VU 29

CAS No. 890764-36-0

VU 29( —— )

Catalog No. M22409 CAS No. 890764-36-0

VU-29 is a positive allosteric mGlu5 receptor modulator with EC50=9 nM and Ki=244 nM for rmGluR5.

Purity : >98% (HPLC)

COA Datasheet HNMR HPLC MSDS Handing Instructions
Size Price / USD Stock Quantity
2MG 43 In Stock
5MG 72 In Stock
10MG 125 In Stock
25MG 260 In Stock
50MG 430 In Stock
100MG 620 In Stock
200MG Get Quote In Stock
500MG Get Quote In Stock
1G Get Quote In Stock

Biological Information

  • Product Name
    VU 29
  • Note
    Research use only, not for human use.
  • Brief Description
    VU-29 is a positive allosteric mGlu5 receptor modulator with EC50=9 nM and Ki=244 nM for rmGluR5.
  • Description
    VU-29 is a positive allosteric mGlu5 receptor modulator with EC50=9 nM and Ki=244 nM for rmGluR5. It is selective for mGluR5 relative to other mGluR subtypes (EC50: rmGluR1/rmGluR2=557 nM/1.5 μM; hmGluR4=154 nM).
  • In Vitro
    ——
  • In Vivo
    VU-29 (500 nM) potentiates DHPG induced increases in phosphoinositide (PI) hydrolysis in rat hippocampal slices. VU-29 potentiates threshold TBS-induced long term potentiation (LTP) in rat hippocampal CA1 region. VU-29 (1 μM) potentiates chemically induced mGluR-long term depression (LTD) in area CA1 of the rat hippocampus. VU-29 (1 μM) potentiates stimulus-induced NMDA receptor-independent LTD.
  • Synonyms
    ——
  • Pathway
    Neuroscience
  • Target
    GluR
  • Recptor
    mGluR
  • Research Area
    ——
  • Indication
    ——

Chemical Information

  • CAS Number
    890764-36-0
  • Formula Weight
    384.39
  • Molecular Formula
    C22H16N4O3
  • Purity
    >98% (HPLC)
  • Solubility
    In Vitro:?DMSO : 50 mg/mL (130.08 mM)
  • SMILES
    [O-][N+](=O)c1ccc(cc1)C(=O)Nc1cc(nn1-c1ccccc1)-c1ccccc1
  • Chemical Name
    ——

Shipping & Storage Information

  • Storage
    (-20℃)
  • Shipping
    With Ice Pack
  • Stability
    ≥ 2 years

Reference

1.Chen Y , Nong Y , Goudet C , et al. Interaction of novel positive allosteric modulators of metabotropic glutamate receptor 5 with the negative allosteric antagonist site is required for potentiation of receptor responses.[J]. Molecular Pharmacology, 2007, 71(5):1389-1398.
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