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Astelin (Azelastine)

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Astelin is a nasal spray which is used for treating allergy symptoms and symptoms of nasal passage inflammation. Astelin contains azelastine, an antihistamine. It blocks the effects of the chemical histamine in your body. Astelin prevents sneezing, itching, runny nose, and other nasal symptoms of allergies.

Other names for this medication:
Adomessen, Afluon, Afluon nasal, Alager, Allergodil, Allergospray, Amsler, Antalerg, Armin, Astepro, Asutoputin, Az ofteno, Azel, Azelastin, Azelastina, Azelastine, Azelastinum, Azelone, Azen, Azep, Azepit, Azeptin, Bifertin, Brixia, Cobatect, Corifina, Lasticom, Lastin, Oculastin, Optilast, Optivar, Otrivin azelastine, Otrivin heuschnupfen, Otrivine, Prorhinite, Raspjine, Rhinolast, Rinalin, Rino-lastin, Snizex, Sophistina, Xanaes

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Also known as:  Azelastine.


Astelin belongs to a group of medicines called antihistamines.

Astelin provides relief from bothersome nasal symptoms such as congestion, itchy/runny nose, sneezing and postnasal drip due to seasonal allergens or environmental irritants.

Astelin is steroid-free, does not contain pseudoephedrine, and relieves your symptoms by blocking the effects of histamine - the primary cause of allergy symptoms.

What makes Astelin unique is that it is a steroid-free antihistamine nasal spray that provides symptom relief whether the trigger is an allergen (grass, trees, pollen, mold, etc.), an irritant (cigarette smoke, perfume, cleaning agents, car exhaust, cold air, etc.), or both.

Astelin is also know as Azelastine, Arzep, Rhinolast, Alerdual, Allergodil, Rinalin.

Generic name of Astelin is Azelastine.


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

Astelin can be used by patients as young as 5 years of age, depending on what type of rhinitis they have been diagnosed with.

For those with seasonal allergic rhinitis, patients from 5 to 11 years of age should administer 1 spray in each nostril twice daily.

Patients 12 years of age and older with seasonal allergic rhinitis should administer 2 sprays of Astelin in each nostril twice daily.

For those with nonallergic vasomotor rhinitis, patients 12 years of age and older should administer 2 sprays of Astelin in each nostril twice daily.

Before using Astelin for the first time, remove the child-resistant screw cap and replace with the pump unit. Prime the delivery system (pump unit) with four sprays or until a fine mist appears. If 3 days or more have elapsed since your last use of the nasal spray, reprime the pump with two sprays or until a fine mist appears.


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


Store at a room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and sunlight. Keep in a tightly closed container. 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 Astelin 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 Astelin if you are allergic to Astelin components.

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

The medicine has a antihistamine in it. Before you start any new medicine, check the label to see if it has an antihistamine (e.g., diphenhydramine) in it too. If it does or if you are not sure, check with your doctor or pharmacist.

Astelin may cause harm if it is swallowed. If you may have taken it by mouth, contact your poison control center or emergency room right away.

Astelin should be used with extreme caution in children younger than 5 years old; safety and effectiveness in these children have not been confirmed.

Do not drink alcohol or use medicines that may cause drowsiness (e.g., sleep aids, muscle relaxers) while you are using Astelin; it may add to their effects. Ask your pharmacist if you have questions about which medicines may cause drowsiness.

Astelin may cause drowsiness. These effects may be worse if you take it with alcohol or certain medicines. Use Astelin with caution. Do not drive or perform other possibly unsafe tasks until you know how you react to it.

Do not stop taking Astelin suddenly.

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In this study the effect of azelastine on the activation (antigen-dependent, Ca(2+)-dependent, Stage I) and release (antigen-independent, Ca(2+)-dependent, Stage II) phases of allergen-induced histamine secretion in rabbit mixed leukocytes (basophils) was investigated. Azelastine (5 microM, 10-min) and diltiazem (5 microM: a Ca2+ antagonist, 10 min) inhibited ragweed extract-induced histamine secretion during the Stage II (release) phase. Theophylline (100 microM), a phosphodiesterase inhibitor, added immediately before antigen challenge, inhibited allergic histamine secretion during the Stage I (activation) phase. The data obtained in this study suggest that diltiazem and azelastine act on the Ca(2+)-dependent and antigen-independent phase (Stage II) of allergic histamine secretion in rabbit basophils.

