Clenbuterol
Drug Residues
Receptors, Adrenergic, beta-2
A subclass of beta-adrenergic receptors (RECEPTORS, ADRENERGIC, BETA). The adrenergic beta-2 receptors are more sensitive to EPINEPHRINE than to NOREPINEPHRINE and have a high affinity for the agonist TERBUTALINE. They are widespread, with clinically important roles in SKELETAL MUSCLE; LIVER; and vascular, bronchial, gastrointestinal, and genitourinary SMOOTH MUSCLE.
beta2-adrenergic receptor-selective agonist clenbuterol prevents Fas-induced liver apoptosis and death in mice. (1/192)
Stimulation of the cAMP-signaling pathway modulates apoptosis in several cell types and inhibits Jo2-mediated apoptosis in cultured rat hepatocytes. No information is yet available as to whether the hepatic beta2-adrenergic receptor (AR) expression level, including beta2-AR-dependent adenylyl cyclase activation, modulates hepatocyte sensitivity to apoptosis in vivo or whether this sensitivity can be modified by beta2-AR ligands. We have examined this using C57BL/6 mice, in which hepatic beta2-AR densities are low, and transgenic F28 mice, which overexpress beta2-ARs and have elevated basal liver adenylyl cyclase activity. The F28 mice were resistant to Jo2-induced liver apoptosis and death. The beta-AR antagonist propranolol sensitized the F28 livers to Jo2. In normal mice clenbuterol, a beta2-AR-specific agonist, considerably reduced Jo2-induced liver apoptosis and death; salbutamol, another beta2-AR-selective agonist, also reduced Jo2-induced apoptosis and retarded death but with less efficacy than clenbuterol; and propranolol blocked the protective effect of clenbuterol. This indicates that the expression level of functional beta2-ARs modulates Fas-regulated liver apoptosis and that this apoptosis can be inhibited in vivo by giving beta2-AR agonists. This may well form the basis for a new therapeutic approach to diseases involving abnormal apoptosis. (+info)Study of interaction between agonists and asn293 in helix VI of human beta(2)-adrenergic receptor. (2/192)
Previously, we demonstrated the involvement of Asn293 in helix VI of the human beta(2)-adrenergic receptor in stereoselective agonist recognition and activation. In the present study, we have further explored the role of this residue by synthesizing derivatives of isoproterenol and clenbuterol, two beta-adrenergic receptor agonists. We analyzed their efficacy and affinity on the wild-type and a mutant receptor (Asn293Leu). Each compound had similar efficacy (tau values) on both the wild-type and mutant receptor, although tau values varied considerably among the eight compounds studied. It appeared that one derivative of isoproterenol, but not of clenbuterol, showed a gain in affinity from the wild type to the mutant receptor. This derivative had a methyl substituent instead of the usual beta-OH group in the aliphatic side chain of isoproterenol, compatible with the more lipophilic nature of the leucine side chain. Such a "gain of function" approach through a combination of synthetic chemistry with molecular biology, may be useful to enhance our insight into the precise atomic events that govern ligand-receptor interactions. (+info)Rapid extraction of clenbuterol from human and calf urine using empore C8 extraction disks. (3/192)
In the present paper, disk extraction was evaluated for the rapid isolation of clenbuterol from human and calf urine, followed by high-performance liquid chromatography analysis with UV detection. A method was developed for the extraction with standard density C8 disks. The disks could be washed with 25% methanol in 0.01M sodium hydroxide without significant losses of clenbuterol. The recovery of denbuterol was about 85%, and the extracts were clean. The detection limit was about 10 ng/mL. The main advantages of these disks were the saving of time and the reduced amounts of organic solvents needed. (+info)Deleterious effects of chronic clenbuterol treatment on endurance and sprint exercise performance in rats. (4/192)
