Visomitin

CAS No. 934826-68-3

Visomitin( SKQ1 bromide | PDTP )

Catalog No. M16686 CAS No. 934826-68-3

Visomitin (SKQ1 bromide, PDTP) is a mitochondria-targeted antioxidant that decreases transmembrane potential and production of reactive oxygen species (ROS).

Purity : >98% (HPLC)

COA Datasheet HNMR HPLC MSDS Handing Instructions
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Biological Information

  • Product Name
    Visomitin
  • Note
    Research use only, not for human use.
  • Brief Description
    Visomitin (SKQ1 bromide, PDTP) is a mitochondria-targeted antioxidant that decreases transmembrane potential and production of reactive oxygen species (ROS).
  • Description
    Visomitin (SKQ1 bromide, PDTP) is a mitochondria-targeted antioxidant that decreases transmembrane potential and production of reactive oxygen species (ROS); prevents neuronal loss and synaptic damage in a rat model of spontaneous Alzheimer’s disease, slows development of age-related ocular pathologies in murine, porcine, bovine, and canine model systems.(In Vitro):Direct treatment of tumor infiltrating leukocytes with Visomitin (SkQ1) does not influence their cytotoxicity against Panc02 cells. While Visomitin does not affect viability of the cell lines, this drug at 500 nM concentration reduces heavily the proliferation of human PDAC cells.(In Vivo):Regarding systemic angiogenic factors, it is observed in serum of Pancreatic ductal adenocarcinoma (PDAC) bearing mice a decrease in KC in the group of continuous treatment with Visomitin (SkQ1). Treatment of the mice with Visomitin increases the level of VEGF molecules. The amount of MIP1a and prolactin is reduced in all Visomitin treatment groups or after the follow-up treatment, respectively. Also, an increase in the IL-6 and IL-13 amount is found in the Visomitin treated groups. TGF-b amount is decreased in the pretreatment setting. On the contrary, all schemes of the Visomitin treatment decrease the NKT cell percentage. The Visomitin treatment has prolonged the median survival of PDAC-bearing mice, but the difference does not reach the level of significance defined.
  • In Vitro
    Direct treatment of tumor infiltrating leukocytes with Visomitin (SkQ1) does not influence their cytotoxicity against Panc02 cells. While Visomitin does not affect viability of the cell lines, this drug at 500 nM concentration reduces heavily the proliferation of human PDAC cells.
  • In Vivo
    Regarding systemic angiogenic factors, it is observed in serum of Pancreatic ductal adenocarcinoma (PDAC) bearing mice a decrease in KC in the group of continuous treatment with Visomitin (SkQ1). Treatment of the mice with Visomitin increases the level of VEGF molecules. The amount of MIP1a and prolactin is reduced in all Visomitin treatment groups or after the follow-up treatment, respectively. Also, an increase in the IL-6 and IL-13 amount is found in the Visomitin treated groups. TGF-b amount is decreased in the pretreatment setting. On the contrary, all schemes of the Visomitin treatment decrease the NKT cell percentage. The Visomitin treatment has prolonged the median survival of PDAC-bearing mice, but the difference does not reach the level of significance defined.
  • Synonyms
    SKQ1 bromide | PDTP
  • Pathway
    Others
  • Target
    Other Targets
  • Recptor
    Others
  • Research Area
    Other Indications
  • Indication
    Other Disease

Chemical Information

  • CAS Number
    934826-68-3
  • Formula Weight
    617.61
  • Molecular Formula
    C36H42BrO2P
  • Purity
    >98% (HPLC)
  • Solubility
    DMSO: ≥29 mg/mL ( < 1 mg/ml refers to the product slightly soluble or insoluble )
  • SMILES
    CC1=C(C(=O)C(=CC1=O)CCCCCCCCCC[P+](C2=CC=CC=C2)(C3=CC=CC=C3)C4=CC=CC=C4)C.[Br-]
  • Chemical Name
    (10-(4,5-dimethyl-3,6-dioxocyclohexa-1,4-dien-1-yl)decyl)triphenylphosphonium bromide

Shipping & Storage Information

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

Reference

1. Novikova YP, et al. Biochemistry (Mosc). 2014 Oct;79(10):1101-10. 2. Stefanova NA, et al. Aging (Albany NY). 2016 Oct 6;8(11):2713-2733. 3. Skulachev VP, et al. Biochem Biophys Res Commun. 2013 Nov 15;441(2):275-9. 4. Brzheskiy VV, et al. Adv Ther. 2015 Dec;32(12):1263-79.
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