8-Aminoadenosine

98%

Powder: -20 degree C for 3 years
In solvent: -80 degree C for 2 years

Nc1nc2c(N)ncnc2n1[C@@H]1O[C@H](CO)[C@@H](O)[C@H]1O

C10H14N6O4

3868-33-5

<1mg/ml refers to the product slightly soluble or insoluble

8-Aminoadenosine (8-NH2-Ado; 0.1-10 uM; for 48 h) has IC50s of 1.5 uM and 8.88 uM in MM.1S and U266 cells, respectively[1]. 8-Aminoadenosine (10 uM; for 24 h) induces significant apoptotic death of MCF-7 cells in p53-independent pathway. 8-Aminoadenosine causes PARP cleavage in MCF-7 cells[2]. 8-Aminoadenosine (3 uM; 0.5-4 h) induces autophagy in the MM.1S cell line[1]. 8-Aminoadenosine (3 uM; 2-16 h) causes a greater drop in ATP levels in the MM.1S cells[1]. 8-Aminoadenosine (3 uM; 5 h) causes a 50% reduction in glucose consumption in MM.1S cells[1]. 8-Aminoadenosine (3 uM; 5 h) indicates a time-dependent decrease in GLUT1 expression at 5 h, whereas at 24 h there was a down-regulation of both transporters (GLUT1 and GLUT4) in MM.1S cells[1]. 8-Aminoadenosine inhibits cell proliferation, activated cell death, and does not activate transcription of the p53 target gene p21 or increase protein levels of either p53 or p21[1]. The toxic effects of 8-Aminoadenosine require adenosine kinase activity to convert 8-Aminoadenosine to 8-NH2-ATP in adenosine kinase-deficient cells[1]. Cell Viability Assay[1]Cell Line: MM.1S and U266 cells Concentration: 0.1, 0.3, 1, 3, 10 uM Incubation Time: For 48 hours. Result: Had IC 50 s of 1.5 uM and 8.88 uM in MM.1S and U266 cells, respectively. Apoptosis Analysis[2]Cell Line: MCF-7 cells Concentration: 10 uM Incubation Time: For 24 hours. Result: Induced significant apoptotic death. Apoptosis was not inhibited by knockdown of functional p53. Apoptosis Analysis[1]Cell Line: MM.1S cell line Concentration: 3 uM Incubation Time: 0.5, 1, 1.5, 2, 2.5, 3, 3.5, 4 hours. Result: Induced the formation of LC3-II protein. Caused the appearance of a population with a high AVO content with 1 uM for 24 hours.