General
Preferred name
salbutamol
Synonyms
ALBUTEROL ()
Albuterol hemisulfate ()
levalbuterol ()
Salbutamol hemisulfate ()
ALBUTEROL SULFATE ()
Ventolin Sulfate ()
Bronchospray ()
AH-3365 ()
Salbutamol,(+/-) ()
Salbutamol Sulfate ()
Albuterol (hemisulfate) ()
AH-3365 (hemisulfate) ()
Salbutamol (hemisulfate) ()
Albuterol, Ventolin, Aerolin, Ventorlin, Asthalin, Asthavent ()
Ventolin CR ()
Aerolin Auto ()
SCH-13949W ()
Salbutamolum ()
Combivent UDVs ()
Rimasal ()
Salamol E-Breathe ()
Proair Hfa ()
Accuneb ()
Salbulin Novolizer ()
Salbutamol ()
Asmaven ()
Maxivent ()
Aerolin 400 ()
Asmasal Spacehaler ()
SCH 13949W ()
Salapin ()
Ventolin E-Breathe ()
Volmax ()
Salbuvent ()
Libetist ()
Ventodisks ()
Duoneb ()
Airomir ()
Ipramol Steri-Neb ()
Proventil-Hfa ()
Proventil ()
Etinoline ()
Kentamol ()
NSC-757417 ()
Ventolin ()
Proventil Hfa ()
Aerolin ()
Asmavent ()
Salipraneb ()
Steri-Neb Salamol ()
Asmasal Clickhaler ()
Ventolin Hfa ()
Ventmax SR ()
Combivent ()
Cobutolin ()
Airsalb ()
Ventoline ()
Sch-13949w sulphate ()
Salbumol ()
R03AC02 ()
Vospire Er ()
Buventol ()
Proair respiclick ()
Vospire ()
Sultanol ()
SCH-13949W Sulfate ()
Salbutamol (as sulfate) ()
Torpex ()
Venetlin ()
R03CC02 ()
SCH 13949W SULFATE ()
Salamol ()
Salbutamoli sulfas ()
Sch 13949w sulphate ()
Ecovent ()
Albuterol sulphate ()
Hexotonal ()
Ventilastin ()
NSC-289928 ()
Sulbutamol (as sulphate) ()
Loftan ()
Salbutamol sulphate ()
Proair digihaler ()
Ventolin Rotacaps ()
Salbutamol-d9 ()
P&D ID
PD001639
CAS
18559-94-9
51022-70-9
36519-31-0
35763-26-9
148563-15-9
1173021-73-2
Tags
available
biased GPCR ligand
drug
Approved by
FDA
First approval
1982
1981
Drug indication
Bronchodilator
Acute asthma
Drug Status
approved
vet_approved
Max Phase
4.0
Structure
Probe scores
P&D probe-likeness score
[[ v.score ]]%
Structure formats
[[ format ]]
[[ compound[format === 'MOL' ? 'molblock' : format.toLowerCase()] ]]
Description
(extracted from source data)
METABOLISM Salbutamol is not metabolized in the lung but is converted in the liver to the 4'-o-sulphate (salbutamol 4'-O-sulfate) ester, which has negligible pharmacologic activity [F3265, F3268]. It may also be metabolized by oxidative deamination and/or conjugation with glucuronide [F3265, F3268]. Salbutamol is ultimately excreted in the urine as free drug and as the metabolite [F3265, F3268].
INDICATION Salbutamol is indicated for (i) the symptomatic relief and prevention of bronchospasm due to bronchial asthma, chronic bronchitis, reversible obstructive airway disease, and other chronic bronchopulmonary disorders in which bronchospasm is a complicating factor, and/or (ii) the acute prophylaxis against exercise-induced bronchospasm and other stimuli known to induce bronchospasm [FDA Label, F3265, F3268].
