Manganese chloride

CAS No. 7773-01-5

Manganese chloride( —— )

Catalog No. M19828 CAS No. 7773-01-5

Manganese chloride inhibits proliferation in a dose- and time-dependent manner induces G0/G1 and S phase arrest and apoptosis in A549 cells.

Purity : >98% (HPLC)

COA Datasheet HNMR HPLC MSDS Handing Instructions
Size Price / USD Stock Quantity
10MG 49 In Stock
25MG 76 In Stock
50MG 115 In Stock
100MG Get Quote In Stock
200MG Get Quote In Stock
500MG Get Quote In Stock
1G Get Quote In Stock

Biological Information

  • Product Name
    Manganese chloride
  • Note
    Research use only, not for human use.
  • Brief Description
    Manganese chloride inhibits proliferation in a dose- and time-dependent manner induces G0/G1 and S phase arrest and apoptosis in A549 cells.
  • Description
    Manganese chloride inhibits proliferation in a dose- and time-dependent manner induces G0/G1 and S phase arrest and apoptosis in A549 cells.
  • In Vitro
    ——
  • In Vivo
    ——
  • Synonyms
    ——
  • Pathway
    Apoptosis
  • Target
    Apoptosis
  • Recptor
    Apoptosis
  • Research Area
    ——
  • Indication
    ——

Chemical Information

  • CAS Number
    7773-01-5
  • Formula Weight
    125.84
  • Molecular Formula
    Cl2Mn
  • Purity
    >98% (HPLC)
  • Solubility
    Water:794.7 mM
  • SMILES
    [Cl-].[Cl-].[Mn++]
  • Chemical Name
    ——

Shipping & Storage Information

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

Reference

1.Zhao P et al. Manganese chloride-induced G0/G1 and S phase arrest in A549 cells. Toxicology. 2008 Aug 19;250(1):39-46.
molnova catalog
related products
  • BTZO-1

    BTZO-1 is an antioxidant response element (ARE) activator with cardioprotective activity.

  • UCF 101

    UCF 101 is a specific inhibitor of HtrA2 and reduces apoptosis in PC12 cells.

  • GSK854

    GSK854 is a highly selective and potent inhibitor of troponin I interacting kinase (TNNI3K) that inhibits myocardial infarction-injured cellular pyroptosis and apoptosis in mice, which may limit oxidative stress, injury, and adverse remodeling in the ischemic heart.