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About This Item
Linear Formula:
H2NC6H4CONHCH2CH2N(C2H5)2·HCl
CAS Number:
Molecular Weight:
271.79
EC Number:
210-381-7
UNSPSC Code:
12352200
PubChem Substance ID:
Beilstein/REAXYS Number:
3729517
MDL number:
Form:
powder
form
powder
mp
167-169 °C (lit.)
solubility
H2O: soluble, ethanol: soluble
originator
Bristol-Myers Squibb
SMILES string
Cl.CCN(CC)CCNC(=O)c1ccc(N)cc1
InChI
1S/C13H21N3O.ClH/c1-3-16(4-2)10-9-15-13(17)11-5-7-12(14)8-6-11;/h5-8H,3-4,9-10,14H2,1-2H3,(H,15,17);1H
InChI key
ABTXGJFUQRCPNH-UHFFFAOYSA-N
Gene Information
Biochem/physiol Actions
Inhibits DNA methyltransferase and modulates epigenetic regulation of gene expression. Na+ channel blocker and Class IA anti-arrhythmic.
Features and Benefits
This compound is a featured product for ADME Tox and Gene Regulation research. Discover more featured ADME Tox and Gene Regulation products. Learn more about bioactive small molecules for other areas of research at sigma.com/discover-bsm.
This compound was developed by Bristol-Myers Squibb. To browse the list of other pharma-developed compounds and Approved Drugs/Drug Candidates, click here.
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signalword
Warning
hcodes
Hazard Classifications
Acute Tox. 4 Oral - Eye Irrit. 2 - Skin Irrit. 2 - STOT SE 3
target_organs
Respiratory system
Storage Class
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
dust mask type N95 (US), Eyeshields, Gloves
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Y H Kim et al.
Circulation, 100(6), 666-674 (1999-08-10)
Ventricular fibrillation (VF) is maintained by 2 mechanisms: first by reentry formation and second by spontaneous wave break or wave splitting. We hypothesized that spontaneous wave break results from a critical shortening of the action potential duration (APD) during VF
Assessment of His-Purkinje reserve: what is the mechanism of block?
James Kneller et al.
Heart rhythm, 9(3), 465-466 (2010-12-04)
Yi-Shiuan Lin et al.
Journal of biomedical science, 18, 3-3 (2011-01-12)
Targeting abnormal DNA methylation represents a therapeutically relevant strategy for cancer treatment as demonstrated by the US Food and Drug Administration approval of the DNA methyltransferase inhibitors azacytidine and 5-aza-2'-deoxycytidine for the treatment of myelodysplastic syndromes. But their use is
