Instructions Foster aerosol for inhalation dosed 100 mcg/dose + 6 mcg/dose container 120 doses
Composition
active ingredients: beclomethasone dipropionate and formoterol fumarate dihydrate;
1 inhalation dose contains: 100 mcg of beclomethasone dipropionate and 6 mcg of formoterol fumarate dihydrate;
excipients: anhydrous ethanol; hydrochloric acid; propellant: norflurane (HFA-134a).
Dosage form
Inhalation aerosol, metered.
Main physicochemical properties: solution from colorless to yellowish.
Pharmacotherapeutic group
Drugs for the treatment of obstructive airway diseases. Adrenergic agents for inhalation use.
ATX code R03A K08.
Pharmacological properties
Pharmacodynamics.
Foster contains beclomethasone dipropionate and formoterol, which have different mechanisms of action and exhibit an additive effect in reducing the frequency of asthma exacerbations, similar to other combination products containing inhaled corticosteroids and beta2-agonists.
Beclomethasone dipropionate
Beclomethasone dipropionate is an inhaled glucocorticosteroid (GCS) that, at recommended doses, has an anti-inflammatory effect, leading to relief of symptoms and a reduction in the frequency of exacerbations of bronchial asthma, while having a lower incidence of side effects than systemic GCS.
Formoterol
Formoterol is a selective beta2-adrenergic receptor agonist that causes relaxation of bronchial smooth muscle in patients with reversible airway obstruction. The bronchodilator effect occurs rapidly, within 1–3 minutes after inhalation, and persists for 12 hours after a single dose.
Bronchial asthma
Clinical efficacy of maintenance therapy with Foster
Clinical trials in adult patients showed that adding formoterol to beclomethasone dipropionate relieved asthma symptoms, improved lung function measures, and reduced the frequency of exacerbations.
In a 24-week study, the effect of Foster on respiratory function was at least equal to that of a random combination of beclomethasone dipropionate and formoterol and exceeded that of beclomethasone dipropionate used alone.
Clinical efficacy of supportive therapy and the use of Foster for symptom relief
In a 48-week study in 1701 asthmatic patients, the efficacy of Fostair as maintenance therapy (1 inhalation BID) and reliever therapy (up to 8 puffs per day) was compared with Fostair as maintenance therapy (1 inhalation BID) with the addition of salbutamol as needed in adult patients with uncontrolled moderate to severe asthma. The results of the study showed that Fostair as maintenance therapy and reliever therapy significantly prolonged the time to the first severe exacerbation* compared with its use as maintenance therapy with the addition of salbutamol as needed (p < 0.001 for ITT and RR populations). The number of severe asthma exacerbations (patients/year) was significantly reduced in the maintenance and reliever groups compared with the salbutamol group: 0.1476 vs. 0.2239, respectively (statistically significant reduction: p < 0.001). Patients receiving maintenance and reliever therapy achieved clinically meaningful improvements in asthma control. The mean number of reliever inhalations per day and the percentage of patients using reliever decreased proportionally in both groups.
Note*: Severe exacerbations were defined as worsening of asthma symptoms leading to hospitalization or emergency medical treatment, or requiring systemic steroids for more than 3 days.
In another clinical study, a single dose of Foster (100+6 mcg) provided a rapid bronchodilator effect and immediate relief of symptoms of dyspnea similar to the effect of salbutamol at a dose of 200 mcg in patients with bronchial asthma who were administered methacholine to induce bronchospasm.
Children
The bronchodilator effect of a single dose of Foster, an experimental pediatric formulation of beclomethasone dipropionate and formoterol fumarate 50+6 mcg/dose, administered via the Aerochamber Plus® spacer device to asthmatic children aged 5–11 years was evaluated compared with a random combination of commercially available beclomethasone dipropionate and formoterol fumarate. Non-inferiority of Foster (50+6 mcg) compared with the random combination was demonstrated in terms of mean FEV1 assessed over 12 hours after morning dosing, as the lower 95% CI of the adjusted mean difference was 0.047 L, which exceeded the pre-planned efficacy limit of 0.1 L.
