HIV-1 Integrase Inhibitor 1

CAS No. 2146094-22-4

HIV-1 Integrase Inhibitor 1( —— )

Catalog No. M13429 CAS No. 2146094-22-4

A novel compound that disrupts the HIV-1 integrase LEDGF interaction.

Purity : >98% (HPLC)

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

Biological Information

  • Product Name
    HIV-1 Integrase Inhibitor 1
  • Note
    Research use only, not for human use.
  • Brief Description
    A novel compound that disrupts the HIV-1 integrase LEDGF interaction.
  • Description
    A novel compound that disrupts the HIV-1 integrase LEDGF interaction; produces an ALLINI-like phenotype through engagement of IN sites distinct from the LEDGF pocket.
  • In Vitro
    ——
  • In Vivo
    ——
  • Synonyms
    ——
  • Pathway
    Microbiology/Virology
  • Target
    HIV
  • Recptor
    HIV
  • Research Area
    ——
  • Indication
    ——

Chemical Information

  • CAS Number
    2146094-22-4
  • Formula Weight
    480.579
  • Molecular Formula
    C26H28N2O5S
  • Purity
    >98% (HPLC)
  • Solubility
    ——
  • SMILES
    CC(C)(C)NS(=O)(=O)C1=CC=CC=C1C2=CC(=CC=C2)C(=O)NC3=CC=C(C=C3)CCC(=O)O
  • Chemical Name
    3-(4-(2'-(N-(tert-butyl)sulfamoyl)-[1,1'-biphenyl]-3-carboxamido)phenyl)propanoic acid

Shipping & Storage Information

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

Reference

1. Burlein C, et al. ACS Chem Biol. 2017 Nov 17;12(11):2858-2865.
molnova catalog
related products
  • Atazanavir sulfate

    A highly potent HIV-1 protease inhibitor that exhibits potent anti-HIV activity EC50 of 2.6-5.3 nM and EC90 of 9-15 nM in cell culture.

  • NBD-11021

    A small molecule, full antagonist of CD4 that blocks gp120-CD4 interaction.

  • Escin IA;Aescin IA

    Escin IA is a triterpene saponin isolated from horse chestnut which inhibits HIV-1 protease with IC50 values of 35 μM. Escin IA has anti-TNBC metastasis activity and its action mechanisms involved inhibition of epithelial-mesenchymal transition process by down-regulating LOXL2 expression.