Methoxy-X04CAS# 863918-78-9 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 863918-78-9 | SDF | Download SDF |
PubChem ID | 16049314 | Appearance | Powder |
Formula | C23H20O3 | M.Wt | 344.4 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | Soluble to 100 mM in DMSO and to 20 mM in ethanol | ||
Chemical Name | 4-[(E)-2-[4-[(E)-2-(4-hydroxyphenyl)ethenyl]-3-methoxyphenyl]ethenyl]phenol | ||
SMILES | COC1=C(C=CC(=C1)C=CC2=CC=C(C=C2)O)C=CC3=CC=C(C=C3)O | ||
Standard InChIKey | FGYNZFHVGOFCMD-KHVHPYDTSA-N | ||
Standard InChI | InChI=1S/C23H20O3/c1-26-23-16-19(3-2-17-6-12-21(24)13-7-17)5-11-20(23)10-4-18-8-14-22(25)15-9-18/h2-16,24-25H,1H3/b3-2+,10-4+ | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Description | Fluorescent amyloid β (Aβ) probe for the detection and quantification of plaques, tangles and cerebrovascular amyloid. Displays high in vitro binding affinity (Ki = 26.8 nM); binds selectively to fibrillar β-sheet deposits. Brain penetrant. |
Methoxy-X04 Dilution Calculator
Methoxy-X04 Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.9036 mL | 14.518 mL | 29.036 mL | 58.072 mL | 72.59 mL |
5 mM | 0.5807 mL | 2.9036 mL | 5.8072 mL | 11.6144 mL | 14.518 mL |
10 mM | 0.2904 mL | 1.4518 mL | 2.9036 mL | 5.8072 mL | 7.259 mL |
50 mM | 0.0581 mL | 0.2904 mL | 0.5807 mL | 1.1614 mL | 1.4518 mL |
100 mM | 0.029 mL | 0.1452 mL | 0.2904 mL | 0.5807 mL | 0.7259 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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Synthesis of methoxy-X04 derivatives and their evaluation in Alzheimer's disease pathology.[Pubmed:24080522]
Neurodegener Dis. 2014;13(4):209-13.
BACKGROUND: Alzheimer's disease is characterized by two notorious protein aggregates in the brain: extracellular senile plaques mainly consisting of amyloid-beta peptides and tau-protein-derived intracellular paired helical filaments. The diagnosis of Alzheimer's disease is impaired by insufficient sensitivity and specificity of diagnostic methods to visualize these pathological hallmarks over all disease stages. OBJECTIVE: The established fluorescence marker Methoxy-X04 stains plaques, tau tangles and amyloid-derived angiopathies with good specificity, yet it is limited by slow elimination in vivo. Since the need for new markers is high, we prepared Methoxy-X04 derivatives and evaluated their potential as imaging agents in Alzheimer's disease pathology. METHODS AND RESULTS: In this study, we describe an improved synthesis for Methoxy-X04 and its derivatives and their affinity determination for the respective protein targets by immunohistology and a displacement assay. CONCLUSION: This resulted in the identification of new derivatives of Methoxy-X04 with improved binding affinity.
Imaging Abeta plaques in living transgenic mice with multiphoton microscopy and methoxy-X04, a systemically administered Congo red derivative.[Pubmed:12230326]
J Neuropathol Exp Neurol. 2002 Sep;61(9):797-805.
The identification of amyloid deposits in living Alzheimer disease (AD) patients is important for both early diagnosis and for monitoring the efficacy of newly developed anti-amyloid therapies. Methoxy-X04 is a derivative of Congo red and Chrysamine-G that contains no acid groups and is therefore smaller and much more lipophilic than Congo red or Chrysamine-G. Methoxy-X04 retains in vitro binding affinity for amyloid beta (Abeta) fibrils (Ki = 26.8 nM) very similar to that of Chrysamine-G (Ki = 25.3 nM). Methoxy-X04 is fluorescent and stains plaques, tangles, and cerebrovascular amyloid in postmortem sections of AD brain with good specificity. Using multiphoton microscopy to obtain high-resolution (1 microm) fluorescent images from the brains of living PSI/APP mice, individual plaques could be distinguished within 30 to 60 min after a single i.v. injection of 5 to 10 mg/kg Methoxy-X04. A single i.p. injection of 10 mg/kg Methoxy-X04 also produced high contrast images of plaques and cerebrovascular amyloid in PSI/APP mouse brain. Complementary quantitative studies using tracer doses of carbon- 11-labeled Methoxy-X04 show that it enters rat brain in amounts that suggest it is a viable candidate as a positron emission tomography (PET) amyloid-imaging agent for in vivo human studies.
PPARgamma/RXRalpha-induced and CD36-mediated microglial amyloid-beta phagocytosis results in cognitive improvement in amyloid precursor protein/presenilin 1 mice.[Pubmed:23197723]
J Neurosci. 2012 Nov 28;32(48):17321-31.
Alzheimer's disease (AD) is characterized by the extracellular deposition of amyloid-beta (Abeta), neurofibrillary tangle formation, and a microglial-driven inflammatory response. Chronic inflammatory activation compromises microglial clearance functions. Because peroxisome proliferator-activated receptor gamma (PPARgamma) agonists suppress inflammatory gene expression, we tested whether activation of PPARgamma would also result in improved microglial Abeta phagocytosis. The PPARgamma agonist pioglitazone and a novel selective PPARalpha/gamma modulator, DSP-8658, currently in clinical development for the treatment of type 2 diabetes, enhanced the microglial uptake of Abeta in a PPARgamma-dependent manner. This PPARgamma-stimulated increase of Abeta phagocytosis was mediated by the upregulation of scavenger receptor CD36 expression. In addition, combined treatment with agonists for the heterodimeric binding partners of PPARgamma, the retinoid X receptors (RXRs), showed additive enhancement of the Abeta uptake that was mediated by RXRalpha activation. Evaluation of DSP-8658 in the amyloid precursor protein/presenilin 1 mouse model confirmed an increased microglial Abeta phagocytosis in vivo, which subsequently resulted in a reduction of cortical and hippocampal Abeta levels. Furthermore, DSP-8658-treated mice showed improved spatial memory performance. Therefore, stimulation of microglial clearance by simultaneous activation of the PPARgamma/RXRalpha heterodimer may prove beneficial in prevention of AD.
Dynamics of the microglial/amyloid interaction indicate a role in plaque maintenance.[Pubmed:18417708]
J Neurosci. 2008 Apr 16;28(16):4283-92.
Microglial cells aggregate around amyloid plaques in Alzheimer's disease, but, despite their therapeutic potential, various aspects of their reactive kinetics and role in plaque pathogenesis remain hypothetical. Through use of in vivo imaging and quantitative morphological measures in transgenic mice, we demonstrate that local resident microglia rapidly react to plaque formation by extending processes and subsequently migrating toward plaques, in which individual transformed microglia somata remain spatially stable for weeks. The number of plaque-associated microglia increased at a rate of almost three per plaque per month, independent of plaque volume. Larger plaques were surrounded by larger microglia, and a subset of plaques changed in size over time, with an increase or decrease related to the volume of associated microglia. Far from adopting a more static role, plaque-associated microglia retained rapid process and membrane movement at the plaque/glia interface. Microglia internalized systemically injected amyloid-binding dye at a much higher rate in the vicinity of plaques. These results indicate a role for microglia in plaque maintenance and provide a model with multiple targets for therapeutic intervention.