Foster pediatric formulation 50+6 mcg/dose administered via the Aerochamber Plus® spacer to asthmatic children aged 5–11 years for 12 weeks of treatment was non-inferior to beclomethasone dipropionate monotherapy and non-inferior to any combination of beclomethasone dipropionate and formoterol fumarate on lung function parameters (primary endpoint: change from baseline in morning FEV1 to dose).
Chronic obstructive pulmonary disease (COPD)
Two 48-week studies evaluated the effect on lung function and the frequency of exacerbations (defined by the prescription of oral steroids and/or a course of antibiotics, and/or hospitalization) in patients with severe COPD (30% < FEV1% < 50%).
One pivotal study showed significant improvements in lung function (primary endpoint change from pre-dose (baseline) FEV1) compared with formoterol after 12 weeks of treatment (adjusted mean difference between Foster and formoterol of 69 ml) and at each clinic visit throughout the treatment period (48 weeks). The study showed that the mean number of exacerbations (patients/year) (exacerbation rate, combined primary endpoint) was statistically significantly reduced with Foster compared with formoterol treatment (adjusted mean rate 0.80 compared with 1.12 in the formoterol group, adjustment factor 0.72, p < 0.001) over a 48-week treatment period in 1199 patients with severe COPD. Foster also significantly prolonged the time to first exacerbation compared with formoterol. The superiority of this drug over formoterol was also confirmed by the frequency of exacerbations in subgroups of patients receiving (about 50% in each treatment group) or not receiving tiotropium bromide as concomitant therapy.
Another pivotal randomized, three-arm, parallel-group study in 718 patients confirmed the superiority of Foster over formoterol in terms of change from baseline FEV1 at the end of treatment (48 weeks) and demonstrated non-inferiority of Foster to the fixed combination of budesonide/formoterol on the same parameter.
Pharmacokinetics.
The systemic exposure of beclomethasone dipropionate and formoterol as active ingredients in the fixed combination of the drug Foster was compared with the exposure of the individual components.
In a pharmacokinetic study in healthy volunteers receiving a single dose of the fixed combination of Foster (4 actuations of 100+6 mcg) or a single dose of beclomethasone dipropionate CFC (4 actuations of 250 mcg) and formoterol HFA (4 actuations of 6 mcg), the AUC of the main active metabolite of beclomethasone dipropionate (beclomethasone-17-monopropionate) and its maximum plasma concentration were 35% and 19% lower, respectively, with the fixed combination than with the non-micronized beclomethasone dipropionate CFC formulation, but the relative absorption rate was higher (0.5 hours versus 2 hours) with the fixed combination compared with the non-micronized beclomethasone dipropionate CFC formulation.
The maximum plasma concentration of formoterol was similar after the use of the fixed or temporary combination, but its systemic exposure was slightly higher after the use of Foster than after the administration of the temporary combination.
There is no evidence of a pharmacokinetic or pharmacodynamic (systemic) interaction between beclomethasone dipropionate and formoterol.
Lung deposition studies in patients with stable COPD, healthy volunteers and asthma patients showed that on average 33% of the nominal dose was deposited in the lungs of COPD patients compared to 34% in healthy volunteers and 31% in asthma patients. Plasma concentrations of beclomethasone-17-monopropionate and formoterol were comparable in all three groups within 24 hours after inhalation. The total exposure to beclomethasone dipropionate was higher in COPD patients compared to asthma patients and healthy volunteers.
Children
Foster was not bioequivalent to a random combination of ultrafine beclomethasone dipropionate and formoterol when administered to adolescent asthmatics aged 12–17 years in a single-dose pharmacokinetic study (4 actuations of 100+6 mcg). This result was independent of whether a spacer (Aerochamber Plus®) was used or not.
