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SKLB 1028

CAS No. 1350544-93-2

SKLB 1028( —— )

Catalog No. M34711 CAS No. 1350544-93-2

SKLB 1028 (Ruserontinib) is a new type of oral multikinase inhibitor of EGFR, FLT3, and Abl. SKLB 1028 shows excellent activity in FLT3-driven AML models and considerable potency in CML models containing Abl mutants.

Purity : >98% (HPLC)

COA Datasheet HNMR HPLC MSDS Handing Instructions
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Biological Information

  • Product Name
    SKLB 1028
  • Note
    Research use only, not for human use.
  • Brief Description
    SKLB 1028 (Ruserontinib) is a new type of oral multikinase inhibitor of EGFR, FLT3, and Abl. SKLB 1028 shows excellent activity in FLT3-driven AML models and considerable potency in CML models containing Abl mutants.
  • Description
    Ruserontinib (SKLB1028) is an orally active multikinase inhibitor of EGFR, FLT3 and Abl, with an IC50 value of 55 nM for human FLT3, and has antitumor activity.
  • In Vitro
    ——
  • In Vivo
    Animal Model:MV4-11 and K562 xenograft NOD-SCID modelsDosage:5, 10, 20 mg/kg,70 mg/kg Administration:orally once daily, 18 days Result:Prevented tumor growth at a dose of 5 mg/kg, and caused rapid and complete tumor regression in both groups of mice at a dose of 10 or 20 mg/kg.Significantly inhibited the proliferation and induced apoptosis of MV4-11 and K562 cells at a dose of 70 mg/kg.
  • Synonyms
    ——
  • Pathway
    Angiogenesis
  • Target
    EGFR
  • Recptor
    EGFR | FLT | Bcr-Abl
  • Research Area
    ——
  • Indication
    ——

Chemical Information

  • CAS Number
    1350544-93-2
  • Formula Weight
    443.55
  • Molecular Formula
    C24H29N9
  • Purity
    >98% (HPLC)
  • Solubility
    In Vitro:?DMSO : 250 mg/mL (563.63 mM; Ultrasonic )
  • SMILES
    C(C)(C)N1C=2C(N=C1NC=3C=CC=NC3)=CN=C(NC4=CC=C(C=C4)N5CCN(C)CC5)N2
  • Chemical Name
    ——

Shipping & Storage Information

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

Reference

1. Z-X Cao, et al. SKLB1028, a novel oral multikinase inhibitor of EGFR, FLT3 and Abl, displays exceptional activity in models of FLT3-driven AML and considerable potency in models of CML harboring Abl mutants. Leukemia. 2012 Aug;26(8):1892-5.?
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