4 microg, and all individual doses were within the +/-25% defined limits of the target ex-actuator dose of 21 microg. The FPM results, defined as the mass of particles between 1.1 and 4.7 microm in diameter (the sum of the mass deposited on stages 3-5 of the Andersen Cascade Impactor), were similar for the HFA and CFC products. The mean FPM values of the two HFA clinical batches were 8.7 and 10.1 microg, covering the values obtained during the development, and the one of the CFC clinical batch was 10.0 microg. Comparability in aerosol characteristics was also demonstrated when the salmeterol HFA inhaler was tested using a large volume spacer (Volumatic).

serevent 50 mg 2015-05-31

MedImmune. buy serevent

serevent drug 2016-11-26

The long-acting beta2-agonist salmeterol inhibits in vitro the release of inflammatory mediators up to 20 h. These mediators are involved in ultrasonically nebulized distilled water (UNDW)-induced bronchoconstriction. We investigated whether salmeterol provides prolonged protection against UNDW provocation and whether this effect was paralleled by its bronchodilator effects. Nineteen asthmatic patients (mean forced expiratory volume in Zantac Overdose one second (FEV1) 84.8% predicted, mean provocative concentration of histamine producing a 20% decrease in FEV1 0.65 mg x mL(-1)) participated in this randomized, double-blind, placebo-controlled crossover trial. After measuring baseline FEV1, patients inhaled 50 microg salmeterol or placebo by metered-dose inhaler. FEV1 was measured after 20 and 40 min, and UNDW provocations and FEV1 measurements were performed after 10, 20 and 34 h. Compared to placebo, salmeterol caused marked bronchodilatation from 20 min up to 20 h after inhalation. Salmeterol also provided more than 20 h of protection against UNDW provocation (still more than one doubling dose). Protection beyond the period of bronchodilatation did not occur. Eleven subjects had a significant reduction in provocative dose of UNDW causing a 20% fall in FEV1 (PD20,UNDW) values between 10 and 20 h, at a time when there was still persistent bronchodilation. No correlation existed between changes in FEV1 and changes in PD20,UNDW. From the equations of regression lines between FEV1 and corresponding PD20,UNDW values, it was calculated that only approximately 25% of the afforded protection was explained by bronchodilatation. In conclusion, a single dose of salmeterol induces both bronchodilatation and protection independently of this bronchodilation against a physiological bronchoconstrictor stimulus for more than 20 h.

serevent inhaler generic 2015-07-08

Current evidence from clinical studies of the safety and tolerability profile of LABAs supports their long-term use Imitrex Pill Identification in COPD.

serevent diskus dosage 2015-09-08

To study the effects and signaling pathways of formoterol and salmeterol on polyriboinosinic polyribocytidylic acid (poly I:C)-induced Risperdal Tablets IP-10 expression in BEAS-2B cells.

serevent medication 2015-06-17

In asthma and chronic obstructive pulmonary disease, activation of G(q)-protein-coupled receptors causes bronchoconstriction. In each case, the management of moderate-to-severe disease uses inhaled corticosteroid (glucocorticoid)/long-acting β(2)-adrenoceptor agonist (LABA) combination therapies, which are more efficacious than either monotherapy alone. In primary human airway smooth muscle cells, glucocorticoid/LABA combinations synergistically induce the expression of regulator of G-protein signaling 2 (RGS2), a GTPase-activating protein that attenuates G(q) signaling. Functionally, RGS2 reduced intracellular free calcium flux elicited by histamine, methacholine, leukotrienes, and other spasmogens. Furthermore, protection against spasmogen-increased intracellular free calcium, following treatment for 6 h with LABA plus corticosteroid, was dependent on RGS2. Finally, Rgs2-deficient mice revealed enhanced bronchoconstriction to spasmogens and an absence Zantac Drug Class of LABA-induced bronchoprotection. These data identify RGS2 gene expression as a genomic mechanism of bronchoprotection that is induced by glucocorticoids plus LABAs in human airway smooth muscle and provide a rational explanation for the clinical efficacy of inhaled corticosteroid (glucocorticoid)/LABA combinations in obstructive airways diseases.

serevent diskus dose 2017-07-12

In a randomized, open-label, placebo-controlled, parallel group study, 66 patients with mild to moderate asthma Zovirax Cream Reviews received one of the following four treatments bid through an MDI for 42 days: mometasone furoate/formoterol (MF/F) 200 μg/10 μg, MF/F 400 μg/10 μg, fluticasone propionate/salmeterol (FP/S) 460 μg/42 μg, or placebo. Plasma cortisol concentrations were measured over 24 h on days -1 (baseline) and 42. Geometric mean ratio (GMR) and 90% CI for mean change from baseline to day 42 in 24-h plasma cortisol area under the curve (AUC) were calculated for each treatment. If the 90% CI for the GMRs fell within 70% to 143%, treatments were deemed comparable.