If a spacer was not used, the available data indicate a lower peak concentration of the inhaled corticosteroid component of Fostair compared to the random combination (point estimate of the adjusted geometric mean Cmax values of beclomethasone-17-monopropionate [B17MP] 84.38%, 90% CI 70.22; 101.38).
When using Foster with a spacer, the peak plasma concentration of formoterol increased by approximately 68% compared to the random combination (point estimate of the ratios of adjusted geometric means Cmax 168.41, 90% CI 138.2; 205.2). The clinical significance of these differences in long-term use is unknown.
The total systemic exposure of formoterol (AUC0-t) was equivalent to that of the random combination regardless of whether a spacer was used or not. For beclomethasone-17-monopropionate, equivalence was demonstrated only when a spacer was not used, while the 90% CI of the AUC0-t was slightly outside the equivalence interval when spacers were used (point estimate of the adjusted geometric mean ratios 89.63%, CI 79.93; 100.50).
Foster, used without a spacer, produced lower amounts of beclomethasone-17-monopropionate or equivalent total systemic exposure (AUC0-t) of formoterol in adolescents compared to adults. In addition, mean peak plasma concentrations (Cmax) for both substances were lower in adolescents than in adults.
In a pharmacokinetic study, a single dose of Foster pediatric formulation 50+6 mcg/dose administered via the Aerochamber Plus® spacer was not bioequivalent to a random combination of beclomethasone dipropionate and formoterol administered to children with asthma aged 5–11 years. The results of the study indicated a lower AUC0-t and peak concentration of the inhaled corticosteroid component of Foster (50+6 mcg) compared to the random combination (point estimate of the ratios of adjusted geometric means AUC0-t beclomethasone-17-monopropionate 81%, 90% CI 69.7; 94.8; Cmax 82%, 90% CI 70.1; 94.7). The total systemic exposure to formoterol (AUC0-t) was equivalent to that of the random combination, while Cmax was slightly lower for Foster (50+6 μg) compared to the random combination (point estimate of the adjusted geometric mean ratios 92%, 90% CI 78; 108).
Beclomethasone dipropionate
Beclomethasone dipropionate is a precursor of the active substance with weak affinity for glucocorticoid receptors and is hydrolyzed by esterases to the active metabolite beclomethasone-17-monopropionate, which has a stronger local anti-inflammatory effect compared to its precursor, beclomethasone dipropionate.
Absorption, distribution and biotransformation
Inhaled beclomethasone dipropionate is rapidly absorbed through the lungs; this is preceded by extensive conversion by esterases to the corresponding active metabolite, beclomethasone-17-monopropionate, which is found in most tissues. The systemic bioavailability of the active metabolite is formed from the dose absorbed from the lungs (36%) and from the dose absorbed from the gastrointestinal tract. The bioavailability of orally administered beclomethasone dipropionate is low, but conversion to beclomethasone-17-monopropionate results in the absorption of 41% of the dose as the active metabolite.
With increasing inhaled dose, systemic exposure increases approximately linearly.
Absolute bioavailability after inhalation is approximately 2% and 62% of the nominal dose for unchanged beclomethasone dipropionate and beclomethasone-17-monopropionate, respectively.
After intravenous administration, the distribution of beclomethasone dipropionate and its active metabolite is characterized by high plasma clearance (150 l/h and 120 l/h, respectively) with a small volume of distribution at steady state for beclomethasone dipropionate (20 l) and a more extensive tissue distribution for its active metabolite (424 l).
Plasma protein binding is moderately high.
Breeding
Faecal excretion is the main route of elimination of beclomethasone dipropionate, mainly in the form of polar metabolites. Renal excretion of beclomethasone dipropionate and its metabolites is negligible. The terminal half-life is 0.5 h and 2.7 h for beclomethasone dipropionate and beclomethasone-17-monopropionate, respectively.
