3868-33-5

3868-33-5 structure

Name: 8-Aminoadenosine
Chemical Name: 8-aminoadenosine
CAS Number: 3868-33-5
Molecular Formula: C₁₀H₁₄N₆O₄
Molecular Weight: 282.26
Catalog: Biochemical Nucleoside drugs Nucleoside intermediate
Create Date: 2018-07-09 02:18:16
Modify Date: 2024-01-13 19:12:05
8-Aminoadenosine (8-NH2-Ado), a RNA-directed nucleoside analogue, reduces cellular ATP levels and inhibits mRNA synthesis. 8-Aminoadenosine blocks Akt/mTOR signaling and induces autophagy and apoptosis in a p53-independent manner. 8-Aminoadenosine has antitumor activity[1][2][3].

Name	8-aminoadenosine
Synonyms	8-Amino-adenosin 8-Amino Adenosine 8-Aminoadenosine 8-Amino-D-adenosine

Description	8-Aminoadenosine (8-NH2-Ado), a RNA-directed nucleoside analogue, reduces cellular ATP levels and inhibits mRNA synthesis. 8-Aminoadenosine blocks Akt/mTOR signaling and induces autophagy and apoptosis in a p53-independent manner. 8-Aminoadenosine has antitumor activity[1][2][3].
Related Catalog	Signaling Pathways >> PI3K/Akt/mTOR >> mTOR Signaling Pathways >> Apoptosis >> Apoptosis Research Areas >> Cancer Signaling Pathways >> Cell Cycle/DNA Damage >> DNA/RNA Synthesis Signaling Pathways >> Autophagy >> Autophagy Signaling Pathways >> PI3K/Akt/mTOR >> Akt
Target	Akt mTOR
In Vitro	8-Aminoadenosine (8-NH2-Ado; 0.1-10 μM; for 48 h) has IC50s of 1.5 μM and 8.88 μM in MM.1S and U266 cells, respectively[1]. 8-Aminoadenosine (10 μM; 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 μM; 0.5-4 h) induces autophagy in the MM.1S cell line[1]. 8-Aminoadenosine (3 μM; 2-16 h) causes a greater drop in ATP levels in the MM.1S cells[1]. 8-Aminoadenosine (3 μM; 5 h) causes a 50% reduction in glucose consumption in MM.1S cells[1]. 8-Aminoadenosine (3 μM; 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 μM Incubation Time: For 48 hours Result: Had IC50s of 1.5 μM and 8.88 μM in MM.1S and U266 cells, respectively. Apoptosis Analysis[2] Cell Line: MCF-7 cells Concentration: 10 μM 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 μM 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 μM for 24 hours.
References	[1]. Mala Shanmugam, et al. Targeting glucose consumption and autophagy in myeloma with the novel nucleoside analogue 8-aminoadenosine. J Biol Chem. 2009 Sep 25;284(39):26816-30. [2]. Alla Polotskaia, et al. 8-Amino-adenosine activates p53-independent cell death of metastatic breast cancers. Mol Cancer Ther. 2012 Nov;11(11):2495-504. [3]. Jennifer Ann Frey, et al. 8-Amino-adenosine inhibits multiple mechanisms of transcription. Mol Cancer Ther. 2010 Jan;9(1):236-45.

Density	2.25g/cm3
Boiling Point	747.1ºC at 760mmHg
Melting Point	180-185ºC dec.
Molecular Formula	C₁₀H₁₄N₆O₄
Molecular Weight	282.26
Flash Point	405.6ºC
Exact Mass	282.10800
PSA	165.56000
Appearance	white to beige
Storage condition	-20?C Freezer
Water Solubility	H2O: soluble2mg/mL, clear (warmed)

Symbol	GHS06
Signal Word	Danger
Hazard Statements	H301
Precautionary Statements	P301 + P310
Hazard Codes	T
Risk Phrases	25
Safety Phrases	45
RIDADR	UN 2811 6.1 / PGIII

4372-67-2

~95%

3868-33-5

Literature: Postigo, Al; Kopsov, Sergey; Ferreri, Carla; Chatgilialoglu, Chryssostomos Organic Letters, 2007 , vol. 9, # 25 p. 5159 - 5162

2946-39-6

~29%

3868-33-5

Literature: Repkova; Ivanova; Komarova; Meshchaninova; Kuznetsova; Venyaminova Russian Journal of Bioorganic Chemistry, 1999 , vol. 25, # 9 p. 612 - 622