D5446
7,8-Dihydroxyflavone hydrate
≥98% (HPLC)
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About This Item
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Quality Level
assay
≥98% (HPLC)
form
solid
storage condition
desiccated
solubility
DMSO: 24 mg/mL
storage temp.
room temp
SMILES string
Oc1ccc2C(=O)C=C(Oc2c1O)c3ccccc3
InChI
1S/C15H10O4/c16-11-7-6-10-12(17)8-13(19-15(10)14(11)18)9-4-2-1-3-5-9/h1-8,16,18H
InChI key
COCYGNDCWFKTMF-UHFFFAOYSA-N
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Application
7,8-Dihydroxyflavone hydrate has been used as tropomyosin-receptor-kinase B (TrkB) agonist in mice and to inhibit TrkB for monitoring evoked excitatory postsynaptic currents (eEPSCs).
Biochem/physiol Actions
7,8-Dihydroxyflavone (7,8-DHF) may be used to help identify and differentiate the physiological effects and cell signaling pathways mediated by TrkB activation, such as those involving, memory, vasorelaxation and hypertension. 7,8-DHF elicits protection in scopolamine induced Alzheimer-like pathologic dysfunction.
7,8-Dihydroxyflavone is a selective tyrosine kinase receptor B (TrkB) receptor agonist. It manifests all the therapeutic effects of brain-derived neurotrophic factor (BDNF)—such as protecting neurons from apoptosis, inhibiting kainic acid-induced toxicity, decreasing infarct volumes in stroke, and neuroprotecting in an animal model of Parkinson′s disease—without the poor pharmacokinetic profile of BDNF limiting its therapeutic potential.
Storage Class
11 - Combustible Solids
wgk_germany
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
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7, 8-dihydroxyflavone ameliorates scopolamine-induced Alzheimer-like pathologic dysfunction
Rejuvenation Research, 17(3), 249-254 (2014)
Autism-like behavior caused by deletion of vaccinia-related kinase 3 is improved by TrkB stimulation
The Journal of Experimental Medicine, 214(10), 2947-2966 (2017)
Vasorelaxing and antihypertensive effects of 7, 8-dihydroxyflavone
American Journal of Hypertension, 27(5), 750-760 (2013)
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Angelman syndrome is a rare neurodevelopmental disorder caused by a mutation in the maternal allele of the gene Ube3a The primary symptoms of Angelman syndrome are severe cognitive deficits, impaired motor functions, and speech disabilities. Analogous phenotypes have been detected
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