(-)-[3R,4S]-Chromanol 293B - CAS 163163-24-4
Category: Inhibitor
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Molecular Formula:
C15H20N2O4S
Molecular Weight:
324.39
COA:
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Targets:
Potassium Channel
Description:
(-)-[3R,4S]-Chromanol 293B is one of the chromanols, which inhibits cAMP-mediated Cl- secretion in colon crypts by a blockade of a cAMP-activated K+ conductance. It selectively inhibits the slow component of delayed rectifier K+ current. It has negligible inhibitory action at KV11.1 (hERG) channels. It may be a useful research chemical.
Purity:
≥99% by HPLC
Synonyms:
N-[(3R,4S)-6-Cyano-3,4-dihydro-3-hydroxy-2,2-dimethyl-2H-1-benzopyran-4-yl]-N-methylethanesulfonamide
MSDS:
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InChIKey:
HVSJHHXUORMCGK-UONOGXRCSA-N
InChI:
InChI=1S/C15H20N2O4S/c1-5-22(19,20)17(4)13-11-8-10(9-16)6-7-12(11)21-15(2,3)14(13)18/h6-8,13-14,18H,5H2,1-4H3/t13-,14+/m0/s1
Canonical SMILES:
CCS(=O)(=O)N(C)C1C(C(OC2=C1C=C(C=C2)C#N)(C)C)O
1.Estrogen inhibits chloride secretion caused by cholera and Escherichia coli enterotoxins in female rat distal colon.
Alzamora R;O'Mahony F;Harvey BJ Steroids. 2011 Aug;76(9):867-76. doi: 10.1016/j.steroids.2011.04.016. Epub 2011 May 8.
Excessive Cl(-) secretion is the driving force for secretory diarrhea. 17β-Estradiol has been shown to inhibit Cl(-) secretion in rat distal colon through a nongenomic pathway. We examined whether 17β-estradiol inhibits Cl(-) secretion in an animal model of secretory diarrhea and the downstream effectors involved. The effect of 17β-estradiol on cholera toxin and heat-stable enterotoxin induced Cl(-) secretion in rat colonic mucosal sheets was studied by current-voltage clamping. Selective permeabilization of apical or basolateral membranes with amphotericin B or nystatin was used to isolate basolateral K(+) channel and apical Cl(-) channel activity, respectively. 17β-Estradiol dose-dependently inhibited secretory responses to both toxins with IC(50) values of approximately 1nM. This effect was female-gender specific, with no inhibition observed in male tissues. 17β-Estradiol responses were insensitive to the pure anti-estrogen ICI 182,720. 17β-Estradiol exerted its effects downstream of enterotoxin-induced production of second messengers (cAMP and cGMP) but was dependent on PKCδ activation. In nystatin-permeabilized tissues, apical Cl(-) currents were unaffected by 17β-estradiol treatment while basolateral K(+) current was profoundly inhibited by the hormone.
2.Palmatine, a protoberberine alkaloid, inhibits both Ca(2+)- and cAMP-activated Cl(-) secretion in isolated rat distal colon.
Wu DZ;Yuan JY;Shi HL;Hu ZB Br J Pharmacol. 2008 Mar;153(6):1203-13. doi: 10.1038/sj.bjp.0707684. Epub 2008 Jan 21.
BACKGROUND AND PURPOSE: ;The protoberberine alkaloid berberine has been reported to inhibit colonic Cl(-) secretion. However, it is not known if other protoberberine alkaloids share these effects. We have therefore selected another protoberberine alkaloid, palmatine, to assess its effects on active ion transport across rat colonic epithelium.;EXPERIMENTAL APPROACH: ;Rat colonic mucosa was mounted in Ussing chambers and short circuit current (I (SC)), apical Cl(-) current and basolateral K(+) current were recorded. Intracellular cAMP content was determined by an enzyme immunoassay. Intracellular Ca(2+) concentration was measured with Fura-2 AM.;KEY RESULTS: ;Palmatine inhibited carbachol-induced Ca(2+)-activated Cl(-) secretion and the carbachol-induced increase of intracellular Ca(2+) concentration. Palmatine also inhibited cAMP-activated Cl(-) secretion induced by prostaglandin E(2) (PGE(2)) or forskolin. Palmatine prevented the elevation of intracellular cAMP by forskolin. Determination of apical Cl(-) currents showed that palmatine suppressed the forskolin-stimulated, apical cAMP-activated Cl(-) current but not the carbachol-stimulated apical Ca(2+)-activated Cl(-) current. Following permeabilization of apical membranes with nystatin, we found that palmatine inhibited a carbachol-stimulated basolateral K(+) current that was sensitive to charybdotoxin and resistant to chromanol 293B.
3.Renal defects in KCNE1 knockout mice are mimicked by chromanol 293B in vivo: identification of a KCNE1-regulated K+ conductance in the proximal tubule.
Neal AM;Taylor HC;Millar ID;Kibble JD;White SJ;Robson L J Physiol. 2011 Jul 15;589(Pt 14):3595-609. doi: 10.1113/jphysiol.2011.209155. Epub 2011 May 16.
KCNE1 is a protein of low molecular mass that is known to regulate the chromanol 293B and clofilium-sensitive K+ channel, KCNQ1, in a number of tissues. Previous work on the kidney of KCNE1 and KCNQ1 knockout mice has revealed that these animals have different renal phenotypes, suggesting that KCNE1 may not regulate KCNQ1 in the renal system. In the current study, in vivo clearance approaches and whole cell voltage-clamp recordings from isolated renal proximal tubules were used to examine the physiological role of KCNE1. Data from wild-type mice were compared to those from KCNE1 knockout mice. In clearance studies the KCNE1 knockout mice had an increased fractional excretion of Na+, Cl−, HCO3(−) and water. This profile was mimicked in wild-type mice by infusion of chromanol 293B, while chromanol was without effect in KCNE1 knockout animals. Clofilium also increased the fractional excretion of Na+, Cl− and water, but this was observed in both wild-type and knockout mice, suggesting that KCNE1 was regulating a chromanol-sensitive but clofilium-insensitive pathway. In whole cell voltage clamp recordings from proximal tubules, a chromanol-sensitive, K+-selective conductance was identified that was absent in tubules from knockout animals.
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CAS 163163-24-4 (-)-[3R,4S]-Chromanol 293B

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