MOA In vitro studies and in vivo pharmacologic studies have shown that salbutamol has a preferential effect on beta2-adrenergic receptors compared with isoproterenol [FDA Label, F3265, F3268]. Although beta2­ adrenoceptors are the predominant adrenergic receptors in bronchial smooth muscle and beta1 adrenoceptors are the predominant receptors in the heart, there are also beta2-adrenoceptors in the human heart comprising 10% to 50% of the total beta-adrenoceptors [FDA Label, F3265, F3268]. The precise function of these receptors has not been established, but their presence raises the possibility that even selective beta2-agonists may have cardiac effects [FDA Label, F3265, F3268]. Activation of beta2-adrenergic receptors on airway smooth muscle leads to the activation of adenyl cyclase and to an increase in the intracellular concentration of cyclic-3′,5′-adenosine monophosphate (cyclic AMP)[FDA Label, F3265, F3268]. This increase of cyclic AMP leads to the activation of protein kinase A, which inhibits the phosphorylation of myosin and lowers intracellular ionic calcium concentrations, resulting in relaxation [FDA Label, F3265, F3268]. Salbutamol relaxes the smooth muscles of all airways, from the trachea to the terminal bronchioles [FDA Label, F3265, F3268]. Salbutamol acts as a functional antagonist to relax the airway irrespective of the spasmogen involved, thus protecting against all bronchoconstrictor challenges [FDA Label, F3265, F3268]. Increased cyclic AMP concentrations are also associated with the inhibition of release of mediators from mast cells in the airway [FDA Label, F3265, F3268]. Salbutamol has been shown in most controlled clinical trials to have more effect on the respiratory tract, in the form of bronchial smooth muscle relaxation, than isoproterenol at comparable doses while producing fewer cardiovascular effects [FDA Label, F3265, F3268]. Controlled clinical studies and other clinical experience have shown that inhaled albuterol, like other beta-adrenergic agonist drugs, can produce a significant cardiovascular effect in some patients, as measured by pulse rate, blood pressure, symptoms, and/or electrocardiographic changes [FDA Label, F3265, F3268]. A measurable decrease in airway resistance is typically observed within 5 to 15 minutes after inhalation of salbutamol [FDA Label, F3265, F3268]. The maximum improvement in pulmonary function usually occurs 60 to 90 minutes after salbutamol treatment, and significant bronchodilator activity has been observed to persist for 3 to 6 hours [FDA Label, F3265, F3268].
ROE After oral administration, 58-78% of the dose is excreted in the urine in 24 hours, approximately 60% as metabolites [F3265, F3268]. A small fraction is excreted in the feces [F3265, F3268].
ABSORPTION Following inhalation, salbutamol acts topically on bronchial smooth muscle and the drug is initially undetectable in the blood [F3265]. After 2 to 3 hours low concentrations are seen, due presumably to the portion of the dose which is swallowed and absorbed in the gut [F3265]. In particular, the systemic levels of salbutamol are low after inhalation of recommended doses [FDA Label]. A trial conducted in 12 healthy male and female subjects using a higher dose (1,080 mcg of albuterol base) showed that mean peak plasma concentrations of approximately 3 ng/mL occurred after dosing when salbutamol was delivered using propellant HFA-134a [FDA Label]. The mean time to peak concentrations (Tmax) was delayed after administration of VENTOLIN (salbutamol) HFA (Tmax = 0.42 hours) as compared with CFC-propelled salbutamol inhaler (Tmax = 0.17 hours) [FDA Label].
HALF-LIFE The elimination half-life of inhaled or oral salbutamol has been recorded as being between 2.7 and 5 hours [F3265] while the apparent terminal plasma half-life of albuterol has been documented as being approximately 4.6 hours [FDA Label].
PHARMACODYNAMICS Salbutamol (INN) or albuterol (USAN), a moderately selective beta(2)-receptor agonist similar in structure to terbutaline, is widely used as a bronchodilator to manage asthma and other chronic obstructive airway diseases.[Label,F3265,F3268] The R-isomer, levalbuterol, is responsible for bronchodilation while the S-isomer increases bronchial reactivity.[A174400] The R-enantiomer is available and sold in its pure form as levalbuterol and subsequently may produce fewer side-effects with only the R-enantiomer present - although this has not been formally demonstrated.[A174400]; ; After oral and parenteral administration, stimulation of the beta receptors in the body, both beta-1 and beta-2, occurs because (a) beta-2 selectivity is not absolute, and (b) higher concentrations of salbutamol occur in the regions of these receptors with these modes of administration.[Label,F3265,F3268] This results in the beta-1 effect of cardiac stimulation, though not so much as with isoprenaline, and beta-2 effects of peripheral vasodilatation and hypotension, skeletal muscle tremor, and uterine muscle relaxation.[Label,F3265,F3268]; ; Metabolic effects such as hyperinsulinemia and hyperglycemia also may occur, although it is not known whether these effects are mediated by beta-1 or beta-2 receptors.[Label,F3265,F3268] The serum potassium levels have a tendency to fall.[F3265]
INDICATION Salbutamol is indicated for (i) the symptomatic relief and prevention of bronchospasm due to bronchial asthma, chronic bronchitis, reversible obstructive airway disease, and other chronic bronchopulmonary disorders in which bronchospasm is a complicating factor, and/or (ii) the acute prophylaxis against exercise-induced bronchospasm and other stimuli known to induce bronchospasm.[Label,F3265,F3268]
ROE After oral administration, 58-78% of the dose is excreted in the urine in 24 hours, approximately 60% as metabolites.[F3265,F3268] A small fraction is excreted in the feces.[F3265,F3268]
METABOLISM Salbutamol is not metabolized in the lung but is converted in the liver to the 4'-o-sulphate (salbutamol 4'-O-sulfate) ester, which has negligible pharmacologic activity.[F3265,F3268] It may also be metabolized by oxidative deamination and/or conjugation with glucuronide.[F3265,F3268] Salbutamol is ultimately excreted in the urine as free drug and as the metabolite.[F3265,F3268]
HALF-LIFE The elimination half-life of inhaled or oral salbutamol has been recorded as being between 2.7 and 5 hours while the apparent terminal plasma half-life of albuterol has been documented as being approximately 4.6 hours.[F3265,Label]
DESCRIPTION The approved drug salbutamol is a racemic mixture of two enantiomers: ((R)-salbutamol) and (S)-salbutamol. The structure shown here does not specify stereochemistry and represents the mixture. The US FDA approved this drug with the name albuterol.