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Pranlukast (SB 205312, ONO-1078) is an orally active, potent, selective blocker of peptidyl-leukotriene receptors. Pranlukast has been studied in a worldwide clinical development program and recently was approved in Japan for the treatment of asthma. This worldwide experience includes a pivotal safety and efficacy study conducted in Japan, a leukotriene D4 (LTD4) challenge study conducted in Europe, and two safety, tolerability, and clinical activity studies conducted in Europe and North America. The pivotal study was a randomized, double-blind, 8-week comparison of pranlukast, 225 mg bid, and azelastine, 2 mg bid. Improvements in asthma symptom scores, morning and evening peak expiratory flow rate (PEFR), and a decreased need for bronchodilators and corticosteroids in the pranlukast-treated group were statistically significant when compared with those in the azelastine-treated group. The most common adverse experiences were GI. The European challenge study evaluated the ability of 5-day therapy with pranlukast, 450 mg bid, to block the bronchoconstrictor effect of inhaled LTD4. A single dose of pranlukast resulted in a 10.6-fold increase in the concentration of LTD4 required to produce a 35% decrease in specific airways conduction; following 5 days of therapy, this increased to 25.9-fold. The two safety, tolerability, and clinical activity studies were randomized, double-blind, placebo-controlled, 4-week evaluations of pranlukast, 225 to 450 mg bid. Improvements in FEV1, PEFR, and asthma symptoms were noted. Ongoing studies will define further the role of pranlukast as a treatment for asthma and allergic rhinitis.

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Alcohol-induced bronchoconstriction is due to high blood concentrations of acetaldehyde, a metabolic product of ethanol, which lead to the release of histamine from basophils and mast cells.

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1. The capacity of various drugs (acetylsalicylic acid (ASA), ketoprofen, diclofenac, piroxicam, BW 755C, BW A4C, nedocromil sodium and azelastine) to inhibit human polymorphonuclear neutrophil (PMN)-mediated platelet activation was investigated. In this model, stimulated PMN release cathepsin G (Cat G), a serine proteinase which, in turn, induces platelet activation. 2. Among the different tested drugs, azelastine (100 microM for 1 min) was the only one able to prevent platelet aggregation. The cyclo-oxygenase inhibitors were all inactive, although used at effective concentrations as judged by inhibition of thromboxane B2 (TxB2) formation. Inhibition of platelet aggregation by azelastine was concentration-dependent, the range of active concentrations being of 20-70 microM. Release from platelets of 5-hydroxytryptamine was also inhibited at 30 microM and above, but never reached 100%. 3. The inhibition by azelastine is due to an effect on both cells. Indeed, beta-glucuronidase release from activated PMN and platelet activation by purified Cat G were both affected. 4. However, used at high concentrations (greater than 100 microM) azelastine was toxic since it released significant amounts of lactate dehydrogenase (LDH) from PMN and platelets. 5. These results show the capacity of azelastine, an anti-allergic and anti-asthmatic compound, to inhibit the cell-to-cell communication between PMN and platelets, an effect which may be relevant for its therapeutic efficacy or for a new application in diseases in which PMN and platelets are involved.

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A simple, noninvasive, bias-flow ventilated wholebody plethysmographic technique and noninvasive pulmonary analyzer (Buxco dyspnea monitor) were used to quantitate allergic dyspnea in chronically sensitized freely moving guinea pigs. In this study, the effect of azelastine on aeroallergen-induced dyspnea in allergic guinea pigs was investigated. Aeroallergen challenge produced severe dyspnea which was characterized by a 390% increase in the amplitude of pseudo flow signal, a 93% increase in box pressure (delta P) and a 68% decline in relaxation time; these changes signify a tremendous increase in the effort of breathing. The oral administration of azelastine (1 mg/kg) two hours before aeroallergen provocation significantly inhibited allergic dyspnea in this acute allergic asthma model. This technique permits quantitative measurement of the severity of the airway allergic responses in freely moving guinea pigs.

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The present study was undertaken to examine the influence of antihistamines on TARC and MDC production from CD14+ cells after antigenic stimulation in vitro.

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The AR+NoTr group showed the worst allergic symptoms, cilia loss and greater inflammation. In the AR+Aze and AR+Cin groups, allergic symptom scores were higher than those in the control group. However, between AR+Aze and AR+Cin groups, there were no significant differences in the allergic symptom scores Histopathological analysis revealed vascular congestion and an increase in goblet cell numbers in the AR+Cin group. However, AR+Cin rat nasal mucosa had less plasma cell infiltration compared with the AR+NoTr group. In rats from the AR+Aze group, analysis of the nasal mucosa revealed less eosinophil infiltration than that seen in the AR+NoTr group. A lower score for mast cell (MC) infiltration was observed in the nasal mucosa of rats treated with Azelastine HCl compared with cinnamaldehyde.

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The study was approved by the Johns Hopkins University institutional review board, and all subjects gave written consent. We studied 20 asymptomatic subjects with seasonal allergic rhinitis. The study had 2 randomized, double-blind, placebo-controlled, crossover phases that evaluated 2 concentrations of olopatadine, 0.1% and 0.2%. In a third exploratory phase, olopatadine, 0.1%, was compared with topical azelastine, 0.1%, in a patient-masked design. Efficacy variables were the allergen-induced sneezes, other clinical symptoms, and the levels of histamine, tryptase, albumin, lysozyme, and cysteinyl-leukotrienes (third study only) in nasal lavage fluids.