The pharmacokinetics of beclomethasone dipropionate in patients with renal or hepatic insufficiency have not been studied; however, since beclomethasone dipropionate is very rapidly metabolized by esterases present in intestinal juice, blood plasma, lungs and liver to form the more polar substances beclomethasone-21-monopropionate, beclomethasone-17-monopropionate and beclomethasone, hepatic insufficiency is not considered to affect the pharmacokinetics and safety profile of beclomethasone dipropionate.
Since beclomethasone dipropionate or its metabolites were not detected in urine, the increase in its systemic exposure in patients with renal insufficiency has not been studied.
Formoterol
Absorption and distribution
After inhalation, formoterol is absorbed from the lungs and the gastrointestinal tract. The fraction of the inhaled dose reaching the gastrointestinal tract after use of a metered dose inhaler (MDI) can vary from 60 to 90%. At least 65% of the orally administered fraction is absorbed from the gastrointestinal tract. Maximum plasma concentrations of unchanged drug are reached within 0.5–1 hour after oral administration. Formoterol is 61–64% bound to plasma proteins and 34% bound to albumin. There was no saturation of binding over the concentration range obtained with therapeutic doses. The elimination half-life determined after oral administration is 2–3 hours. Absorption of formoterol is linear after inhalation of 12–96 μg formoterol fumarate.
Biotransformation
Formoterol is extensively metabolized, the main metabolic pathway involving direct conjugation to the phenolic hydroxyl group. The glucuronic acid conjugate is inactive. The second major metabolic pathway involves O-dimethylation after conjugation to the phenolic 2'-hydroxyl group. The cytochrome P450 isoenzymes CYP2D6, CYP2C19 and CYP2C9 are involved in the O-dimethylation of formoterol. The liver appears to be the primary site of metabolism. Formoterol does not inhibit CYP450 enzymes at therapeutically relevant concentrations.
Breeding
The total urinary excretion of formoterol after a single inhalation from a dry powder inhaler increased linearly over the dose range of 12–96 μg. On average, 8 and 25% of the dose were excreted as unchanged and total formoterol, respectively. Based on plasma concentrations determined after inhalation of a single dose of 120 μg in twelve healthy volunteers, the mean terminal half-life was 10 hours. The (R,R)- and (S,S)-enantiomers accounted for approximately 40 and 60% of the unchanged drug excreted in the urine, respectively. The relative proportions of the two enantiomers remained constant over the dose range studied, and there was no evidence of relative accumulation of one enantiomer over the other during multiple dosing.
After oral administration (40–80 mcg) to healthy volunteers, 6–10% of the dose was recovered in the urine as unchanged drug and up to 8% of the dose was recovered as the glucuronide.
Overall, 67% of an oral dose of formoterol is excreted in the urine (mainly as metabolites), the remainder in the feces. Renal clearance of formoterol is 150 ml/min.
Pharmacokinetics in specific patient groups
Renal/hepatic failure:
The pharmacokinetics of formoterol in patients with renal/hepatic insufficiency have not been studied, however, given that formoterol is excreted mainly by hepatic metabolism, an increase in the drug's effect can be expected in patients with severe liver cirrhosis.
Indication
Bronchial asthma
Foster is used for the regular treatment of bronchial asthma when the use of a combination agent (inhaled glucocorticosteroid and long-acting beta2-agonist) is appropriate:
- patients whose symptoms are not adequately controlled with inhaled corticosteroids and short-acting beta2-agonists used as needed, or
- patients for whom inhaled glucocorticosteroids and long-acting beta2-agonists provide adequate disease control.
Chronic obstructive pulmonary disease (COPD)
Symptomatic treatment of patients with severe COPD (FEV1 < 50% predicted) and a history of recurrent exacerbations who have clinically significant symptoms of the disease despite regular treatment with long-acting bronchodilators.
