Albuterol 6mg/ml, 60ML

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  • Product Code:AB60
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  • $44.00


Albuterol is a Beta-2 agonist also known internationally as salbutamol, similar to clenbuterol but shorter-acting.  Therapeutic uses of B2 agonists include treatment of bronchial asthma.  This class of drug has also been demonstrated to lower C-reactive proteins, an important inflammation marker, in individuals with chronic obstructive pulmonary disease.[1] Adrenergic receptors exist in many cells throughout the body and react with catecholamines such as norepinephrine/noradrenaline and adrenaline/epinephrine when a fight-or-flight response is induced.  When this occurs heart rate increases, pupils dilate, blood flow is diverted to skeletal muscle, and energy is mobilized.

Albuterol as a selective Beta-2 adrenercic agonist that is preferred for emergency situations due to its shorter active life and fast onset.   In such situations the preferred route of administration is via nebulized albuterol mixed with oxygen when symptoms such as wheezing or bronchiospasm, especially where asthma has been previously diagnosed.

Albuterol and other B2 agonists are of interest to bodybuilders, athletes, and those who work with obese patients in a clinical setting.  Because of the effect of B2 agonists on energy regulation, in certain environments anabolism to skeletal muscle as well as mobilization of fat stores have been demonstrated.  Despite the fact that B2 agonists have been shown to have no demonstrable use in performance enhancement[2], they are on the WADA ban list for athletes[3].

The effects of B2 adrenergic agonists on fat are more publicized than their potential anabolic effects on muscle tissue:

Although there is little evidence that the inhalation of therapeutic doses of β2-AR agonists enhances performance, the anabolic effects on muscle could potentially be observed if very high doses were inhaled, or if another route of administration was used. Anabolic effects have been studied particularly for clenbuterol, a long-acting β2-AR agonist that is licensed for the treatment of asthma in a limited number of countries (but not including the United Kingdom, the United States or Australia). It is of interest that clenbuterol was originally developed as a non-steroidal anabolic agent to improve the conversion rate (or efficiency of converting food into body mass) in animals. The anabolic effects of oral β2-AR agonists have been well documented in animals (Zeman et al., 1988; Moore et al., 1994; Ryall et al., 2006) and are associated with an increase in skeletal muscle protein, largely due to the inhibition of protein degradation (Reeds et al., 1986; Yang and McElligott, 1989; Maltin et al., 1993). In addition to the increase in muscle mass, β2-AR agonists also decrease body fat (Yang and McElligott, 1989), hence their classification as ‘repartitioning agents'. The increase in muscle mass is associated with an increase in muscle force production (Zeman et al., 1988; Dodd et al., 1996).[2]

Albuterol and similar drugs do still affect the metabolism of obese individuals, but to a lesser degree than lean individuals studied:

The aim of this study was to elucidate the roles of the beta(1)- and the beta(2)-adrenoceptors in thermogenesis and lipid utilization in obesity. The beta(1)-adrenoceptor study was performed in 9 obese and 10 lean men and consisted of 4 30-min periods during which subjects received consecutive infusions of 0, 3, 6, and 9 microg/kg fat-free mass (FFM).min dobutamine. Energy expenditure, lipid oxidation, and plasma nonesterified fatty acids and glycerol concentrations increased similarly in both groups during beta(1)-adrenergic stimulation. The beta(2)-adrenoceptor study was performed in 10 obese and 11 lean men and involved 3 45-min periods during which 0, 50, and 100 ng/kg FFM.min salbutamol were given in combination 1.2 microg/kg FFM.min atenolol (bolus, 50 microg/kg FFM). During beta(2)-adrenergic stimulation, the increases in energy expenditure and plasma nonesterified fatty acids and glycerol concentrations were reduced in the obese group. Furthermore, lipid oxidation significantly increased in the normal weight group, but remained similar in the overweight group. In conclusion, these data suggest that beta(1)-adrenoceptor-mediated metabolic processes are similar in both groups, but beta(2)-adrenoceptor-mediated increases in thermogenesis and lipid utilization are impaired in the obese.[4]

Albuterol increase fat loss primarily through mobilization of FFAs and increases energy expenditure even in the absence of circulating FFAs:


In humans, beta-adrenergic stimulation increases energy and fat metabolism. In the case of beta1-adrenergic stimulation, it is fueled by an increased lipolysis. We examined the effect of beta2-adrenergic stimulation, with and without a blocker of lipolysis, on thermogenesis and substrate oxidation. Furthermore, the effect of beta1-and beta2-adrenergic stimulation on uncoupling protein 3 (UCP3) mRNA expression was studied. Nine lean males received a 3-h infusion of dobutamine (DOB, beta1) or salbutamol (SAL, beta2). Also, we combined SAL with acipimox to block lipolysis (SAL+ACI). Energy and substrate metabolism were measured continuously, blood was sampled every 30 min, and muscle biopsies were taken before and after infusion. Energy expenditure significantly increased approximately 13% in all conditions. Fat oxidation increased 47 +/- 7% in the DOB group and 19 +/- 7% in the SAL group but remained unchanged in the SAL+ACI condition. Glucose oxidation decreased 40 +/- 9% upon DOB, remained unchanged during SAL, and increased 27 +/- 11% upon SAL+ACI. Plasma free fatty acid (FFA) levels were increased by SAL (57 +/- 11%) and DOB (47 +/- 16%), whereas SAL+ACI caused about fourfold lower FFA levels compared with basal levels. No change in UCP3 was found after DOB or SAL, whereas SAL+ACI downregulated skeletal muscle UCP3 mRNA levels 38 +/- 13%. In conclusion, beta2-adrenergic stimulation directly increased energy expenditure independently of plasma FFA levels. Furthermore, this is the first study to demonstrate a downregulation of skeletal muscle UCP3 mRNA expression after the lowering of plasma FFA concentrations in humans, despite an increase in energy expenditure upon beta2-adrenergic stimulation.[5]



[1] Tang YJ, Wang K, Yuan T, Qiu T, Xiao J, Yi Q, Feng YL. Salmeterol/fluticasone treatment reduces circulating C-reactive protein level in patients with stable chronic obstructive pulmonary disease. Chin Med J (Engl). 2010 Jul;123(13):1652-7.

[2] Br J Pharmacol. 2008 June; 154(3): 584–597. E Davis, R Loiacono,and R J Summers. The rush to adrenaline: drugs in sport acting on the β-adrenergic system.

[3]WADA List of Prohibited Substances.  Available online:

[4]Schiffelers SL, Saris WH, Boomsma F, van Baak MA. beta(1)- and beta(2)-Adrenoceptor-mediated thermogenesis and lipid utilization in obese and lean men. J Clin Endocrinol Metab. 2001 May;86(5):2191-9.

[5] Hoeks J, van Baak MA, Hesselink MK, Hul GB, Vidal H, Saris WH, Schrauwen P. Effect of beta1- and beta2-adrenergic stimulation on energy expenditure, substrate oxidation, and UCP3 expression in humans. Am J Physiol Endocrinol Metab. 2003 Oct;285(4):E775-82.


*The latter article is intended for educational / informational purposes only. THIS PRODUCT IS INTENDED AS A RESEARCH CHEMICAL ONLY. This designation allows the use of research chemicals strictly for in vitro testing and laboratory experimentation only. Bodily introduction of any kind into humans or animals is strictly forbidden by law.

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