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KT5823

CAS No. 126643-37-6

KT5823( —— )

Catalog No. M33394 CAS No. 126643-37-6

KT5823 is a selective and potent cGMP-dependent protein kinase (PKG) inhibitor with inhibitory effects on PKA and PKC.KT5823 increases thyroid-stimulating hormone-induced (Na+/I- symporter) NIS expression and iodide ion uptake by modulating sodium iodide symporter protein expression and activity in thyroid cells. KT5823 induces apoptosis.

Purity : >98% (HPLC)

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Biological Information

  • Product Name
    KT5823
  • Note
    Research use only, not for human use.
  • Brief Description
    KT5823 is a selective and potent cGMP-dependent protein kinase (PKG) inhibitor with inhibitory effects on PKA and PKC.KT5823 increases thyroid-stimulating hormone-induced (Na+/I- symporter) NIS expression and iodide ion uptake by modulating sodium iodide symporter protein expression and activity in thyroid cells. KT5823 induces apoptosis.
  • Description
    KT5823, a selective the cGMP-dependent protein kinase (PKG) inhibitor with an Ki value of 0.23 μM, it also inhibits PKA and PKC with Ki values of 10 μM and 4 μM, respectively. KT5823 is a staurosporine-related protein kinase inhibitor, increases thyroid-stimulating hormone-induced (Na+/I- symporter) NIS expression, and iodide uptake in thyroid cells. KT5823 arrests cells after the G0/G1 boundary and causes increases in the levels of apoptotic DNA fragmentation.
  • In Vitro
    ——
  • In Vivo
    ——
  • Synonyms
    ——
  • Pathway
    Apoptosis
  • Target
    Apoptosis
  • Recptor
    Apoptosis | PKA
  • Research Area
    ——
  • Indication
    ——

Chemical Information

  • CAS Number
    126643-37-6
  • Formula Weight
    495.53
  • Molecular Formula
    C29H25N3O5
  • Purity
    >98% (HPLC)
  • Solubility
    ——
  • SMILES
    C[C@]12N3C=4C5=C(C6=C(C4C=7C3=CC=CC7)CN(C)C6=O)C=8C(N5[C@](O1)(C[C@@]2(C(OC)=O)OC)[H])=CC=CC8
  • Chemical Name
    ——

Shipping & Storage Information

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

Reference

1. Gadbois DM, et al. Multiple kinase arrest points in the G1 phase of nontransformed mammalian cells are absent in transformed cells. Proc Natl Acad Sci U S A. 1992 Sep 15;89(18):8626-30.?
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