Open Access Articles- Top Results for Solabegron


Systematic (IUPAC) name
3'-[(2-{[(2R)-2-(3-chlorophenyl)-2-hydroxyethyl]amino}ethyl)amino]biphenyl-3-carboxylic acid
Clinical data
451470-34-1 7pxY
PubChem CID 9887812
ChemSpider 8063484 7pxN
UNII 55P6YH9O6N 7pxY
KEGG D05879 7pxY
Synonyms 3-(3-(2-[(2-(3-chlorophenyl)-2-hydroxyethyl)amino]ethylamino)phenyl)benzoic acid
Chemical data
Formula C23H23ClN2O3
410.892 g/mol
 14pxN (what is this?)  (verify)

Solabegron (GW-427,353) is a drug which acts as a selective agonist for the β3 adrenergic receptor. It is being developed for the treatment of overactive bladder and irritable bowel syndrome.[1][2][3] It has been shown to produce visceral analgesia by releasing somatostatin from adipocytes.[4][5]

Solabegron was discovered by GlaxoSmithKline and acquired by AltheRx in March 2011. Solabegron relaxes the bladder smooth muscle by stimulating beta-3 adrenoceptors, a novel mechanism compared to older established drug treatments for overactive bladder syndrome such as the anticholinergic agents. Astellas Pharma have developed the first commercially available β3 adrenergic receptor, mirabegron, which is now licensed in Japan[6] and the US[7] for overactive bladder. Mirabegron is not licensed for irritable bowel syndrome.

A Phase II study of Solabegron for overactive bladder (OAB) looked at 258 patients with moderate to severe incontinence experiencing an average of 4.5 wet episodes per day. Results demonstrated a statistically significant improvement with Solabegron as compared to placebo, as measured by the percent reduction of the number of wet episodes and the absolute number of daily voids.

A Phase II study for irritable bowel syndrome (IBS) evaluated 102 patients with IBS. Solabegron demonstrated significant reduction in pain associated with the disorder and a trend for greater improvement in the quality of life, compared to placebo.

Both Phase II studies indicated a tolerability profile for Solabegron that was similar to placebo. The OAB patients did not suffer from dry mouth, constipation, increase in heart rate or cognitive issues.

AltheRx is currently preparing to advance Solabegron into a large clinical study in OAB.


  1. ^ Hicks, A; McCafferty, GP; Riedel, E; Aiyar, N; Pullen, M; Evans, C; Luce, TD; Coatney, RW; Rivera, GC; Westfall, TD; Hieble, JP (Oct 2007). "GW427353 (solabegron), a novel, selective beta3-adrenergic receptor agonist, evokes bladder relaxation and increases micturition reflex threshold in the dog". Journal of Pharmacology and Experimental Therapeutics 323 (1): 202–9. PMID 17626794. doi:10.1124/jpet.107.125757. 
  2. ^ Grudell, AB; Camilleri, M; Jensen, KL; Foxx-Orenstein, AE; Burton, DD; Ryks, MD; Baxter, KL; Cox, DS; Dukes, GE; Kelleher, DL; Zinsmeister, AR (May 2008). "Dose-response effect of a beta3-adrenergic receptor agonist, solabegron, on gastrointestinal transit, bowel function, and somatostatin levels in health". American Journal of Physiology. Gastrointestinal and Liver Physiology 294 (5): G1114–9. PMID 18372395. doi:10.1152/ajpgi.00051.2008. 
  3. ^ Kelleher, DL; Hicks, KJ; Cox, DS et al. (2008). "Randomized, double-blind, placebo (PLA)-controlled, crossover study to evaluate efficacy and safety of the beta 3-adrenergic receptor agonist solabegron (SOL) in patients with irritable bowel syndrome (IBS)". Neurogastroenterol Motil 20 (Suppl 2): 131. 
  4. ^ Cellek, S; Thangiah, R; Bassil, AK; Campbell, CA; Gray, KM; Stretton, JL; Lalude, O; Vivekanandan, S; Wheeldon, A; Winchester, WJ; Sanger, GJ; Schemann, M; Lee, K (Jul 2007). "Demonstration of functional neuronal beta3-adrenoceptors within the enteric nervous system". Gastroenterology 133 (1): 175–83. doi:10.1053/j.gastro.2007.05.009. 
  5. ^ Schemann M, Hafsi N, Michel K, Kober OI, Wollmann J, Li Q, Zeller F, Langer R, Lee K, Cellek S. The beta3-adrenoceptor agonist GW427353 (solabegron) decreases excitability of human enteric neurons via release of somatostatin. Gastroenterology 2009 Sep 25. [Epub ahead of print]
  6. ^ "Mirabegron for the treatment of overactive bladder". Drugs of Today 48 (1): 25–32. January 2012. PMID 22384458. doi:10.1358/dot.2012.48.1.1738056. 
  7. ^