This compound is a customized synthesis product. We have a strong synthesis team with excellent synthesis technology and capabilities. However, due to various objective factors, there is a low probability that the synthesis will not be successful. If you need to learn more, please feel free to consult us, we will serve you wholeheartedly.
This compound is a customized synthesis product. We have a strong synthesis team with excellent synthesis technology and capabilities. However, due to various objective factors, there is a low probability that the synthesis will not be successful. If you need to learn more, please feel free to consult us, we will serve you wholeheartedly.
Gambogic Acid is a caged xanthone that is derived from Garcinia hanburyi and functions as a strong apoptotic inducer in many types of cancer cells by inhibiting human Bcl-2 family proteins and activating caspases. Gambogic Acid also blocks Kir2.1 channels with EC50 of ≤ 100 nM.[1] [2] [3] Gambogic Acid significantly inhibits human umbilical vein endothelial cell (HUVEC) proliferation, migration, invasion, tube formation, and micro-vessel growth at nM concentration. [4]
In vivo
Gambogic Acid effectively inhibits tumor angiogenesis and suppressed tumor growth with low side effects using metronomic chemotherapy with Gambogic Acid. [4] Gambogic Acid has multiple functional effects including the induction of apoptosis, the inhibition of proliferation and the prevention of cancer metastasis and tumor angiogenesis. [5] In both animal tumor models and Clinicalal trials, Gambogic Acid efficiently inhibits tumor growth with minimal side effects, with little toxicity on immune and hemopoietic systems. Gambogic Acid can produce tissue-specific proteasome inhibition and tumor-specific toxicity. [6] LD50: Mice 45 mg/kg (i.p.). [7]
Kinase Assay
The fluorescence polarization reactions are performed. For Kidetermination, duplicate 200 μL reactions are set up at eight different ATP concentrations from 200 μM (2-fold serial dilutions) in the presence of either DMSO or R406 at 125, 62.5, 31.25, 15.5, or 7.8 nM. At different time points, 20 μL of each reaction is removed and quenched to stop the reaction. For each concentration of R406, the rate of reaction at each concentration of ATP is determined and plotted against the ATP concentration to determine the apparent Km and Vmax (maximal rate). Finally the apparent Km (or apparent Km/Vmax) is plotted against the inhibitor concentration to determine the Ki. All data analysis is performed using Prism and Prism enzyme kinetics programs[1]
Method for preparing DMSO master liquid: mg
drug pre-dissolved in μL DMSO (Master liquid concentration
mg/mL),
Method for preparing in vivo formulation:Take μL
DMSO master liquid, next add μL PEG300, mix and clarify, next add μL
Tween 80,mix and clarify, next add μL ddH2O, mix and clarify.
Method for preparing in vivo formulation:Take μL
DMSO master liquid, next add μL Corn oil,mix and clarify.
Note:
Be sure to add the solvent(s) in order. Physical methods such as vortex, ultrasound or hot water bath can be used to aid dissolving.
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Tech Support
Please see Inhibitor Handling Instructions for more frequently ask questions. Topics include: how to prepare stock solutions, how to store products, and cautions on cell-based assays & animal experiments, etc.