1223397-11-2 Usage
Description
WZB117 (1223397-11-2) is an inhibitor of Glucose Transporter 1 (GLUT1). It inhibited cell proliferation in lung cancer A549 cells and breast cancer MCF7 cells with an IC50 of approximately 10 μM. Daily intraperitoneal injection of WZB117 at 10mg/kg resulted in 70% reduction in tumor volume of human A549 lung cancer grafted on nude mice.
Uses
Different sources of media describe the Uses of 1223397-11-2 differently. You can refer to the following data:
1. WZB 117 is a GLUT1 inhibitor.
2. WZB-117 has been used to study its tumor initiating ability in cancer stem cells. It has also been used to study the effect of glucose antagonists on 2-NBDG (2-(N-(7-Nitrobenz-2-oxa-1,3-diazol-4-yl)Amino)-2-Deoxyglucose) uptake.
General Description
A bis-hydroxybenzoate compound that acts as a fast-acting, irreversible blocker of glucose transport by GLUT1 in red blood cells. Shown to rapidly inhibit glucose transport in cancer cells (IC50 ~ 500 nM in A549 cells) and block proliferation. Its inhibitory effects are more pronounced in hypoxic cancer cells. It binds directly to GLUT1 involving three hydrogen bonds, one each with Asn34, Arg126, and Trp412. Also shown to reduce the levels of GLUT1 protein, intracellular ATP levels, and glycolytic enzymes and increase the level of AMPK in tumor cells. Preferentially induces cell cycle arrest and causes senescence and necrosis in red blood cells and tumor cells (IC50 = 10 μM) over non cancerous cells and synergizes the anti-tumor effects of cisplatin (Cat. No. 232120) and paclitaxel (Cat. No. 580555). Also, effectively suppresses tumor growth in human A549 lung cancer grafted nude mice model (10 mg/kg, i.p., daily).
Biochem/physiol Actions
Cell permeable: yes
in vitro
previous study found that wzb117 could inhibit glucose transport in human red blood cells expressing glut1 as their sole glucose transporter. moreover, cancer cell treatment with wzb117 resulted in decreased levels of glut1 protein, intracellular atp, as well as glycolytic enzymes. all these changes were followed by increase in atp-sensing enzyme amp-activated protein kinase and declined in cyclin e2 as well as phosphorylated retinoblastoma, leading to cell-cycle arrest, senescence, and necrosis [1].
in vivo
animal study showed that the daily ip injection of wzb117 at 10 mg/kg led to a more than 70% reduction in the size of human lung cancer of a549 cell origin [1].
IC 50
~0.6 μm for blocking glucose transport in diverse cancer cells
References
1) Liu?et al. (2012),?A small-molecule inhibitor of glucose transporter 1 downregulates glycolysis, induces cell-cycle arrest, and inhibits cancer cell growth in vitro and in vivo; Mol. Cancer Ther.,?11?1672
Check Digit Verification of cas no
The CAS Registry Mumber 1223397-11-2 includes 10 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 7 digits, 1,2,2,3,3,9 and 7 respectively; the second part has 2 digits, 1 and 1 respectively.
Calculate Digit Verification of CAS Registry Number 1223397-11:
(9*1)+(8*2)+(7*2)+(6*3)+(5*3)+(4*9)+(3*7)+(2*1)+(1*1)=132
132 % 10 = 2
So 1223397-11-2 is a valid CAS Registry Number.
1223397-11-2Relevant articles and documents
COMPOSITIONS AND METHODS FOR GLUCOSE TRANSPORT INHIBITION
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Page/Page column 26-27, (2011/10/13)
Glucose deprivation is an attractive strategy in cancer research and treatment. Cancer cells upregulate glucose uptake and metabolism for maintaining accelerated growth and proliferation rates. Specifically blocking these processes is likely to provide new insights to the role of glucose transport and metabolism in tumorigenesis, as well as in apoptosis. As solid tumors outgrow the surrounding vasculature, they encounter microenvironments with a limited supply of nutrients leading to a glucose deprived environment in some regions of the tumor. Cancer cells living in the glucose deprived environment undergo changes to prevent glucose deprivation-induced apoptosis. Knowing how cancer cells evade apoptosis induction is also likely to yield valuable information and knowledge of how to overcome the resistance to apoptosis induction in cancer cells. Disclosed herein are novel anticancer compounds that inhibit basal glucose transport, resulting in tumor suppression and new methods for the study of glucose deprivation in animal cancer research.
