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Last updated on: November 22nd, 2021

Drug Approvals

(British Approved Name, US Adopted Name, rINN)

Synonyms: Fenoterol; Fenoteroli; Fenoterolum
BAN: Fenoterol
USAN: Fenoterol
INN: Fenoterol [rINN (en)]
INN: Fenoterol [rINN (es)]
INN: Fénotérol [rINN (fr)]
INN: Fenoterolum [rINN (la)]
INN: Фенотерол [rINN (ru)]
Chemical name: 1-(3,5-Dihydroxyphenyl)-2-(4-hydroxy-αmethylphenethylamino)ethanol
Molecular formula: C17H21NO4 =303.4
CAS: 13392-18-2
ATC code: G02CA03; R03AC04; R03CC04

Fenoterol Hydrobromide

Drug Approvals

(British Approved Name Modified, rINNM)

International Nonproprietary Names (INNs) in main languages (French, Latin, and Spanish):

Synonyms: Fenoterol, hidrobromuro de; Fenoterol-hidrobromid; Fenoterol-hydrobromid; Fenoterolhydrobromid; Fenoteroli Hydrobromidum; Fenoterolihydrobromidi; Fenoterolio hidrobromidas; TH-1165a
BAN: Fenoterol Hydrobromide [BANM]
INN: Fenoterol Hydrobromide [rINNM (en)]
INN: Hidrobromuro de fenoterol [rINNM (es)]
INN: Fénotérol, Bromhydrate de [rINNM (fr)]
INN: Fenoteroli Hydrobromidum [rINNM (la)]
INN: Фенотерола Гидробромид [rINNM (ru)]
Chemical name: 1-(3,5-Dihydroxyphenyl)-2-(4-hydroxy-αmethylphenethylamino)ethanol hydrobromide
Molecular formula: C17H21NO4,HBr =384.3
CAS: 1944-12-3
ATC code: G02CA03; R03AC04; R03CC04
Read code: y01pc

Pharmacopoeias. In Europe.

European Pharmacopoeia, 6th ed. (Fenoterol Hydrobromide). A white or almost white, crystalline powder. Soluble in water and in alcohol. A 4% solution in water has a pH of 4.2 to 5.2. Protect from light.


Adverse Effects and Precautions

As for Salbutamol.

Increased mortality.

Since the introduction of metered-dose aerosols of beta agonists there have been two reported epidemics of increased morbidity and mortality in asthmatic patients associated with their use. The first occurred in the 1960s and was linked with the use of high-dose isoprenaline inhalers. The use of isoprenaline was subsequently largely stopped in favour of more selective beta2 agonists.

The second epidemic occurred in New Zealand in the late 1970s and 1980s and was associated with the use of fenoterol. When use of fenoterol fell in New Zealand, so too did the asthma mortality rate. Heavy or regular use of fenoterol was implicated. Fenoterol was also implicated in increased asthma morbidity and mortality in a study in Canada, as was salbutamol, and results from Japan also suggested a relation between asthma deaths and excessive use of beta agonists, particularly fenoterol. However, an analysis of the New Zealand deaths could not identify such a risk with beta agonists other than fenoterol.

There is still debate about this second epidemic. The individual case control studies, including the one from Canada, showed an increased morbidity and mortality in patients taking fenoterol, but a meta-analysis of the accumulated data to 1992 suggested that the increase in mortality in the patients taking beta2 agonists was slight and only significant when they were given by nebuli-sation. Also a working party of the UK CSM considered that a causal link between asthma mortality and beta-agonist use could neither be confirmed nor refuted.

Not surprisingly there are different views on the cause of the increased asthma mortality. The cardiotoxicity of the beta agonist might have to be considered, although evidence for such an effect is felt by some to be slight. The severity of the asthma might have been a factor in two different ways. One hypothesis is that patients used more fenoterol because they had severe asthma and were already at increased risk of dying. Another proposes that heavy beta-agonist use led to an increase in asthma severity which could be explained by a down regulation of beta receptors.

This may appear to be only of historical interest since mortality rates have fallen and current recommendations for the use of short-acting beta2 agonists, which are generally more selective than fenoterol, are for them to be taken as required rather than on a regular basis indeed increasing use of such drugs is seen as an indication to amend the treatment schedule. Moreover, the dose of fenoterol has been reduced in recent years. However, controversy over regular use of short-acting beta2 agonists continues to be fed by conflicting studies of their benefit.

More recently 2 further observational studies have reported an association between use of short-acting beta2 agonists and adverse effects on mortality. A cohort study, designed to evaluate the effect of respiratory medications on asthma death, found an association between the excessive use of short-acting beta2 agonists and an increased risk of asthma death no additional risk was found with fenoterol beyond the risk associated with beta2 agonists as a class. It was unknown whether excessive use was a symptom or a cause of worsening asthma. A case-control study similarly found a modestly increased risk ofmortality associated with use of short-acting beta2 agonists in the previous 1 to 5 years.

