Home - Products - Cell Cycle/DNA Damage - HDAC - 4-(1H-Pyrazol-4-yl)-7-((2-(trimethylsilyl)ethoxy)-methyl)-7H-pyrrolo[2,3-d]pyrimidine

4-(1H-Pyrazol-4-yl)-7-((2-(trimethylsilyl)ethoxy)-methyl)-7H-pyrrolo[2,3-d]pyrimidine

CAS No. 941685-27-4

4-(1H-Pyrazol-4-yl)-7-((2-(trimethylsilyl)ethoxy)-methyl)-7H-pyrrolo[2,3-d]pyrimidine( —— )

Catalog No. M17678 CAS No. 941685-27-4

Detail unknown.

Purity : >98% (HPLC)

COA Datasheet HNMR HPLC MSDS Handing Instructions
Size Price / USD Stock Quantity
25MG 48 Get Quote
50MG 67 Get Quote
100MG 104 Get Quote
200MG Get Quote Get Quote
500MG Get Quote Get Quote
1G Get Quote Get Quote

Biological Information

  • Product Name
    4-(1H-Pyrazol-4-yl)-7-((2-(trimethylsilyl)ethoxy)-methyl)-7H-pyrrolo[2,3-d]pyrimidine
  • Note
    Research use only, not for human use.
  • Brief Description
    Detail unknown.
  • Description
    Detail unknown.
  • In Vitro
    ——
  • In Vivo
    ——
  • Synonyms
    ——
  • Pathway
    Cell Cycle/DNA Damage
  • Target
    HDAC
  • Recptor
    Others
  • Research Area
    ——
  • Indication
    ——

Chemical Information

  • CAS Number
    941685-27-4
  • Formula Weight
    315.45
  • Molecular Formula
    C15H21N5OSi
  • Purity
    >98% (HPLC)
  • Solubility
    In Vitro:?DMSO : 100 mg/mL (317.01 mM)
  • SMILES
    C[Si](C)(C)CCOCn1ccc2c(ncnc12)c1c[nH]nc1
  • Chemical Name
    ——

Shipping & Storage Information

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

Reference

molnova catalog
related products
  • BRD4097

    BRD4097, a negative control in the HDAC1/2/3/8 assay, is a selective histone deacetylase (HDAC3) inhibitor that can be used to protect b-cells and improve insulin resistance, help promote cognitive function and enhance learning and memory formation.

  • TH34

    TH34 is an HDAC6/8/10 inhibitor (IC50s: 4.6/1.9/7.7 μM). It shows high selectivity over HDAC1/2/3.

  • Valproic acid sodium...

    A HDAC inhibitor that selectively inhibits the catalytic activity of class I HDACs, and induces proteasomal degradation of HDAC2.