product name Fesoterodine Fumarate
Description: Fesoterodine Fumarate (also known as SPM 907) is a prodrug of 5-hydroxymethyl tolterodine that is a muscarinic AChR receptor antagonist, used to treat overactive bladder syndrome. Fesoterodine was approved by the European Medicines Agency in April 2007, the US FDA on October 31, 2008 and Health Canada on February 9, 2012. Fesoterodine has the advantage of allowing more flexible dosage than other muscarinic antagonists. Its tolerability and side effects are similar to other muscarinic antagonists and as a new drug seems unlikely to make great changes in practices of treatment for overactive bladder.
References: Curr Med Chem. 2009;16(33):4481-9; BJU Int. 2008 Apr;101(8):1036-42.
527.65
Formula
C26H37NO3.C4H4O4
CAS No.
286930-03-8
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 100 mg/mL (189.5 mM)
Water: 100 mg/mL (189.5 mM)
Ethanol: 100 mg/mL (189.5 mM)
Solubility (In vivo)
Synonyms
SPM 907
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19390431
| In Vitro |
In vitro activity: Fesoterodine is rapidly and extensively converted to 5-HMT, such that the pharmacologic activity appears to be primarily attributable to 5-HMT. Fesoterodine is a competitive antagonist of cholinergic agonist-stimulated responses in human M1-M5 cell lines and has a similar potency and selectivity profile to the radioligand-binding studies. Fesoterodine causes a rightward shift of the concentration-response curve for carbachol with no depression of the maximum in rat bladder strips, and concentration-dependently reduces contractions induced by electrical field stimulation (EFS). Fesoterodine is hydrolyzed by nonspecific esterases to 5-hydroxmethyl tolterodine (5-HMT), which is the active metabolite and is responsible for all its antimuscarinic activity. Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | |
| Animal model | |
| Formulation & Dosage | |
| References | Curr Med Chem. 2009;16(33):4481-9; BJU Int. 2008 Apr;101(8):1036-42. |
Related Posts
product name Fesoterodine Fumarate
Description: Fesoterodine Fumarate (also known as SPM 907) is a prodrug of 5-hydroxymethyl tolterodine that is a muscarinic AChR receptor antagonist, used to treat overactive bladder syndrome. Fesoterodine was approved by the European Medicines Agency in April 2007, the US FDA on October 31, 2008 and Health Canada on February 9, 2012. Fesoterodine has the advantage of allowing more flexible dosage than other muscarinic antagonists. Its tolerability and side effects are similar to other muscarinic antagonists and as a new drug seems unlikely to make great changes in practices of treatment for overactive bladder.
References: Curr Med Chem. 2009;16(33):4481-9; BJU Int. 2008 Apr;101(8):1036-42.
527.65
Formula
C26H37NO3.C4H4O4
CAS No.
286930-03-8
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 100 mg/mL (189.5 mM)
Water: 100 mg/mL (189.5 mM)
Ethanol: 100 mg/mL (189.5 mM)
Solubility (In vivo)
Synonyms
SPM 907
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19390431
| In Vitro |
In vitro activity: Fesoterodine is rapidly and extensively converted to 5-HMT, such that the pharmacologic activity appears to be primarily attributable to 5-HMT. Fesoterodine is a competitive antagonist of cholinergic agonist-stimulated responses in human M1-M5 cell lines and has a similar potency and selectivity profile to the radioligand-binding studies. Fesoterodine causes a rightward shift of the concentration-response curve for carbachol with no depression of the maximum in rat bladder strips, and concentration-dependently reduces contractions induced by electrical field stimulation (EFS). Fesoterodine is hydrolyzed by nonspecific esterases to 5-hydroxmethyl tolterodine (5-HMT), which is the active metabolite and is responsible for all its antimuscarinic activity. Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | |
| Animal model | |
| Formulation & Dosage | |
| References | Curr Med Chem. 2009;16(33):4481-9; BJU Int. 2008 Apr;101(8):1036-42. |