Contraindication
Hypersensitivity to beclomethasone dipropionate, formoterol fumarate dihydrate or to any of the excipients of the drug.
Interaction with other medicinal products and other types of interactions
Pharmacokinetic interactions
Beclomethasone dipropionate is rapidly metabolized by esterase enzymes.
Beclomethasone is less dependent on CYP3A metabolism than some other corticosteroids and interactions are generally unlikely; however, the possibility of systemic effects cannot be excluded with concomitant use of strong CYP3A inhibitors (e.g. ritonavir, cobicistat) and therefore caution and appropriate monitoring are recommended when using such drugs.
Patients with bronchial asthma should avoid the use of beta-blockers (including eye drops). If the use of a beta-blocker cannot be avoided, the effect of formoterol will be weakened or eliminated.
On the other hand, when used simultaneously with other bronchodilators, potentiation of effects is possible, therefore caution should be exercised when using theophylline or other beta-adrenergic agents together with formoterol.
Concomitant use with quinidine, disopyramide, procainamide, phenothiazines, antihistamines, monoamine oxidase inhibitors and tricyclic antidepressants may increase the duration of the QTc interval and the risk of developing ventricular arrhythmia.
In addition, L-dopa, L-thyroxine, oxytocin, and alcohol may impair the cardiac tolerance of beta2-sympathomimetics.
Concomitant use of monoamine oxidase inhibitors, including drugs with similar properties such as furazolidone and procarbazine, may cause hypertensive reactions.
There is an increased risk of arrhythmia in patients receiving concomitant anesthesia with halogenated hydrocarbons.
Concomitant use of xanthine derivatives, steroids or diuretics may potentiate the potential hypokalemic effect of beta2-sympathomimetics (see section 4.4). Hypokalemia may increase the susceptibility to arrhythmias in patients taking cardiac glycosides.
Foster contains a small amount of ethanol. There is a theoretical possibility of interaction in particularly sensitive patients taking disulfiram or metronidazole.
Application features
Fostair should be used with caution (monitoring is recommended) in patients with arrhythmias, including third-degree atrioventricular block and tachyarrhythmia (rapid and/or irregular heartbeat), idiopathic subvalvular aortic stenosis, hypertrophic obstructive cardiomyopathy, severe heart disease such as acute myocardial infarction, ischemic heart disease, chronic heart failure, and in patients with occlusive vascular disease, including atherosclerosis, arterial hypertension and aneurysm.
Caution should be exercised when prescribing the drug to patients with established or suspected prolongation of the QTc interval (congenital or drug-induced) (QTc > 0.44 sec), as formoterol may prolong the QTc interval.
Fostair should be administered with caution to patients with thyrotoxicosis, diabetes mellitus, pheochromocytoma and untreated hypokalemia.
Treatment with beta2-agonists may cause potentially serious hypokalemia. Caution should be exercised in severe bronchial asthma, as this effect may be potentiated by hypoxia. Hypokalemia may also be potentiated by concomitant use of other agents that can cause hypokalemia, such as xanthine derivatives, steroids and diuretics (see section "Interaction with other medicinal products and other forms of interaction"). Caution is recommended in patients with unstable bronchial asthma who may be taking a number of so-called rescue bronchodilators. In such cases, monitoring of serum potassium levels is recommended.
Formoterol inhalation may increase blood glucose levels. For this reason, patients with diabetes should monitor their blood glucose levels closely.
When planning anesthesia with halogenated anesthetics, it should be ensured that Foster has not been used for at least 12 hours before the start of anesthesia, as there is a risk of developing cardiac arrhythmia.
As with other inhaled corticosteroids, Foster should be used with caution in patients with active or latent pulmonary tuberculosis, as well as in patients with fungal and viral respiratory tract infections.
It is not recommended to abruptly stop treatment with Foster.
