InChI key
QIKYZXDTTPVVAC-UHFFFAOYSA-N
InChI
1S/C7H8N2O/c8-6-3-1-5(2-4-6)7(9)10/h1-4H,8H2,(H2,9,10)
SMILES string
NC(=O)c1ccc(N)cc1
assay
98%
form
solid
mp
181-183 °C (lit.)
functional group
amide
Quality Level
Application
4-氨基苯甲酰胺作为多聚 ADP 核糖聚合酶 (PADPRP) 抑制剂,利用核酶多聚 ADP 核糖聚合酶 (PADPRP) 研究细胞毒性效应细胞对靶细胞的死亡作用 。
signalword
Warning
hcodes
Hazard Classifications
Eye Irrit. 2 - STOT SE 3
target_organs
Respiratory system
存储类别
11 - Combustible Solids
wgk
WGK 1
ppe
dust mask type N95 (US), Eyeshields, Gloves
P Burgman et al.
Radiation research, 119(2), 380-386 (1989-08-01)
The purpose of this study was to investigate possible involvement of poly(ADP-ribosyl)ation reactions in X-ray-induced cell killing, repair of potentially lethal damage (PLD), and formation and repair of radiation-induced DNA damage. As tools we used the inhibitors of poly(ADP-ribose)polymerase, 3-aminobenzamide
R J Baugh et al.
The Journal of biological chemistry, 275(37), 28826-28833 (2000-07-13)
The initiation of coagulation results from the activation of factor X by an enzyme complex (Xase) composed of the trypsin-like serine proteinase, factor VIIa, bound to tissue factor (TF) on phospholipid membranes. We have investigated the basis for the protein
P Burgman et al.
Radiation research, 116(3), 406-415 (1988-12-01)
The purpose of this study was to investigate a possible involvement of poly(ADP-ribosyl)ation reactions in hyperthermic cell killing and hyperthermic DNA strand-break induction and repair in HeLa S3 cells. The inhibitors of poly(ADP-ribose) polymerase, 3-aminobenzamide (3AB) and 4-aminobenzamide (4AB), were
E Ben-Hur et al.
Radiation research, 97(3), 546-555 (1984-03-01)
Postirradiation incubation of V79 Chinese hamster cells with inhibitors of poly(ADP-ribose) synthesis was found to potentiate the killing of cells by X rays. Potentiation increased with incubation time and with concentration of the inhibitor. Preirradiation incubation had only a small
R Laffranchi et al.
Experimental cell research, 237(1), 217-222 (1998-01-07)
Interferon-gamma is among the cytokines which have been implicated as effector molecules of beta-cell destruction in autoimmune diabetes. Its mechanism of action is, however, largely unknown. In the present study rat pancreatic beta-cells, INS-1, were incubated with rat interferon-gamma (rIRN-gamma)
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