Marketed formulations may contain salbutamol sulfate (PubChem CID 9884233).
Salbutamol is termed a 'short-acting beta-agonist' (SABA). (GtoPdb)
DESCRIPTION The approved drug salbutamol is a racemic mixture of two enantiomers: (R)-salbutamol and (S)-salbutamol. The structure shown here does not specify stereochemistry and represents the mixture. The US FDA approved this drug with the name albuterol.
Marketed formulations may contain salbutamol sulfate (PubChem CID 9884233).
Salbutamol is termed a 'short-acting beta-agonist' (SABA).
PHARMACODYNAMICS Salbutamol (INN) or albuterol (USAN), a moderately selective beta(2)-receptor agonist similar in structure to terbutaline, is widely used as a bronchodilator to manage asthma and other chronic obstructive airway diseases [FDA Label, F3265, F3268]. The R-isomer, levalbuterol, is responsible for bronchodilation while the S-isomer increases bronchial reactivity [A174400]. The R-enantiomer is available and sold in its pure form as levalbuterol and subsequently may produce fewer side-effects with only the R-enantiomer present - although this has not been formally demonstrated [A174400]. After oral and parenteral administration, stimulation of the beta receptors in the body, both beta-1 and beta-2, occurs because (a) beta-2 selectivity is not absolute, and (b) higher concentrations of salbutamol occur in the regions of these receptors with these modes of administration [FDA Label, F3265, F3268]. This results in the beta-1 effect of cardiac stimulation, though not so much as with isoprenaline, and beta-2 effects of peripheral vasodilatation and hypotension, skeletal muscle tremor, and uterine muscle relaxation [FDA Label, F3265, F3268]. Metabolic effects such as hyperinsulinemia and hyperglycemia also may occur, although it is not known whether these effects are mediated by beta-1 or beta-2 receptors [FDA Label, F3265, F3268]. The serum potassium levels have a tendency to fall [F3265].
MOA In vitro studies and in vivo pharmacologic studies have shown that salbutamol has a preferential effect on beta2-adrenergic receptors compared with isoproterenol.[Label,F3265,F3268] Although beta2­ adrenoceptors are the predominant adrenergic receptors in bronchial smooth muscle and beta1 adrenoceptors are the predominant receptors in the heart, there are also beta2-adrenoceptors in the human heart comprising 10% to 50% of the total beta-adrenoceptors.[Label,F3265,F3268] The precise function of these receptors has not been established, but their presence raises the possibility that even selective beta2-agonists may have cardiac effects.[Label,F3265,F3268]; ; Activation of beta2-adrenergic receptors on airway smooth muscle leads to the activation of adenyl cyclase and to an increase in the intracellular concentration of cyclic-3′,5′-adenosine monophosphate (cyclic AMP).[Label,F3265,F3268] This increase of cyclic AMP leads to the activation of protein kinase A, which inhibits the phosphorylation of myosin and lowers intracellular ionic calcium concentrations, resulting in relaxation.[Label,F3265,F3268] Salbutamol relaxes the smooth muscles of all airways, from the trachea to the terminal bronchioles.[Label,F3265,F3268] Salbutamol acts as a functional antagonist to relax the airway irrespective of the spasmogen involved, thus protecting against all bronchoconstrictor challenges.[Label,F3265,F3268] Increased cyclic AMP concentrations are also associated with the inhibition of release of mediators from mast cells in the airway.[Label,F3265,F3268]; ; Salbutamol has been shown in most controlled clinical trials to have more effect on the respiratory tract, in the form of bronchial smooth muscle relaxation, than isoproterenol at comparable doses while producing fewer cardiovascular effects.