The beta(2)-adrenergic agonist, clenbuterol, has powerful muscle anabolic and lipolytic effects and is used by athletes to improve exercise performance; however, its use in conjunction with different forms of exercise training has received limited attention. Since previous studies have reported that chronic use of other beta(2)-adrenergic agonists has deleterious effects on cardiac muscle structure and function, the aim of the present study was to determine whether chronic clenbuterol administration would reduce the exercise capabilities of rats subjected to long-term treadmill sprint running, endurance swimming or voluntary wheel running training. The effect of clenbuterol treatment on exercise performance in rats was evaluated in three separate studies. Different groups of male rats were assigned to an endurance swimming (2 h/day, 5/7 days, 18 weeks) group, a treadmill sprint running (8x1 min bouts, 1.05 m/s, 20 weeks) group, or a voluntary wheel running (16 weeks) group. In each study, rats were allocated into either a treated group that received clenbuterol (2 mg.kg(-1).day(-1)) in their drinking water or an untreated control group. In each of the three studies, treated rats exhibited a reduction in exercise performance compared with untreated rats. Treated rats ran approximately 57% less total distance than untreated rats in the voluntary running programme and were unable to complete the swimming and sprinting protocols performed by the untreated rats. In each of the studies, the treated rats exhibited cardiac hypertrophy, with absolute heart mass increased by approximately 19% and heart mass relative to body mass increased by approximately 20%. The hearts of sedentary rats treated with clenbuterol exhibited extensive collagen infiltration surrounding blood vessels and in the wall of the left ventricle. The results indicate strongly that chronic clenbuterol administration deleteriously affects exercise performance in rats, potentially due to alterations in cardiac muscle structure and function. (+info)Effects of beta(2)-agonist clenbuterol on biochemical and contractile properties of unloaded soleus fibers of rat. (5/192)
The effects of clenbuterol beta(2)-agonist administration were investigated in normal and atrophied [15-day hindlimb-unloaded (HU)] rat soleus muscles. We showed that clenbuterol had a specific effect on muscle tissue, since it reduces soleus atrophy induced by HU. The study of Ca(2+) activation properties of single skinned fibers revealed that clenbuterol partly prevented the decrease in maximal tension after HU, with a preferential effect on fast-twitch fibers. Clenbuterol improved the Ca(2+) sensitivity in slow- and fast-twitch fibers by shifting the tension-pCa relationship toward lower Ca(2+) concentrations, but this effect was more marked after HU than in normal conditions. Whole muscle electrophoresis indicated slow-to-fast transitions of the myosin heavy chain isoforms for unloaded and for clenbuterol-treated soleus. The coupling of the two latter conditions did not, however, increase these phenotypical transformations. Our findings indicated that clenbuterol had an anabolic action and a beta(2)-adrenergic effect on muscle fibers and appeared to counteract some effects of unloading disuse conditions. (+info)Differential effects of dexamethasone and clenbuterol on rat growth and on beta2-adrenoceptors in lung and skeletal muscle. (6/192)
Beta-adrenergic agonists increase growth rate, but their efficacy is reduced over time as the number of beta2-adrenoceptors in muscle decreases. Dexamethasone increases beta2-adrenoceptor density in many tissues, but this effect has not been reported in skeletal muscle. In this study, male rats were treated daily for 10 d with either clenbuterol (4 mg/kg of feed), dexamethasone (.2 mg/kg BW, s.c.), or clenbuterol plus dexamethasone. Untreated rats served as controls. Dexamethasone caused a marked suppression of growth rate, which resulted in decreased (P < .001) body weight (-29%), carcass weight (-30%), hind-limb muscles (-22%), omental fat (-22%), and heart weight (-10%). Feed intake was reduced (-26%), but feed conversion efficiency was also impaired (P < .001). Clenbuterol caused a small increase in growth rate (+6%; P < .05), with an increase in leg muscle (+7%; P < .01) and heart mass (+8%; P < .05). Feed efficiency was improved (P < .001) by clenbuterol. Rats given the combined treatment still showed a reduction in growth rate (-81%). Clenbuterol caused only a mild attenuation of the effects of dexamethasone on feed intake, BW, and carcass weight, but reduced the catabolic effect of dexamethasone on hind-limb muscle to only -8%. Clenbuterol caused a slight increase in the affinity beta2-adrenoceptors in lung for binding to the radioligand (-)[125I]iodocyanopindolol. Relative to control values, the