246-Tribromophenyl caproate

CAS No. 16732-09-5

246-Tribromophenyl caproate( —— )

Catalog No. M20929 CAS No. 16732-09-5

246-Tribromophenyl caproate is a potent antifungal agent.

Purity : >98% (HPLC)

COA Datasheet HNMR HPLC MSDS Handing Instructions
Size Price / USD Stock Quantity
200MG 43 Get Quote
500MG Get Quote Get Quote
1G Get Quote Get Quote

Biological Information

  • Product Name
    246-Tribromophenyl caproate
  • Note
    Research use only, not for human use.
  • Brief Description
    246-Tribromophenyl caproate is a potent antifungal agent.
  • Description
    246-Tribromophenyl caproate is a potent antifungal agent.
  • In Vitro
    ——
  • In Vivo
    2,4,6-Tribromophenyl caproate (2,4,6-tribromophenyl caproic acid ester) contains at least one selected from Sharon skin or a salt thereof transdermal absorption patch according to any one of the first term through the fifth term.
  • Synonyms
    ——
  • Pathway
    Microbiology/Virology
  • Target
    Antifungal
  • Recptor
    Antifungal
  • Research Area
    ——
  • Indication
    ——

Chemical Information

  • CAS Number
    16732-09-5
  • Formula Weight
    428.94
  • Molecular Formula
    C12H13Br3O2
  • Purity
    >98% (HPLC)
  • Solubility
    DMSO:50 mg/mL (116.57 mM)
  • SMILES
    CCCCCC(=O)Oc1c(Br)cc(Br)cc1Br
  • Chemical Name
    ——

Shipping & Storage Information

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

Reference

molnova catalog
related products
  • Hyodeoxycholic acid

    Hyodeoxycholic Acid has been used in trials studying the treatment of Hypercholesterolemia.

  • Gamitrinib TPP hexaf...

    Gamitrinib TPP hexafluorophosphate is a mitochondrial-targeted HSP90 inhibitor with anticancer activity, which can regulate cell cycle and cell homeostasis and can be used to study cancer, neurodegenerative diseases and viral infections.

  • Asebogenin

    Asebogenin is a compound fractionated from Salvia miltiorrhiza with antifungal activity, inhibition of GPVI-induced platelet reactions, and inhibition of NET formation induced by pro-inflammatory stimuli.