serevent reviews 2015-10-10

There are limited data describing patients with moderate COPD exacerbations and evaluating comparative effectiveness of maintenance treatments in this patient population. The study examined COPD patients with moderate COPD exacerbations. COPD-related outcomes were compared between patients initiating fluticasone propionate-salmeterol Vasotec 20 Mg 250/50 mcg (FSC) vs anticholinergics (ACs) following a moderate COPD exacerbation.

serevent generic name 2016-02-25

The combination of an inhaled corticosteroid and a long acting beta-2 agonist is indicated for the regular treatment of persistent moderate-to-severe asthmatics whose asthma is not controlled by inhaled corticosteroids and the occasional use of a short acting beta-2 agonist. The aim of this review is to give an overview of the rationale of combining formoterol and fluticasone and to analyze the clinical data concerning a new fixed combination of fluticasone and formoterol in a pressurised metered-dose inhaler with a dose counter (Flutiform(®)) that was approved for the treatment of asthma in France in 2013. The clinical studies provide evidence that combined fluticasone/formoterol is more efficacious than fluticasone or formoterol given alone, and provides similar improvements in lung function to fluticasone (Flixotide(®)) and formoterol (Foradil(®)) administered concurrently. The combination of fluticasone/formoterol gave a more rapid bronchodilatation than the combination fluticasone/salmeterol. As a whole, the combination of fluticasone/formoterol had similar efficacy and tolerability profiles to the combinations of either Biogesic Paracetamol Tablet budesonide/formoterol or fluticasone/salmeterol.

serevent 25 mg 2017-11-15

Phosphodiesterase (PDE)4 inhibition attenuates neutrophilic inflammation in chronic obstructive pulmonary disease. The objective of the present study was to examine the efficacy and mechanism by which PDE4 inhibition blocks adhesion of beta(2)-integrin to an endothelial counterligand. Neutrophils (polymorphonuclear leukocytes (PMNs)) were isolated from humans receiving no medication. Adhesion was analysed by myeloperoxidase activity. The effects of cilomilast+/-salmeterol on the following were determined: 1) surface CD11b expression; 2) adhesion; 3) intracellular cyclic adenosine monophosphate (cAMP) concentration; and 4) extracellular signal-regulated kinase (ERK)-1/2-mediated group IVA-phospholipase A(2) (gIVA-PLA(2)) phosphorylation caused by leukotriene (LT)B(4) or tumour necrosis factor (TNF)-alpha activation. Either cilomilast or rolipram+/-salmeterol caused concentration-related blockade of LTB(4)-induced adhesion to counterligand, but had no effect on TNF-alpha-activated PMNs. A comparable increase in intracellular cAMP concentration for PMNs activated with LTB(4) and TNF-alpha was caused by 1 muM cilomilast and 0.1 microM Prilosec Heartburn Medicine salmeterol. Upregulation of surface CD11b expression and ERK-1/2 phosphorylation were blocked by cilomilast or rolipram+/-salmeterol for PMNs activated by LTB(4), but not for cells stimulated by TNF-alpha. Cilomilast+/-salmeterol also blocked gIVA-PLA(2) phosphorylation caused by LTB(4) but not TNF-alpha. In conclusion, the current study demonstrates that both leukotriene B(4) and tumour necrosis factor-alpha upregulate cyclic adenosine monophosphate. However, cyclic adenosine monophosphate does not block beta(2)-integrin adhesion caused by tumour necrosis factor-alpha. It was concluded that tumour necrosis factor-alpha prevents inhibition of extracellular signal-regulated kinase-1/2-mediated group IVA-phospholipase A(2) activation, which is essential for beta(2)-integrin adhesion in polymorphonuclear leukocytes.

serevent generic drug 2016-08-14

Eleven outpatient Lasix 40mg Tab clinical centers.

generic serevent inhaler 2015-12-21

A total of 1,481 women and 4,631 men with COPD were enrolled in TORCH, a trial comparing salmeterol, 50 μg, plus fluticasone propionate, 500 μg, twice a day and each component individually. Causes of death were determined by an endpoint committee. Sex differences in survival were explored using a Cox proportional hazards model adjusted for other baseline factors. Exacerbation rate was compared using a negative binomial model. Dyspnea was evaluated using the Medical Research Council scale and health status using the St. George's Respiratory Questionnaire.

serevent buy 2016-06-05

The study population included 33,939 adult asthmatics (at least 12 years of age) continuously enrolled in 1 of 4 participating health plans for the 6-month study period. Every subject was in 1 of 10 different pharmacotherapy treatment groups. Univariate and multivariate analyses were used to compare the rates and costs of pharmaceutical prescriptions and medical care services between patients on salmeterol plus fluticasone and patients with other pharmacologic therapies.

serevent max dose 2015-09-28

There is conflicting clinical evidence describing the response to long-acting beta-agonist (LABA) bronchodilators for patients with Arg16Gly beta(2)-adrenergic receptor (ADRB2 ) genotype differences. Furthermore, the role of inhaled corticosteroids (ICS) in modulating Arg16Gly clinical responses is not well understood. The objective of this study was to investigate the effects of Arg16Gly polymorphism on the 12 hour post-dose bronchodilator response to the LABA salmeterol (SAL) or SAL plus fluticasone propionate (FSC) on first administration and following 12 weeks of treatment.

