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经验公式(希尔记法):
C15H15N3O6
化学文摘社编号:
分子量:
333.30
NACRES:
NA.77
PubChem Substance ID:
UNSPSC Code:
12352200
MDL number:
InChI key
UUIYULWYHDSXHL-NSHDSACASA-N
SMILES string
N[C@@H](CN1C=CC(=O)N(Cc2ccccc2C(O)=O)C1=O)C(O)=O
InChI
1S/C15H15N3O6/c16-11(14(22)23)8-17-6-5-12(19)18(15(17)24)7-9-3-1-2-4-10(9)13(20)21/h1-6,11H,7-8,16H2,(H,20,21)(H,22,23)/t11-/m0/s1
assay
≥98% (HPLC)
form
powder
color
white to off-white
solubility
DMSO: ≥5 mg/mL at 60 °C (with warming for 5 minutes)
storage temp.
−20°C
Biochem/physiol Actions
UBP302 is a selective GluR5 antagonist.
UBP302 is a selective GluR5 antagonist. UBP302 is the active enantiomer of UB296 and is one of the most potent GluR5 antagonists available for research use.
Preparation Note
UBP302 is soluble in DMSO at a concentration ≥5 mg/ml.
Sandy Stayte et al.
Experimental neurology, 323, 113062-113062 (2019-09-13)
The excitatory neurotransmitter glutamate is essential in basal ganglia motor circuits and has long been thought to contribute to cell death and degeneration in Parkinson's disease (PD). While previous research has shown a significant role of NMDA and AMPA receptors
Steven L Miller et al.
Toxicology and applied pharmacology, 284(2), 204-216 (2015-02-18)
Inhibition of acetylcholinesterase (AChE) after nerve agent exposure induces status epilepticus (SE), which causes brain damage or death. The development of countermeasures appropriate for the pediatric population requires testing of anticonvulsant treatments in immature animals. In the present study, exposure
James P Apland et al.
The Journal of pharmacology and experimental therapeutics, 351(2), 359-372 (2014-08-27)
Exposure to nerve agents induces prolonged status epilepticus (SE), causing brain damage or death. Diazepam (DZP) is the current US Food and Drug Administration-approved drug for the cessation of nerve agent-induced SE. Here, we compared the efficacy of DZP with
Kelli Solly et al.
Journal of biomolecular screening, 20(6), 708-719 (2015-02-24)
GluK1, a kainate subtype of ionotropic glutamate receptors, exhibits an expression pattern in the CNS consistent with involvement in pain processing and migraine. Antagonists of GluK1 have been shown to reduce pain signaling in the spinal cord and trigeminal nerve
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