C1081
8-Chloroadenosine 3′,5′-cyclic-monophosphate
≥85%
别名:
8-Chloro-cAMP, 8-Chloroadenosine 3′,5′-monophosphate, 8-Cl-cAMP
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关于此项目
经验公式（希尔记法）:
C10H11ClN5O6P
化学文摘社编号:
分子量:
363.65
MDL编号:
UNSPSC代码:
41106305
PubChem化学物质编号:
NACRES:
NA.77
生化/生理作用
Membrane-permeable cAMP analog; resistant to hydrolysis by phosphodiesterases.
储存分类代码
11 - Combustible Solids
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
个人防护装备
Eyeshields, Gloves, type N95 (US)
法规信息
新产品
此项目有
Audrey J Robinson-White et al.
The Journal of clinical endocrinology and metabolism, 93(3), 1020-1029 (2007-12-13)
Protein kinase A (PKA) affects cell proliferation in many cell types and is a potential target for cancer treatment. PKA activity is stimulated by cAMP and cAMP analogs. One such substance, 8-Cl-cAMP, and its metabolite 8-Cl-adenosine (8-Cl-ADO) are known inhibitors
R G Halgren et al.
Blood, 92(8), 2893-2898 (1998-10-09)
We have examined the cytotoxic effects of cyclic adenosine-3', 5'-monophosphate (cAMP) derivatives on multiple myeloma cells lines and determined that the 8-Chloro substituted derivative (8Cl-cAMP) is one of the most potent. We report here that 8Cl-cAMP is cytotoxic to both
Young-Ho Ahn et al.
Journal of cellular physiology, 209(3), 1039-1045 (2006-09-15)
8-Cl-cAMP, which is known to induce differentiation, growth inhibition, and apoptosis in various cancer cells, has been investigated as a putative anti-cancer drug. Previously, we reported that 8-Cl-cAMP and its metabolite 8-Cl-adenosine induce growth inhibition and apoptosis through p38 mitogen-activated
Dragana Janković et al.
Investigational new drugs, 24(1), 15-25 (2005-12-28)
To identify purine analogs that could be effective in treating neuroblastomas, we tested the anticancer properties of sulfinosine, 8-Cl-cAMP and 8-Cl-adenosine in the SK-N-SH cell line. First we examined the effects of these three agents on cell growth inhibition and
Linda Melotti et al.
Oncology reports, 45(2), 752-763 (2021-01-09)
The Ras/Raf/MEK/MAPK signaling cascade is frequently activated in human cancer and serves a crucial role in the oncogenesis of pediatric low‑grade gliomas (PLGGs). Therefore, drugs targeting kinases among the mitogen‑activated protein kinase (MAPK) effectors of receptor tyrosine kinase signaling may represent promising
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