SR 33805 oxalate
Potent Ca2+ channel antagonist; binds allosterically to the a1-subunit of L-type Ca2+ channels (Kd = 20 pM), at a site distinct from other types of blocker. Shows some selectivity for vascular smooth muscle, inducing vasorelaxation without producing inotropic or chronotropic effects. Inhibits PDGF-stimulated smooth muscle cell proliferation.
|Storage||Store at RT|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 654.77. Batch specific molecular weights may vary from batch to batch due to solvent of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||1.53 mL||7.64 mL||15.27 mL|
|5 mM||0.31 mL||1.53 mL||3.05 mL|
|10 mM||0.15 mL||0.76 mL||1.53 mL|
|50 mM||0.03 mL||0.15 mL||0.31 mL|
References are publications that support the biological activity of the product.
Chatelain et al (1993) In vitro characterization of a novel Ca2+ entry blocker: SR 33805. Eur.J.Pharmacol. 246 181 PMID: 8223943
Magnier-Gaubil et al (1996) Smooth muscle cell cycle and proliferation. Relationship between calcium influx and sarco-endoplasmic reticulum Ca2+ATPase regulation. J.Biol.Chem. 271 27788 PMID: 8910375
Romey and Lazdunski (1994) Effects of a new class of calcium antagonists, SR33557 (fantofarone) and SR33805, on neuronal voltage-activated Ca++ channels. J.Pharmacol.Exp.Ther. 271 1348 PMID: 7996445
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Keywords: SR 33805 oxalate, SR 33805 oxalate supplier, Ca2+, channel, blockers, L-type, Calcium, CaV, Channels, voltage-gated, voltage-dependent, SR33805, oxalate, Cav1.x, 1806, Tocris Bioscience
1 Citation for SR 33805 oxalate
Citations are publications that use Tocris products. Selected citations for SR 33805 oxalate include:
Wu et al (2008) Coupling of L-type Ca2+ channels to KV7/KCNQ channels creates a novel, activity-dependent, homeostatic intrinsic plasticity. J Neurophysiol 100 1897 PMID: 18715900
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Literature in this Area
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