density of beta2-adrenoceptors in lung was +31% with dexamethasone treatment, -45% with clenbuterol, and -23% with the combined treatment. Clenbuterol also decreased beta2-adrenoceptors in skeletal muscle (-35%), but so did dexamethasone (-13%), so the effects of the beta-adrenergic agonist were not attenuated through use of the combined treatment (-40%). The results show that the inductive effect of glucocorticoids on beta2-adrenoceptors is tissue-specific and that glucocorticoid treatment is not a useful adjunct to beta-adrenergic agonist treatment in animal production. (+info)Power output of fast and slow skeletal muscles of mdx (dystrophic) and control mice after clenbuterol treatment. (7/192)
The mdx mouse is the most commonly used animal model for Duchenne muscular dystrophy. We tested the null hypothesis that 20 weeks of clenbuterol treatment ( approximately 2 mg kg-1 day-1) of mdx and control mice would have no effect on the absolute and specific force (Po, kN m-2) and absolute and normalised power output (W kg-1) of extensor digitorum longus (EDL) and soleus muscles. For mdx and control mice, clenbuterol treatment produced modest increases in the mass of the two muscles but did not increase absolute or specific force or normalised power output. For absolute power output, only the EDL muscles of mdx mice showed a difference following treatment, with the power output of treated mice being 118 % that of the untreated mice. The modest effects of clenbuterol treatment on the dynamic properties of skeletal muscle provide little support for any improvement in muscle function for the dystrophic condition. (+info)Function and distribution of beta3-adrenoceptors in rat, rabbit and human urinary bladder and external urethral sphincter. (8/192)
1. Activation of beta-adrenoceptors causes relaxation of the urinary bladder and contraction of the external urethral sphincter, which consists of fast-contracting skeletal muscles. A beta2-adrenoceptor agonist, clenbuterol, recently has been developed as a therapeutic drug for the treatment of urinary incontinence, however beta2-adrenoceptor agonists have undesirable effects on cardiac and striated muscle function. 2. In this study, we compared the effects of the beta2-adrenoceptor agonist, clenbuterol and of a novel beta3-adrenoceptor agonist, GS332, on urinary bladder and external urethral sphincter function in rat, rabbit and human. We also determined the distribution of beta3-adrenoceptors in human urinary bladder and external urethral sphincter, using radioligand-binding techniques. 3. Clenbuterol induced marked relaxations in rat, rabbit and human urinary bladder smooth muscles and also induced marked contractions in rat periurethral striated muscles (external urethral sphincter), while GS332 induced marked relaxations in rat and human, but not in rabbit, urinary bladder smooth muscles and induced small contractions in rat periurethral striated muscles. 4. The radioligand binding studies showed presence of beta2- and beta3-adrenoceptors in human urinary bladder, external urethral sphincter and abdominal rectus muscles. The affinities of GS332 were the highest in urinary bladder and the lowest in the skeletal (abdominal rectus) muscles, while the affinities of clenbuterol were similar in urinary bladder, external urethral sphincter and the skeletal (abdominal rectus) muscles. 5. These results suggest that GS332 could, similarly clenbuterol, have a role in the treatment of urinary frequency and urinary incontinence. (+info)Clenbuterol is a sympathomimetic amine, often used as a bronchodilator in some countries to treat asthma, but it's also infamous for its off-label use as a performance-enhancing drug due to its ability to stimulate beta-2 adrenergic receptors, leading to increased metabolic rate and fat loss.
Clenbuterol is a sympathomimetic amine, which is a type of medication that stimulates the sympathetic nervous system. It is primarily used as a bronchodilator to treat asthma and other respiratory disorders because it helps to relax the muscles in the airways and increase airflow to the lungs.
Clenbuterol works by binding to beta-2 receptors in the body, which triggers a series of reactions that lead to bronchodilation. However, it also has anabolic effects, which means that it can promote muscle growth and fat loss. This has led to its abuse as a performance-enhancing drug among athletes and bodybuilders.
