Clenbuterol (NAB-365) is a β2-adrenergic agonist that is selective (β2/β1 ratio = 4.0). TNF-α and IL-1β released in response to lipopolysaccharide (LPS) are strongly inhibited by clenbuterol. The inflammatory process can be inhibited by clenbuterol[2]. For a duration of 24 or 48 hours, clenbuterol (10-200 µM) reduces the viability of C2C12 myoblasts. At 100 µM, clenbuterol dramatically reduces DNA synthesis. The percentage of cells in the G0/G1 phase rises when exposed to 100 µM clenbuterol for 12 hours. Cell cycle progression is delayed by clenbuterol therapy. In C2C12 myoblasts, clenbuterol (100 µM) causes cell cycle arrest but not apoptosis[3].

In young male Mecp2-null (Mecp2−/y) mice, treatment with clenbuterol improves motor coordination, recovers deficits in respiratory function and social recognition, and enhances survival[4]. One bronchodilator is clenbuterol. Five horses receive intratracheal clenbuterol (90 µg). Serum concentrations peak at around 230 pg/mL 10 minutes after treatment, then fall to about 50 pg/mL in 30 minutes, and then decline considerably more slowly after that. This serum test can be used to identify clenbuterol administered intratracheally just prior to the start of the race[5].

Cell Viability Assay[3]
Cell Types: C2C12 cells.
Tested Concentrations: 0, 10, 100, and 200 µM.
Incubation Duration: 24 and 48 hrs (hours).
Experimental Results: Treatment decreased viability of C2C12 cells for 24 and 48 h.

Animal/Disease Models: Male Mecp2−/y and female Mecp2−/+ mice[4]
Doses: 5 or 0.1 mg/kg.
Route of Administration: Injected ip; daily for 5 d, followed by a 2-d off period , repeated weekly
Experimental Results: Dramatically improved the phenotype during the second but not first day of testing, implying a modest effect on motor coordination in Mecp2-null mice.

Absorption, Distribution and Excretion
89-98% orally

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Biological Half-Life
36-39 hours

[1]. Gilad Barnea, et al. The genetic design of signaling cascades to record receptor activation. Proc Natl Acad Sci U S A. 2008 Jan 8;105(1):64-9.
[2]. Olga Witkowska-Piłaszewicz, et al. The Effect of the Clenbuterol-β2-Adrenergic Receptor Agonist on the Peripheral Blood Mononuclear Cells Proliferation, Phenotype, Functions, and Reactive Oxygen Species Production in Race Horses In Vitro. Cells. 2021 Apr
[3]. Min Chen, et al. Clenbuterol Induces Cell Cycle Arrest in C2C12 Myoblasts by Delaying p27 Degradation through β-arrestin 2 Signaling. Int J Biol Sci. 2017 Oct 17;13(10):1341-1350.
[4]. Nikolaos Mellios, et al. β2-Adrenergic receptor agonist ameliorates phenotypes and corrects microRNA-mediated IGF1 deficits in a mouse model of Rett syndrome. Proc Natl Acad Sci U S A. 2014 Jul 8;111(27):9947-52.
[5]. A F Lehner, et al. Clenbuterol in the horse: confirmation and quantitation of serum clenbuterol by LC-MS-MS after oral and intratracheal administration. J Anal Toxicol. May-Jun 2001;25(4):280-7.

Clenbuterol is a substituted aniline that is 2,6-dichloroaniline in which the hydrogen at position 4 has been replaced by a 2-(tert-butylamino)-1-hydroxyethyl group. It has a role as a bronchodilator agent, a beta-adrenergic agonist and a sympathomimetic agent. It is a member of ethanolamines, a primary arylamine, a secondary amino compound, an amino alcohol, a substituted aniline and a dichlorobenzene. It is a conjugate base of a clenbuterol(1+).
A substituted phenylaminoethanol that has beta-2 adrenomimetic properties at very low doses. It is used as a bronchodilator in asthma.
Clenbuterol is a substituted phenylaminoethanol and a long-acting beta-2 adrenergic agonist with sympathomimetic activity. Clenbuterol selectively binds to and activates beta-2 adrenergic receptors in bronchiolar smooth muscle, thereby causing stimulation of adenyl cyclase, the enzyme that catalyzes the conversion of adenosine triphosphate (ATP) to cyclic-3',5'-adenosine monophosphate (cAMP). Increased intracellular cAMP levels cause relaxation of smooth muscle. In addition, clenbuterol also stimulates central nervous system (CNS), and causes an increase in blood pressure and heart rate due to both beta-2 and beta-1 adrenergic activities. This agent may also exert an anabolic or anti-catabolic effect due to as of yet unidentified mechanisms.
A substituted phenylaminoethanol that has beta-2 adrenomimetic properties at very low doses. It is used as a bronchodilator in asthma.
See also: Clenbuterol Hydrochloride (has salt form); (S)-Clenbuterol (annotation moved to).

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Drug Indication
Used as a bronchodilator in the treatment of asthma patients.

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Mechanism of Action
Clenbuterol is a Beta(2) agonist similar in some structural respects to salbutamol. Agonism of the beta(2) receptor stimulates adenylyl cyclase activity which ultimately leads to downstream effects of smooth muscle relaxation in the bronchioles.

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Pharmacodynamics
Clenbuterol is a substituted phenylaminoethanol that has beta-2 adrenomimetic properties at very low doses. It is used as a bronchodilator in asthma. Although approved for use in some countries, as of fall, 2006, clenbuterol is not an ingredient of any therapeutic drug approved by the U.S. Food and Drug Administration.

C12H18CL2N2O

277.189

276.079

37148-27-9

Clenbuterol hydrochloride;21898-19-1

2783

Typically exists as solid at room temperature

1.3±0.1 g/cm3

404.9±40.0 °C at 760 mmHg

174-175.5

198.7±27.3 °C

0.0±1.0 mmHg at 25°C

1.577

2.61

3

3

4

17

233

0

CC(C)(C)NCC(C1=CC(=C(C(=C1)Cl)N)Cl)O

STJMRWALKKWQGH-UHFFFAOYSA-N

InChI=1S/C12H18Cl2N2O/c1-12(2,3)16-6-10(17)7-4-8(13)11(15)9(14)5-7/h4-5,10,16-17H,6,15H2,1-3H3

1-(4-amino-3,5-dichlorophenyl)-2-(tert-butylamino)ethanol

Clenbuterol PlanipartNAB 365 P 5369

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)