[Label,F3265,F3268] Controlled clinical studies and other clinical experience have shown that inhaled albuterol, like other beta-adrenergic agonist drugs, can produce a significant cardiovascular effect in some patients, as measured by pulse rate, blood pressure, symptoms, and/or electrocardiographic changes.[Label,F3265,F3268]; ; A measurable decrease in airway resistance is typically observed within 5 to 15 minutes after inhalation of salbutamol.[Label,F3265,F3268] The maximum improvement in pulmonary function usually occurs 60 to 90 minutes after salbutamol treatment, and significant bronchodilator activity has been observed to persist for 3 to 6 hours.[Label,F3265,F3268]
ABSORPTION Following inhalation, salbutamol acts topically on bronchial smooth muscle and the drug is initially undetectable in the blood.[F3265] After 2 to 3 hours low concentrations are seen, due presumably to the portion of the dose which is swallowed and absorbed in the gut.[F3265]; ; In particular, the systemic levels of salbutamol are low after inhalation of recommended doses.[Label] A trial conducted in 12 healthy male and female subjects using a higher dose (1,080 mcg of albuterol base) showed that mean peak plasma concentrations of approximately 3 ng/mL occurred after dosing when salbutamol was delivered using propellant HFA-134a.[Label] The mean time to peak concentrations (Tmax) was delayed after administration of VENTOLIN (salbutamol) HFA (Tmax = 0.42 hours) as compared with CFC-propelled salbutamol inhaler (Tmax = 0.17 hours).[Label]
DESCRIPTION beta Adrenoceptor agonist (LOPAC library)
DESCRIPTION beta2-Adrenoceptor agonist (LOPAC library)
DESCRIPTION 5-HT1B agonist (Tocris Bioactive Compound Library)
Cell lines
0
Organisms
1
Compound Sets
33
AdooQ Bioactive Compound Library
A10819
BiasDB
Salbutamol
Cayman Chemical Bioactives
21003
25234
ChEMBL Approved Drugs
CHEMBL714
CHEMBL1441059
ChEMBL Drugs
CHEMBL714
CHEMBL1441059
Concise Guide to Pharmacology 2017/18
558
Concise Guide to Pharmacology 2019/20
558
Concise Guide to Pharmacology 2021/22
558
Concise Guide to Pharmacology 2023/24
558
DrugBank
DB01001
DrugBank Approved Drugs
DB01001
DrugCentral
105
DrugCentral Approved Drugs
105
DrugMAP
DMN9CWF
DrugMAP Approved Drugs
DMN9CWF
DrugMatrix
Enamine BioReference Compounds
Guide to Pharmacology
558
Ki Database
Albuterol
Salbutamol,(+/-)
LOPAC library
LSP-MoA library (Laboratory of Systems Pharmacology)
CHEMBL714
Mcule NIBR MoA Box Subset
MCULE-4493408325
MedChem Express Bioactive Compound Library
HY-B1037
HY-B0436
NCATS Inxight Approved Drugs
QF8SVZ843E
NIH Clinical Collections (NCC)
Novartis Chemogenetic Library (NIBR MoA Box)
NPC Screening Collection
Prestwick Chemical Library
ReFrame library
Selleckchem Bioactive Compound Library
salbutamol
Salbutamol-sulfate(Albuterol)
TargetMol Bioactive Compound Library
T1139
T6652
The Spectrum Collection
Tocris Bioactive Compound Library
0634
External IDs
96
Properties
(calculated by RDKit )
Molecular Weight
239.15
Hydrogen Bond Acceptors
4
Hydrogen Bond Donors
4
Rotatable Bonds
4
Ring Count
1
Aromatic Ring Count
1
cLogP
1.31
TPSA
72.72
Fraction CSP3
0.54
Chiral centers
1.0
Largest ring
6.0
QED
0.64
Structural alerts
0
No structural alerts detected
Related compounds
Custom attributes
(extracted from source data)
Selectivity
beta2
Pathway
Neuroscience
GPCR/G protein
Autophagy
Neuronal Signaling
MAPK/ERK Pathway
Stem Cell/Wnt
Target
??2-adrenergic receptor
??-adrenergic receptor
??adrenergic receptor
Adrenergic Receptor
ERK
Primary Target
Adrenergic ?2 Receptors
MOA
Agonist
beta2-Adrenoceptor Agonists
Member status
member
Therapeutic Class
Bronchodilator Agents
Source data