It's important to note that Clenbuterol is not approved for use in humans in many countries, including the United States, due to concerns about its potential side effects and lack of proven benefits for athletic performance. It is also banned by most major sports organizations. The use of Clenbuterol for non-medical purposes can be dangerous and may lead to serious health complications, such as heart problems, muscle tremors, and anxiety.
"Drug residues refer to the remaining amounts of a veterinary drug or its metabolites that can be found in edible animal tissues, after the drug has been administered and the animal has gone through a withdrawal period."
Drug residues refer to the remaining amount of a medication or drug that remains in an animal or its products after the treatment period has ended. This can occur when drugs are not properly metabolized and eliminated by the animal's body, or when withdrawal times (the recommended length of time to wait before consuming or selling the animal or its products) are not followed.
Drug residues in animals can pose a risk to human health if consumed through the consumption of animal products such as meat, milk, or eggs. For this reason, regulatory bodies set maximum residue limits (MRLs) for drug residues in animal products to ensure that they do not exceed safe levels for human consumption.
It is important for farmers and veterinarians to follow label instructions and recommended withdrawal times to prevent the accumulation of drug residues in animals and their products, and to protect public health.
Adrenergic beta-Agonists are medications that stimulate beta-adrenergic receptors, leading to increased intracellular cyclic AMP levels and activation of various physiological responses such as bronchodilation, cardiac stimulation, and vasodilation.
Adrenergic beta-agonists are a class of medications that bind to and activate beta-adrenergic receptors, which are found in various tissues throughout the body. These receptors are part of the sympathetic nervous system and mediate the effects of the neurotransmitter norepinephrine (also called noradrenaline) and the hormone epinephrine (also called adrenaline).
When beta-agonists bind to these receptors, they stimulate a range of physiological responses, including relaxation of smooth muscle in the airways, increased heart rate and contractility, and increased metabolic rate. As a result, adrenergic beta-agonists are often used to treat conditions such as asthma, chronic obstructive pulmonary disease (COPD), and bronchitis, as they can help to dilate the airways and improve breathing.
There are several different types of beta-agonists, including short-acting and long-acting formulations. Short-acting beta-agonists (SABAs) are typically used for quick relief of symptoms, while long-acting beta-agonists (LABAs) are used for more sustained symptom control. Examples of adrenergic beta-agonists include albuterol (also known as salbutamol), terbutaline, formoterol, and salmeterol.
It's worth noting that while adrenergic beta-agonists can be very effective in treating respiratory conditions, they can also have side effects, particularly if used in high doses or for prolonged periods of time. These may include tremors, anxiety, palpitations, and increased blood pressure. As with any medication, it's important to use adrenergic beta-agonists only as directed by a healthcare professional.
Adrenergic beta-2 receptor agonists are medications that bind to and stimulate beta-2 adrenergic receptors, leading to relaxation of smooth muscle in the bronchioles, uterus, and blood vessels, and increased heart rate and force of contraction. They are primarily used to treat respiratory conditions such as asthma and COPD, and are also used in the treatment of preterm labor.
Adrenergic beta-2 receptor agonists are a class of medications that bind to and stimulate beta-2 adrenergic receptors, which are found in various tissues throughout the body, including the lungs, blood vessels, and skeletal muscles. These receptors are part of the sympathetic nervous system and play a role in regulating various physiological processes such as heart rate, blood pressure, and airway diameter.
When beta-2 receptor agonists bind to these receptors, they cause bronchodilation (opening of the airways), relaxation of smooth muscle, and increased heart rate and force of contraction. These effects make them useful in the treatment of conditions such as asthma, chronic obstructive pulmonary disease (COPD), and premature labor.
Examples of adrenergic beta-2 receptor agonists include albuterol, terbutaline, salmeterol, and formoterol. These medications can be administered by inhalation, oral administration, or injection, depending on the specific drug and the condition being treated.
It's important to note that while adrenergic beta-2 receptor agonists are generally safe and effective when used as directed, they can have side effects such as tremors, anxiety, palpitations, and headaches. In addition, long-term use of some beta-2 agonists has been associated with increased risk of severe asthma exacerbations and even death in some cases. Therefore, it's important to use these medications only as directed by a healthcare provider and to report any concerning symptoms promptly.