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astelin maximum dosage 2016-11-02

In order to clarify the mechanism of the antitussive effects of azelastine hydrochloride (azelastine, CAS 790307-93-0), the cough responses to inhaled capsaicin and substance P (SP) were evaluated before and after the administration of azelastine in conscious guinea pigs. The concentrations of SP were also measured before and after the administration of azelastine by radioimmunoassay in anesthetized guinea pigs. Capsaicin and SP caused coughing in conscious guinea pigs in a dose-dependent fashion. After the treatment with azelastine, capsaicin-induced cough decreased significantly, and the dose-response curve to capsaicin was shifted to a higher concentration in comparison with the the controls. SP-induced cough was not inhibited by the treatment with azelastine, and the dose-response curves to SP did not change. The concentrations of SP recovered in bronchoalveolar lavage fluid and in the trachea Protonix Yellow Pill were decreased statistically significantly in a dose-dependent manner after the treatment with azelastine, while the SP concentrations of the subjects not treated with azelastine were not inhibited. These results suggest that the antitussive effect of azelastine might be partly due to the inhibition of SP release from sensory nerves in guinea pigs.

astelin usual dosage 2016-09-27

Nonallergic rhinitis is a common disease that probably affects as many as 17 million Americans. Of equal importance is that, based on available data, approximately 22 million people suffer with a combination of nonallergic rhinitis and allergic diseases (mixed rhinitis). Both nonallergic and mixed rhinitis occur more frequently in adults than in children, may be more common in female patients than in male Zithromax 250 Dosage patients, and are more likely to be perennial than seasonal. Agents demonstrating efficacy (based on controlled trials or having approval by the FDA) for the therapy of nonallergic rhinitis are azelastine and topical nasal steroids.

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We found that the combination of intranasal azelastine and mometasone synergistically Diflucan Dosage Pediatrics suppressed Th17 responses and (reciprocally) elevated Treg responses. Therefore, this combination not only ameliorated allergic inflammation by suppressing Th2 responses, but also usefully modified the Treg/Th17 balance.

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Azelastine has previously been demonstrated to inhibit histamine release, to antagonize histamine-mediated responses, and to be a bronchodilator. To determine the mechanism by which azelastine has antihistaminic and bronchodilatory actions, we studied its interaction with relevant human lung receptors. We performed competitive radioligand binding assays and determined the affinity of azelastine for [3H]pyrilamine (histamine H1), [125I]pindolol (beta), and [3H]quinuclidinyl benzilate (muscarinic) binding sites. Azelastine had a relatively high affinity for histamine H1 receptors with IC50 values consistently as low or lower than values measured for other antihistamines. In contrast, azelastine had a very low affinity for both beta-receptors and muscarinic receptors with IC50 values greater than 2 logs greater than those determined for beta-agonists and muscarinic antagonists, respectively. Thus, bronchodilatory activity of azelastine does not appear to result from either beta-agonist or muscarinic-antagonist properties. Azelastine does, however, have the ability to inhibit the release of histamine and to bind to histamine H1 receptors, thereby effectively antagonizing histamine H1 receptor-mediated responses in the lung. These characteristics make azelastine a potentially very useful drug to treat allergic responses Lamictal 150 Mg in the respiratory tract.

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To compare Diovan Tablet 80mg an azelastine-fluticasone combination nasal spray administered in a single-delivery device with a commercially available azelastine nasal spray and fluticasone nasal spray.

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Efficacy of azelastine nasal spray was significantly superior compared to desloratadine tablets (p = 0.005) and placebo (p < 0.001). Desloratadine was significantly better than placebo (p < 0.001). Decrease both in Major Nasal Symptom Score (MNSS) and in Total Nasal Symptom Score (TNSS) was fastest after azelastine treatment. Improvement of nasal symptom severity was most pronounced after azelastine treatment for all nasal symptoms including nasal congestion Benicar Dose Sizes . Onset of action was 15 min for azelastine compared to 150 min for desloratadine. Both active preparations were safe and well tolerated.

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We have evaluated the efficacy of azelastine, a new long acting antihistamine, in the topic treatment of seasonal allergic rhinitis to Parietaria officinalis. Forty five patients have been considered, 20 males and 25 females, mean age 28.5 years, suffering from seasonal rhinitis to Parietaria officinalis for at least 4 years. Azelastine was administered twice a day for 4 weeks in the pollen season. On a daily diary-card, patients had to record the severity of the symptoms considered: runny nose, sneeze, itching nose, nasal obstruction, following an arbitrary score from 0 to 3. At the end of the study, patients obtained a Prograf Medication Cost significant improvement of the symptoms considered without the addition of any other topical or systemic therapy. No side effects have been reported. Therefore azelastine is an effective drug in the treatment of seasonal allergic rhinitis to Parietaria officinalis.

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The pathogenesis of vasomotor rhinitis is not understood. It is unlikely that antihistamines, based on their H1 antagonist Diflucan Iv Dose activity alone, would be effective in this disorder.