serevent brand name 2015-10-18

The deltaPpl and RL were improved 15 minutes through 6 hours after administration of salmeterol, compared with values obtained from horses receiving no treatment. The RAO was improved 15 minutes through 2 hours after administration of salmeterol. The maximal response to salmeterol was evident 30 to 60 minutes after administration and was characterized by a 59 + 19% decrease in deltaPpl and a 56 +/- 13% decrease in RL. The deltaPpl and RL were not different from baseline values 8 hours after salmeterol administration.

serevent drug category 2015-09-18

Changes in weekly PEF from the last week of the run-in period to the last week of treatment (primary end point: change in PEF) were -3.9 ± 4.87 L/min (n = 128) for tiotropium and -3.2 ± 4.64 L/min (n = 134) for salmeterol, and these were superior to placebo (-24.6 ± 4.84 L/min, n = 125, P < .05). Tiotropium was noninferior to salmeterol (estimated difference, -0.78 L/min [95% CI, -13.096 to 11.53]; P = .002; α = .025, 1-sided; noninferiority, 20 L/min). Tiotropium and salmeterol were numerically superior to placebo in some patient-reported secondary outcomes. Adverse events were comparable across treatments.

serevent drug card 2016-06-29

1. Partial agonists of the beta2-adrenoceptor which activate adenylyl cyclase are widely used as bronchodilators for the relief of bronchoconstriction accompanying many disease conditions, including bronchial asthma. The bronchodilator salmeterol has both a prolonged duration of action in bronchial tissue and the ability to reassert this activity following the temporary blockade of human beta2-adrenoceptors with antagonist. 2. We have compared the activation and desensitization of human beta2-adrenoceptor stimulation of adenylyl cyclase induced by salmeterol, adrenaline and salbutamol in a human lung epithelial line, BEAS-2B, expressing beta2-adrenoceptor levels of 40-70 fmol mg(-1), and in human embryonic kidney (HEK) 293 cell lines expressing 2-10 pmol mg(-1). The efficacy observed for the stimulation of adenylyl cyclase by salmeterol was only approximately 10% of that observed for adrenaline in BEAS-2B cells expressing low levels of beta2-adrenoceptor, but similar to adrenaline in HEK 293 cells expressing very high levels of receptors. Salmeterol pretreatment of these cells induced a rapid and stable activation of adenylyl cyclase activity which resisted extensive washing and beta2-adrenoceptor antagonist blockade, consistent with binding to a receptor exosite and/or to partitioning into membrane lipid. 3. The desensitization and internalization of beta2-adrenoceptors induced by the partial agonists salmeterol and salbutamol were considerably reduced relative to the action of adrenaline. Consistent with these observations, the initial rate of phosphorylation of the receptor induced by salmeterol and salbutamol was much reduced in comparison to adrenaline. 4. Our data suggest that the reduction in the rapid phase of desensitization of beta2-adrenoceptors after treatment with salmeterol or salbutamol is caused by a decrease in the rate of beta2-adrenoceptor kinase (betaARK) phosphorylation and internalization. In contrast, the rate of cyclic AMP-dependent protein kinase (PKA)-mediated phosphorylation by these partial agonists appears to be similar to adrenaline.

serevent maximum dose 2016-12-02

1. The potential for tachyphylaxis to the non-pulmonary effects of salmeterol, a long-acting selective beta 2-adrenoceptor agonist was investigated in 12 healthy male subjects in a double-blind two period crossover study design. 2. Subjects received cumulative doses of up to 400 micrograms (50 + 50 + 100 + 100 + 100 micrograms at 45 min intervals) inhaled salmeterol prior to a 13 day dosing schedule of twice-daily inhaled salmeterol 100 micrograms or placebo. Twelve hours after the last dose of salmeterol or placebo, subjects again received cumulative doses of up to 400 micrograms inhaled salmeterol. 3. Pulse rate, blood pressure, 12-lead ECG, physiological tremor and peak expiratory flow rate (PEFR) were measured before administration of cumulative doses of salmeterol, at 10, 20, 30 and 40 min after each incremental dose of salmeterol and at 4, 6 and 8 h after the first dose. Blood samples were taken for plasma potassium, magnesium, non-esterified fatty acids (NEFA) and blood glucose concentrations at 20 and 40 min after each dose and at 4, 6 and 8 h after the first dose. 4. Eleven subjects completed the study. One subject withdrew due to beta 2-adrenoceptor related adverse events. All other adverse events reported were mild in nature. 5. Dose-related changes to the effects of salmeterol on pulse rate, QTc interval, tremor, PEFR, blood glucose and plasma potassium were seen, but there was no dose-related effect of salmeterol on blood pressure, plasma magnesium and NEFA. 6. Tachyphylaxis occurred to the effects of salmeterol on tremor, QTc and blood glucose.(ABSTRACT TRUNCATED AT 250 WORDS)