2,5-Pyrazinediethanol,-bta--hydroxy-(9CI) - CAS 220150-12-9
Category:
Main Product
Product Name:
2,5-Pyrazinediethanol,-bta--hydroxy-(9CI)
Catalog Number:
220150-12-9
Synonyms:
220150-12-9; 1-[5-(2-hydroxyethyl)pyrazin-2-yl]ethane-1,2-diol; (1R)-1-[5-(2-HYDROXYETHYL)PYRAZIN-2-YL]ETHANE-1,2-DIOL; 104670-30-6; ACMC-20m7gh; 2,5-Pyrazinediethanol,b-hydroxy-,(bR)-(9CI)
CAS Number:
220150-12-9
Molecular Weight:
184.19248;g/mol
Molecular Formula:
C8 H12 N2 O3
COA:
Inquire
MSDS:
Inquire
Canonical SMILES:
C1=C(N=CC(=N1)C(CO)O)CCO
InChI:
InChI=1S/C8H12N2O3/c11-2-1-6-3-10-7(4-9-6)8(13)5-12/h3-4,8,11-13H,1-2,5H2
InChIKey:
UHLOTLAGSJOGNS-UHFFFAOYSA-N
Chemical Structure
CAS 220150-12-9 2,5-Pyrazinediethanol,-bta--hydroxy-(9CI)

Reference Reading


1.Induction of nitric oxide production by the cytostatic macrolide apicularen A [2,4-heptadienamide, N-[(1E)-3-[(3S,5R,7R,9S)-3,4,5,6,7,8,9,10-octahydro-7,14 dihydroxy-1-oxo-5,9-epoxy-1H-2-benzoxacyclododecin-3-yl]-1 propenyl]-, (2Z,4Z)-(9CI)] and possible role of nitric oxide in apicularen A-induced apoptosis in RAW 264.7 cells.
Hong J1, Yokomakura A, Nakano Y, Ban HS, Ishihara K, Ahn JW, Zee O, Ohuchi K. J Pharmacol Exp Ther. 2005 Mar;312(3):968-77. Epub 2004 Nov 23.
We previously reported that apicularen A [2,4-heptadienamide, N-[(1E)-3-[(3S,5R,7R,9S)-3,4,5,6,7,8,9,10-octahydro-7,14 dihydroxy-1-oxo-5,9-epoxy-1H-2-benzoxacyclododecin-3-yl]-1 propenyl]-, (2Z,4Z)-(9CI)], a highly cytostatic macrolide isolated from the myxobacterial genus Chondromyces, induces apoptosis in the mouse leukemic monocyte cell line RAW 264.7. To analyze the action mechanism of apicularen A for the induction of apoptosis, effects of apicularen A on nitric oxide (NO) production in RAW 264.7 cells were examined. It was demonstrated that apicularen A at 10 and 100 nM induced nitrite production, whereas apicularen B [2,4-heptadienamide, N-[(1E)-3-[(3S,5R,7R,9S)-7-[[2-(acetylamino)-2-deoxy-beta-d-glucopyranosyl]oxy]-3,4,5,6,7,8,9,10-octahydro-14-hydroxy-1-oxo-5,9-epoxy-1H-2-benzoxacyclododecin-3-yl]-1 propenyl]-, (2Z,4Z)-(9CI)], an N-acetyl-glucosamine glycoside of apicularen A, had no effect at 100 nM. The apicularen A-induced nitrite production was accompanied by an increase in the level of inducible nitric-oxide synthase (iNOS) and its mRNA and was suppressed by the NOS inhibitor N(G)-monomethyl-l-arginine acetate (l-NMMA).
2.Differential effects of the Gβ5-RGS7 complex on muscarinic M3 receptor-induced Ca2+ influx and release.
Karpinsky-Semper D1, Volmar CH, Brothers SP, Slepak VZ. Mol Pharmacol. 2014 May;85(5):758-68. doi: 10.1124/mol.114.091843. Epub 2014 Feb 28.
The G protein β subunit Gβ5 uniquely forms heterodimers with R7 family regulators of G protein signaling (RGS) proteins (RGS6, RGS7, RGS9, and RGS11) instead of Gγ. Although the Gβ5-RGS7 complex attenuates Ca(2+) signaling mediated by the muscarinic M3 receptor (M3R), the route of Ca(2+) entry (i.e., release from intracellular stores and/or influx across the plasma membrane) is unknown. Here, we show that, in addition to suppressing carbachol-stimulated Ca(2+) release, Gβ5-RGS7 enhanced Ca(2+) influx. This novel effect of Gβ5-RGS7 was blocked by nifedipine and 2-aminoethoxydiphenyl borate. Experiments with pertussis toxin, an RGS domain-deficient mutant of RGS7, and UBO-QIC {L-threonine,(3R)-N-acetyl-3-hydroxy-L-leucyl-(aR)-a-hydroxybenzenepropanoyl-2,3-idehydro-N-methylalanyl-L-alanyl-N-methyl-L-alanyl-(3R)-3-[[(2S,3R)-3-hydroxy-4- methyl-1-oxo-2-[(1-oxopropyl)amino]pentyl]oxy]-L-leucyl-N,O-dimethyl-,(7→1)-lactone (9CI)}, a novel inhibitor of Gq, showed that Gβ5-RGS7 modulated a Gq-mediated pathway.
3.Phosphoinositide 3-kinase-dependent antagonism in mammalian olfactory receptor neurons.
Ukhanov K1, Brunert D, Corey EA, Ache BW. J Neurosci. 2011 Jan 5;31(1):273-80. doi: 10.1523/JNEUROSCI.3698-10.2011.
Phosphoinositide signaling, in particular, phosphoinositide 3-kinase (PI3K) signaling, has been implicated in mediating inhibitory odorant input to mammalian olfactory receptor neurons (ORNs). To better understand this phenomenon we investigated PI3K-dependent inhibition between single odorant pairs. The concentration-dependent inhibition of the response of native rat ORNs to octanol by citral is PI3K dependent; blocking PI3K activity with the β and γ isoform-specific inhibitors AS252424 (5-[5-(4-fluoro-2-hydroxy-phenyl)-furan-2-ylmethylene]-thiazolidine-2,4-dione) and TGX221(7-methyl-2-(4-morpholinyl)-9-[1-(phenylamino)ethyl]-4H-pyrido [1,2-a]pyrimidin-4-one) eliminated or strongly reduced the inhibition. Interestingly, blocking PI3K also changed the apparent agonist strength of the otherwise noncompetitive antagonist citral. The excitation evoked by citral after blocking PI3K, could be suppressed by the adenylate cyclase III (ACIII) blockers MDL12330A (cis-N-(2-phenylcyclopentyl)-azacyclotridec-1-en-2-amine hydrochloride) and SQ22536 [9-(tetrahydro-2-furanyl)-9H-purin-6-amine], indicating that citral could also activate ACIII, presumably through the canonical olfactory receptor (OR).