If the patient considers the treatment ineffective, it is recommended to consult a doctor. Increased use of rescue bronchodilators indicates a worsening of the condition and requires a review of the treatment of bronchial asthma. Sudden and progressive deterioration in the control of bronchial asthma or COPD is potentially life-threatening and the patient should undergo an urgent medical examination. If infection is suspected, the need for increasing the intensity of inhaled treatment or the appropriateness of prescribing oral corticosteroids or antibiotic treatment should be assessed.
As with any inhalation therapy, paradoxical bronchospasm with immediate increase in wheezing and respiratory rate may occur after administration of the drug. In such cases, a fast-acting inhaled bronchodilator should be used immediately. Use of Foster should be discontinued immediately, the patient should undergo a medical examination and, if necessary, alternative treatment should be initiated.
Foster should not be used as the first-line treatment for bronchial asthma.
For the treatment of acute attacks of bronchial asthma, patients are recommended to always carry a fast-acting bronchodilator both when using Foster as maintenance therapy and to relieve symptoms, and when using the drug solely as maintenance therapy.
Patients should be advised to take Fostair daily as prescribed, even when symptoms are absent. Fostair inhalation should be used to relieve symptoms when asthma flares up, but is not intended for regular prophylactic use, e.g. before exercise. In such cases, a separate rapid-acting bronchodilator should be considered.
Once asthma symptoms are controlled, consideration should be given to gradually reducing the dose, with regular review of the patient. The lowest effective dose of Foster should be used (see section 4.2).
Systemic effects may occur with any inhaled corticosteroid, especially at high doses and over long periods of time. The likelihood of such effects is much lower with inhaled corticosteroids than with oral corticosteroids. Possible systemic effects include Cushing's syndrome, Cushingoid features, adrenal suppression, decreased bone mineral density, growth retardation in children and adolescents, cataracts and glaucoma, and less commonly, a number of psychological or behavioral effects, including psychomotor hyperactivity, sleep disturbances, anxiety, depression, or aggression (especially in children).
For this reason, regular monitoring of the patient's condition is important, as well as reducing the dose of inhaled corticosteroids to the lowest possible dose that provides effective control of bronchial asthma.
Pharmacokinetic data obtained after a single dose (see section "Pharmacokinetics") showed that the use of Foster with the Aerochamber Plus® spacer compared with the use of a standard device does not increase the total systemic exposure of formoterol and reduces the systemic exposure of beclomethasone-17-monopropionate. In addition, the level of unchanged beclomethasone dipropionate entering the systemic circulation from the lungs increases, but the total systemic exposure of beclomethasone dipropionate and its active metabolites is not changed, and therefore the risk of systemic effects when used with the spacer is not increased.
Prolonged treatment of patients with high doses of inhaled corticosteroids may cause adrenal suppression and acute adrenal insufficiency. Children under 16 years of age who ingest/inhale doses of beclomethasone dipropionate in excess of those recommended are at particular risk. Situations that may potentially cause acute adrenal insufficiency include trauma, surgery, infection or any rapid dose reduction. Symptoms are usually vague and may include anorexia, abdominal pain, weight loss, fatigue, headache, nausea, vomiting, hypotension, decreased level of consciousness, hypoglycaemia and convulsions. Additional systemic corticosteroids should be considered during times of stress or elective surgery.
Caution should be exercised when transferring patients to Fostair when adrenal function is impaired, possibly due to previous treatment with systemic steroids.
When switching from oral to inhaled corticosteroids, the risk of impaired adrenal reserve persists for a significant period of time. Patients who have received high doses of corticosteroids as emergency treatment in the past or who have received long-term treatment with high doses of inhaled corticosteroids may also be at risk. The possibility of residual impairment should always be borne in mind in emergencies and certain other situations that may cause stress; the appropriateness of appropriate corticosteroid treatment should be considered. Depending on the degree of adrenal impairment, medical advice may be required before individual procedures.
