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Fórmula empírica (notación de Hill):
C6H9BrO3
Número CAS:
Peso molecular:
209.04
UNSPSC Code:
12352200
Assay:
≥98% (GC)
Form:
oil
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Servicio técnico
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Permítanos ayudarleassay
≥98% (GC)
form
oil
color
colorless to yellow
shipped in
ambient
storage temp.
2-8°C
Biochem/physiol Actions
3-BrOP is a cell-permeable ester of the the glycolysis inhibitor 3-bromopyruvate (3-BrPA) that is known to target hexokinase II (HK2) and GAPDH. Upon entering the cells, 3-BrOP is hydrolyzed by intracellular esterase to 3-BrPA. 3-BrOP is shown to synergize cancer cell killing with mTOR inhibitor rapamycin (apoptosis induction with/without 100 ng/mL rapamycin = 64%/36% of Raji human lymphoma cells by 40 μM 3-BrOP and 72%/45% of HL-60 leukemia cells by 20 μM 3-BrOP in 24 h) due to enhanced cellular ATP depletion and glucose uptake inhibition. When administered via tail vein injection, 3-BrOP significantly suppersses SK-N-SH xenograft-derived neuroblastoma tumor growth in mice in vivo (by 78% in 14 days; 20 mg/kg/day).
Cell-permeable ester of the the glycolysis inhibitor 3-bromopyruvate (3-BrPA) with in vitro and in vivo anti-cancer efficacy.
signalword
Warning
hcodes
Hazard Classifications
Eye Irrit. 2 - Skin Irrit. 2 - STOT SE 3
target_organs
Respiratory system
Clase de almacenamiento
10 - Combustible liquids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
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R-H Xu et al.
Leukemia, 19(12), 2153-2158 (2005-09-30)
The mammalian target of rapamycin (mTOR) pathway plays important roles in regulating nutrient metabolism and promoting the growth and survival of cancer cells, which exhibit increased glycolysis for ATP generation. In this study, we tested the hypothesis that inhibition of
Alejandro G Levy et al.
Investigational new drugs, 30(1), 191-199 (2010-10-05)
Children with high-risk and recurrent neuroblastoma have poor survival rates, and novel therapies are needed. Many cancer cells have been found to preferentially employ the glycolytic pathway for energy generation, even in the presence of oxygen. 3-BrOP is a novel
H-Q Ju et al.
Leukemia, 31(10), 2143-2150 (2017-02-15)
Internal tandem duplication (ITD) mutation in Fms-like tyrosine kinase 3 gene (FLT3/ITD) represents an unfavorable genetic change in acute myeloid leukemia (AML) and is associated with poor prognosis. Metabolic alterations have been involved in tumor progression and attracted interest as
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