Beta-2 adrenergic receptors are G protein-coupled receptors that mediate the response to catecholamines, such as epinephrine and norepinephrine, and when activated, they stimulate adenylyl cyclase leading to increased levels of intracellular cyclic AMP, which in turn triggers various physiological responses, including smooth muscle relaxation, bronchodilation, and increased heart rate.
Adrenergic receptors are a type of G protein-coupled receptor that bind and respond to catecholamines, such as epinephrine (adrenaline) and norepinephrine (noradrenaline). Beta-2 adrenergic receptors (β2-ARs) are a subtype of adrenergic receptors that are widely distributed throughout the body, particularly in the lungs, heart, blood vessels, gastrointestinal tract, and skeletal muscle.
When β2-ARs are activated by catecholamines, they trigger a range of physiological responses, including relaxation of smooth muscle, increased heart rate and contractility, bronchodilation, and inhibition of insulin secretion. These effects are mediated through the activation of intracellular signaling pathways involving G proteins and second messengers such as cyclic AMP (cAMP).
β2-ARs have been a major focus of drug development for various medical conditions, including asthma, chronic obstructive pulmonary disease (COPD), heart failure, hypertension, and anxiety disorders. Agonists of β2-ARs, such as albuterol and salmeterol, are commonly used to treat asthma and COPD by relaxing bronchial smooth muscle and reducing airway obstruction. Antagonists of β2-ARs, such as propranolol, are used to treat hypertension, angina, and heart failure by blocking the effects of catecholamines on the heart and blood vessels.
Ethanolamines are organic compounds that contain an amino group and an alcohol group, including common biologically occurring ones like neurtransmitter acetylcholine and hormone epinephrine (adrenaline), as well as widely used industrial chemicals.
Ethanolamines are a class of organic compounds that contain an amino group (-NH2) and a hydroxyl group (-OH) attached to a carbon atom. They are derivatives of ammonia (NH3) in which one or two hydrogen atoms have been replaced by a ethanol group (-CH2CH2OH).
The most common ethanolamines are:
* Monethanolamine (MEA), also called 2-aminoethanol, with the formula HOCH2CH2NH2.
* Diethanolamine (DEA), also called 2,2'-iminobisethanol, with the formula HOCH2CH2NHCH2CH2OH.
* Triethanolamine (TEA), also called 2,2',2''-nitrilotrisethanol, with the formula N(CH2CH2OH)3.
Ethanolamines are used in a wide range of industrial and consumer products, including as solvents, emulsifiers, detergents, pharmaceuticals, and personal care products. They also have applications as intermediates in the synthesis of other chemicals. In the body, ethanolamines play important roles in various biological processes, such as neurotransmission and cell signaling.
Fenoterol is a selective beta-2 adrenergic agonist used as a bronchodilator in the management of reversible airways obstruction, such as asthma and chronic obstructive pulmonary disease (COPD), to relieve symptoms like wheezing, shortness of breath, and coughing.
Fenoterol is a short-acting β2-adrenergic receptor agonist, which is a type of medication used to treat respiratory conditions such as asthma and chronic obstructive pulmonary disease (COPD). It works by relaxing the muscles in the airways and increasing the flow of air into the lungs, making it easier to breathe.
Fenoterol is available in various forms, including inhalation solution, nebulizer solution, and dry powder inhaler. It is usually used as a rescue medication to relieve sudden symptoms or during an asthma attack. Like other short-acting β2-agonists, fenoterol has a rapid onset of action but its effects may wear off quickly, typically within 4-6 hours.
It is important to note that the use of fenoterol has been associated with an increased risk of severe asthma exacerbations and cardiovascular events, such as irregular heartbeat and high blood pressure. Therefore, it should be used with caution and only under the supervision of a healthcare professional.