An increased incidence of pneumonia, including pneumonia requiring hospitalization, has been observed in patients with COPD receiving inhaled corticosteroids. There is some evidence of an increased risk of pneumonia with increasing steroid doses, but this has not been consistently demonstrated in all studies. There is no convincing clinical evidence of a difference in the magnitude of the risk of pneumonia between classes of inhaled corticosteroids. Physicians should remain alert for the possible development of pneumonia in patients with COPD, as the clinical features of such infections overlap with symptoms of COPD exacerbations. Risk factors for pneumonia in patients with COPD include smoking, older age, low body mass index (BMI), and severe COPD.
Patients should be advised to rinse or swish their mouth with water or brush their teeth with a toothbrush after inhaling the prescribed dose of the product to reduce the risk of oropharyngeal candidiasis.
Vision impairment
Visual disturbances may occur with systemic and topical corticosteroids. If a patient experiences symptoms such as blurred vision or other visual disturbances, an ophthalmologist should be consulted to evaluate possible causes, which may include cataracts, glaucoma, or rare conditions such as central serous chorioretinopathy (CSCR), which have been reported following the use of systemic and topical corticosteroids.
Excipient content
This medicinal product contains a small amount of ethanol, less than 100 mg/dose. At normal doses, the amount of ethanol is insignificant and does not pose a risk to patients.
After first opening the container, use within 3 months!
Use during pregnancy or breastfeeding
There is no experience with the use of HFA-134a propellant in pregnant or breastfeeding women, nor is there any information on its safety in this group of patients. However, studies of the effects of HFA-134a propellant on reproductive function and embryonic development in animals have not revealed any clinically significant adverse effects.
Pregnancy
There are no clinical data on the use of Foster in pregnant women. Animal studies with the combination of beclomethasone dipropionate and formoterol have shown reproductive toxicity at high systemic doses. Due to the tocolytic effect of beta2-sympathomimetics, special care may be required during labour. Formoterol is not recommended for use during pregnancy, including late pregnancy or during labour, unless there are no approved alternative treatments.
Foster is allowed to be used during pregnancy if the expected benefit to the woman outweighs the potential risks to the fetus.
Lactation
There are no clinical data on the use of this drug during breastfeeding.
Although animal data are not available, it is reasonable to assume that beclomethasone dipropionate, like other corticosteroids, passes into breast milk.
It is not yet known whether formoterol passes into human breast milk, but it has been detected in the milk of lactating animals.
The use of Foster in breastfeeding women is recommended only if the expected benefit to the mother outweighs the potential risks to the child.
Ability to influence reaction speed when driving vehicles or other mechanisms
The drug Foster has virtually no effect on the ability to drive or use other mechanisms.
Method of administration and doses
The drug Foster is used by inhalation.
Dosage
Bronchial asthma
Foster is not intended for the initial treatment of bronchial asthma. The dose of the components of the drug is individual and should be adjusted depending on the severity of the disease. This should be taken into account not only after starting treatment with combination drugs, but also after dose adjustment. If the patient requires a dose combination that differs from that available in the combination inhalation drug, appropriate doses of beta2-agonists and/or corticosteroids should be prescribed separately.
Beclomethasone dipropionate in Foster is characterized by a micronized particle size distribution, resulting in a stronger effect than that of beclomethasone dipropionate dosage forms with a non-micronized particle size distribution (100 μg of beclomethasone dipropionate micronized in Foster is equivalent to 250 μg of beclomethasone dipropionate in a dosage form with non-micronized particles). Therefore, the total daily dose of beclomethasone dipropionate prescribed in Foster should be lower than the total daily dose of beclomethasone dipropionate prescribed in a dosage form with non-micronized beclomethasone dipropionate particles.
This should be taken into account when transferring a patient from a non-micronized beclomethasone dipropionate formulation to Foster; the beclomethasone dipropionate dose should be lower and adjusted according to the individual needs of the patient.
There are two treatment options:
A. Maintenance therapy: Foster is used as a regular maintenance