However, the study had insufficient power to come to any conclusions regarding the effects of fenoterol, which was rarely prescribed alone, and concluded that evidence for a direct adverse effect of beta2 agonists was inconclusive other explanations might include lack of more appropriate asthma care, more severe disease or increasing severity of disease, or a tendency for patients whose disease was not responding to receive a wider range of treatments.

For discussion of similar concerns about the use of long-acting beta2 agonists in asthma, see Salmeterol.

Pulmonary oedema.

Pulmonary oedema has occurred in women given beta agonists, including fenoterol, for premature labour. The risk factors, the most important of which is fluid overload, are discussed under Precautions for Salbutamol.



As for Salbutamol.


Fenoterol is incompletely absorbed from the gastrointestinal tract and is also subject to extensive first-pass metabolism by sulfate conjugation. It is excreted in the urine and bile almost entirely as the inactive sulfate conjugate. Fenoterol is distributed into breast milk.

Uses and Administration

Fenoterol is a direct-acting sympathomimetic with beta-adrenoceptor stimulant activity largely selective for beta2 receptors (a beta2 agonist). It has actions and uses similar to those of salbutamol and is used as a bronchodilator in the management of reversible airways obstruction, as occurs in asthma and in some patients with chronic obstructive pulmonary disease. On inhalation, fenoterol acts rapidly (5 minutes) and has a duration of action of about 6 to 8 hours.

In the management of reversible airways obstruction, fenoterol hydrobromide may be given from a metered-dose aerosol in a dose of 1 or 2 inhalations of 100 micrograms up to 3 or 4 times daily, to a maximum of 800 micrograms daily. Current asthma guidelines recommend that inhaled short-acting beta2 agonists such as fenoterol be used on an ‘as-required’, not regular, basis. In those patients requiring more than occasional use of fenoterol, anti-inflammatory therapy is also needed. An increased requirement for, or decreased duration of effect of, fenoterol indicates deterioration of asthma control and the need for increased anti-inflammatory therapy.

Fenoterol hydrobromide may be given as a nebulised solution the usual dose for inhalation by this route is 0.5 to 1 mg. In more refractory cases up to 2.5 mg may be given. Treatment may be repeated every 6 hours as required.

Fenoterol hydrobromide may also be given orally for the relief of bronchospasm at a dose of 2.5 to 5 mg three times daily.

For doses in children, see Administration in Children, below.

Fenoterol hydrobromide has also been used similarly to salbutamol, in the management of premature labour. A suggested dose, by intravenous infusion, has been 1 to 3 micrograms/minute, up to a maximum of 5 micrograms/minute, followed by oral doses of 5 mg every 3 to 6 hours.

Administration in children.

In some countries fenoterol has been given via a metered-dose inhaler to children over 6 years of age, at the same doses used in adults (see Uses and Administration, above).

Fenoterol hydrobromide is also given orally to children for the relief of bronchospasm in the following doses:

  • children aged 1 to 3 years, 1.25 mg three times daily
  • children aged 4 to 10 years, 2.5 mg three times daily
  • children aged over 10 years, as for adults (see Uses and Administration, above)


British Pharmacopoeia 2008: Fenoterol Pressurised Inhalation.

Proprietary Preparations

Argentina: Alveofen Asmopul Berotec

Australia: Berotec

Austria: Berotec

Belgium: Berotec

Brazil: Berotec Bromifen Bromotec Febiotec Fenozan

Canada: Berotec

Chile: Berotecf Parsistene

Czech Republic: Berotec

Denmark: Berotec

Finland: Berotec

Germany: Berotec Partusisten

Hong Kong: Berotec

Hungary: Berotec

Indonesia: Berotec

Italy: Dosberotecjpn Berotec

Malaysia: Berotec Feno

Mexico: Berotec Partusisten

The Netherlands: Berotec Partusisten

Norway: Berotec

Philippines: Berotec

Poland: Berotec

Portugal: Berotec

Russia: Berotec Partusisten

Singapore: Berotec

Spain: Berotec

Sweden: Berotec

Switzerland: Berotec

Thailand: Berotec

Venezuela: Berotec Segamol.


Argentina: Berodual Duotec Ipradual

Austria: Berodual Berodualin Ditec

Belgium: Duovent

Brazil: Duovent Fymnal

Canada: Duovent

Chile: Berodual

Czech Republic: Berodual Ditec

Denmark: Berodual

Finland: Atrovent Comp

France: Bronchodual

Germany: Berodual Ditec

Greece: Berodual

Hong Kong: Berodual

Hungary: Berodual Duotec

India: Fenovent

Indonesia: Berodual

Ireland: Duovent

Italy: Duovent Iprafen

Malaysia: Berodual Duovent

Mexico: Berodual Berosolvon

The Netherlands: Berodual

Philippines: Berodual

Poland: Berodual

Portugal: Berodual

Russia: Berodual Ditec

South Africa: Atrovent Beta Berodual Duovent Sabax Nebrafen

Singapore Berodual Duovent

Spain: Berodual

Switzerland: Berodual

Thailand: Berodual Inhalex Punol

UK: Duovent

Venezuela: Berodual Berosolvon Duovent Respidual

The symbol denotes a preparation no longer actively marketed

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