Clenbuterol
... has also been used as a performance-enhancing drug. One issue is that clenbuterol is a food contaminant in some ... Clenbuterol is approved for use in some countries as a bronchodilator for asthma.[medical citation needed] Clenbuterol is a β2 ... or using clenbuterol. The situation has dramatically improved in China since September 2011, when a ban of clenbuterol was ... Clenbuterol is a growth-promoting drug in the β agonist class of compounds. It is not licensed for use in China, the United ...
NCAA banned substances
"Clenbuterol Alternative: 3 Legal Alternatives That Give Clen Like Results". CLENBUTEROL. 2018-09-09. Retrieved 2019-03-09. " ... Examples of anabolic agents are boldenone, clenbuterol, dehydrocholormethyl-testosterone (DHEA), nandrolone, stanozolol, ...
Beta-2 adrenergic receptor
April 2008). "Clenbuterol increases lean muscle mass but not endurance in patients with chronic heart failure". The Journal of ... "Clenbuterol" (PDF). Drug and Chemical Evaluation Section. Drug Enforcement Agency. Retrieved 15 November 2021. "Food and Drugs ... Choo JJ, Horan MA, Little RA, Rothwell NJ (July 1992). "Anabolic effects of clenbuterol on skeletal muscle are mediated by beta ... The comprehensive anabolic, lipolytic, and ergogenic effects of long-acting β2 agonists such as clenbuterol render them ...
Sudarshan K. Aggarwal
"Online shop to buy clenbuterol". 2014. "DC Aggarwal". The British Journal of Radiology. 41 (485): 322. 2014. doi:10.1259/0007- ...
History of the Giro d'Italia
Contador raced the 2011 Giro despite having an ongoing trial about his possible use of clenbuterol, a banned substance. On 6 ... "Alberto Contador tests positive for clenbuterol". Cycling News. 30 September 2010. Archived from the original on 14 July 2011. ...
2010 Tour de France
"Alberto Contador Suspended Over Traces of Clenbuterol From Tour de France Test". Cyclingnews.com. Archived from the original on ... "Alberto Contador Tests Positive For Clenbuterol". Cyclingnews.com. 29 September 2010. Archived from the original on 2 October ... had contained traces of clenbuterol. He has stated, due to the number of other tests he passed and that only a tiny amount of ...
2011 Tour de France
"Alberto Contador tests positive for clenbuterol". Cyclingnews.com. 29 September 2010. Archived from the original on 12 November ... Contador announced that he had tested positive for the banned clenbuterol from a sample taken during his now-disqualified 2010 ... CAS removed Alberto Contador's results due to his positive test for clenbuterol at the 2010 Tour. The UCI subsequently revised ... the Court of Arbitration for Sport removed Alberto Contador's results from the 2011 Tour for testing positive for clenbuterol ...
Ion suppression in liquid chromatography-mass spectrometry
I. Determination of clenbuterol in urine". J Chromatogr A. 863 (1): 115-122. doi:10.1016/S0021-9673(99)00959-0. PMID 10591469. ... Determination of clenbuterol in urine using multiple-stage mass spectrometry in an ion-trap mass spectrometer". Rapid ...
Astana Qazaqstan Team
In September 2010, Alberto Contador returned a positive doping test for Clenbuterol at the 2010 Tour de France. After a two- ... "Alberto Contador tests positive for clenbuterol". Cyclingnews.com. 29 September 2010. Barry Ryan (9 December 2014). "Astana ...
Alberto Contador
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2010 Astana season
"Alberto Contador Suspended Over Traces Of Clenbuterol From Tour De France Test". Cyclingnews.com. Archived from the original on ... "Alberto Contador Tests Positive For Clenbuterol". Cyclingnews.com. Archived from the original on 2 October 2010. Retrieved 2010 ... had contained traces of clenbuterol. He has stated, due to the number of other tests he passed and that only a tiny amount of ...
Dan Duchaine
While in prison, he says he learned to make money through "legitimate avenues". In 1988, Duchaine introduced Clenbuterol to ...
Jack Bauer (cyclist)
ahood (23 April 2014). "No ban for Rogers in clenbuterol case". VeloNews.com. Retrieved 10 August 2022. VeloNews.com (5 ... he was upgrade to first place after Michael Rogers was disqualified for failing a drug test for clenbuterol. In the 2014 Jayco ...
