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SR33805

  Cat. No.:  DC41018   Featured
Chemical Structure
121345-64-0
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Field of application
SR33805 is a potent Ca2+ channel antagonist, with EC50s of 4.1 nM and 33 nM in depolarized and polarized conditions, respectively. SR33805 blocks L-type but not T-type Ca2+ channels. SR33805 can be used for the research of acute or chronic failing hearts.
Chemicals PropertiesBiological activity COA & MSDSRelated productsDatasheet
Cas No.: 121345-64-0
Chemical Name: Benzeneethanamine,3,4-dimethoxy-N-methyl-N-[3-[4-[[1-methyl-2-(1-methylethyl)-1H-indol-3-yl]sulfonyl]phenoxy]propyl]-
SMILES: CN(CCCOC1=CC=C(C=C1)S(=O)(=O)C2=C(C(C)C)N(C)C3C2=CC=CC=3)CCC4=CC(OC)=C(OC)C=C4
Formula: C32H40N2O5S
M.Wt: 564.7354
Purity: >98%
Sotrage: Powder-20°C3 years 4°C2 yearsIn solvent-80°C6 months-20°C1 month
Description: SR33805 is a potent Ca2+ channel antagonist, with EC50s of 4.1 nM and 33 nM in depolarized and polarized conditions, respectively. SR33805 blocks L-type but not T-type Ca2+ channels. SR33805 can be used for the research of acute or chronic failing hearts[1][2].
Target: L-type calcium channel:4.1 nM (EC50, in depolarized conditions) L-type calcium channel:33 nM (EC50, in polarized conditions)
In Vivo: SR33805 (20 mg/kg; a single i.p.) improves end-systolic strain and fractional shortening of MI hearts in rats[2]. SR33805 (5 mg/kg/day; p.o. for 38 d) significantly reduces intimal hyperplasia in pigs[3]. Animal Model: Male Wistar rats (5 weeks) are subjected to coronary artery ligature[2] Dosage: 0.2, 2, 20 mg/kg Administration: A single i.p. injection Result: Increased significantly both end-systolic strain (ESS) and fractional shortening (FS) by about +38 and +26%, respectively at the dose of 20 mg/kg. Did not affect other contractile parameters.
In Vitro: SR33805 (0.01-10 µM; 3 d) inhibits growth factor-induced proliferation of SMC (0.2050<0.46 µM) in a dose-dependent manner[3]. SR33805 (10 µM; 10 min) restores the myocardial infarction (MI)-altered cell shortening without affecting the Ca2+ transient amplitude[2]. SR33805 (10 µM) decreases the activity of recombinant PKA[2]. Cell Viability Assay[3] Cell Line: Smooth muscle cells (SMC) Concentration: 0.01, 0.1, 1, 10 µM Incubation Time: 3 days Result: Inhibited in a dose-dependent manner FCS-, bFGF and PDGF-induced proliferation of porcine SMC with IC50s of 0.26±0.08, 0.46±0.1 and 0.20±0.04 µM, respectively.
References: [1]. Romey G, et, al. Effects of two chemically related new Ca2+ channel antagonists, SR33557 (fantofarone) and SR33805, on the L-type cardiac channel. Eur J Pharmacol. 1994 Sep 22; 263(1-2): 101-5. [2]. Mou YA, et, al. Beneficial effects of SR33805 in failing myocardium. Cardiovasc Res. 2011 Aug 1; 91(3): 412-9. [3]. Hainaud P, et, al. The calcium inhibitor SR33805 reduces intimal formation following injury of the porcine carotid artery. Atherosclerosis. 2001 Feb 1; 154(2): 301-8.
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