Michael Rogers (cyclist)
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2011 Saxo Bank-SunGard season
While riding for Astana in the 2010 Tour de France, Contador tested positive for clenbuterol, a bronchodilator and stimulant ... Greg Johnson (2010-09-30). "Alberto Contador suspended over traces of clenbuterol from Tour de France test". Cycling News. ... Cycling News (2011-01-26). "Contador to receive one-year ban for Clenbuterol positive". Cycling News. Future Publishing Limited ... Charles Pelkey (2010-09-29). "Contador tests positive for low levels of clenbuterol". VeloNews. Competitor Group, Inc. Archived ...
2011 Pan American Games
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Bradley Wiggins
Wynn, Nigel (6 February 2012). "Contador banned for two years after clenbuterol positive". Cycling Weekly. Retrieved 29 March ...
Tour de France
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List of wins by TIAA CREF and its successors
"Press Release: Michael Rogers - Clenbuterol Adverse Analytical Finding". Union Cycliste Internationale. 2014-04-23. Archived ...
Zhou Mi (badminton)
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Compounding
"Update on Illegal Compounding of Clenbuterol Veterinary Drug Products". Food and Drug Administration. January 10, 2002. ...
List of Major League Baseball players suspended for performance-enhancing drugs
Raul Mondesi Jr of Royals tests positive for Clenbuterol; suspended 50 games. Reduced from 80G when proved substance was in ...
Adrenergic agonist
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Canelo Álvarez vs. Gennady Golovkin II
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Canelo Álvarez vs. Gennady Golovkin
"Canelo Tests Positive For Clenbuterol Ahead of Golovkin Fight". BoxingScene.com. Retrieved March 6, 2018. Jay, Phil. "EXCLUSIVE ... Álvarez tested positive in two random urine tests for the banned substance clenbuterol. The NAC opened an investigation, and ...
Adalberto Mondesí
Mondesi began the 2016 season in Double-A. On May 10, Mondesi was suspended 50 games after testing positive for clenbuterol ... Raul Mondesi Jr of Royals tests positive for Clenbuterol; suspended 50 games. Reduced from 80G when proved substance was in ...
Adrenergic receptor
2008). "Clenbuterol increases lean muscle mass but not endurance in patients with chronic heart failure". The Journal of Heart ... Kline WO, Panaro FJ, Yang H, Bodine SC (2007). "Rapamycin inhibits the growth and muscle-sparing effects of clenbuterol". ...
Andy Schleck
"CAS Sanction Contador With Two Year Ban In Clenbuterol Case". Cyclingnews.com. February 6, 2012. Retrieved February 23, 2012. ... Greg Johnson (September 30, 2010). "Alberto Contador Suspended Over Traces of Clenbuterol From Tour de France Test". ...
List of doping cases in cycling
On 9 October, Alessandro Colo was given a one-year ban by CONI for testing positive for clenbuterol on the last stage of the ... On 12 August, David Clinger was issued a lifetime ban by the USADA, for a positive test for clenbuterol while serving a ban for ... On 7 April, Ali Hassan Mansoor (VIB Bikes) tested positive for Clenbuterol at the 2017 Tour du Maroc, and was banned for 4 ... On 3 June, Oldemar Vega Murillo tested positive for Clenbuterol at the Copa America and UCI Junior Series XCO, and was banned ...
Shane Gray
In June 2009, Gray tested positive to clenbuterol, a banned substance. He argued that the substance was found in an asthma ...
Clenbuterol - Wikipedia
Clenbuterol has also been used as a performance-enhancing drug. One issue is that clenbuterol is a food contaminant in some ... Clenbuterol is approved for use in some countries as a bronchodilator for asthma.[medical citation needed] Clenbuterol is a β2 ... or using clenbuterol. The situation has dramatically improved in China since September 2011, when a ban of clenbuterol was ... Clenbuterol is a growth-promoting drug in the β agonist class of compounds. It is not licensed for use in China, the United ...
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