KU-55933

SKU: orb1305169

Description

KU-55933

Research Area

Cell Biology, Molecular Biology, Signal Transduction

Key Properties

• CAS Number: 587871-26-9
• MW: 395.49
• Purity: 97.21%
• Formula: C₂₁H₁₇NO₃S₂
• SMILES: O=c1cc(oc(c1)-c1cccc2Sc3ccccc3Sc12)N1CCOCC1
• Target: Autophagy,ATM/ATR,PI3K,mTOR,DNA-PK
• Solubility: Ethanol:19.8 mg/mL (50.06 mM);DMSO:16.67 mg/mL (42.15 mM);10% DMSO+40% PEG300+5% Tween 80+45% Saline:2 mg/mL (5.06 mM)

Bioactivity

• Target IC50:
  PI3K:16600 nM|mTOR:9300 nM|DNA-PK:2500 nM|ATM:12.9 nM
• In Vivo:
  METHODS: To test the anti-infective activity in vivo, Eflornithine hydrochloride hydrate (25-50 mg/kg) and hydroxyurea (50-100 mg/kg) were orally administered to B. microti infected BALB/c mice once daily for 5 days. RESULTS: Oral administration of hydroxyurea and Eflornithine inhibited the proliferation of Bifidobacterium microti in mice by 60.1% and 78.2%, respectively. hydroxyurea-DA and Eflornithine-DA combination treatment showed higher efficacy of chemotherapy than monotherapy.
• In Vitro:
  METHODS: Ovarian cancer cells SKOV-3 were treated with Eflornithine hydrochloride hydrate (1-100 µM) for 48 h. Cell viability was measured by PrestoBlue assay. RESULTS: Eflornithine significantly inhibited the viability of SKOV-3 cells in a dose-dependent manner. METHODS: MYCN2 (-) and MYCN2 (+) NB cells were treated with Eflornithine hydrochloride hydrate (5 mM) and putrescine/spermidine/spermine for 72 h. Cell migration was detected by wound healing assay. RESULTS: Significant differences in cell migration were observed between untreated control cells and Eflornithine-treated cells. eflornithine inhibited cell migration by 73% and 72% in MYCN2 (-) and MYCN2 (+) cells, respectively. Supplementation of the medium with polyamines attenuated the effect of Eflornithine on MYCN2 (-) and MYCN2 (+) cells.
• Cell Research:
  U2OS cells are exposed to ionizing radiation (3, 5, or 15 Gy) or UV (5 or 50 J/m2) and the ATM response determined by Western blot analysis of p53 serine 15 phosphorylation and stabilization of wild-type p53. Whole cell extracts are obtained from each time point, proteins separated by SDS-PAGE, and the ATM-specific increase in phosphorylated serine 15 measured with a p53 phospho-serine 15 specific antibody. Overall p53 stabilization with time is also observed with a p53-specific antibody (DO-1). Similarly, for studying ATM-dependent phosphorylations on H2AX, CHK1, NBS1, and SMC1, the following antibodies are used: CHK1 phospho-serine 345 and NBS1 phospho-serine 343 antibodies. Histone H2A (H-124) and CHK1 antibodies are also used, as well as SMC1 and SMC1 phospho-serine 966 antibodies. For determination of a cellular IC50 for KU-55933, the peak response time for p53 serine 15 phosphorylation of 2 hours is used to monitor inhibition of ATM. KU-55933 is titrated onto cells and preincubated for 1 hour before ionizing radiation. Using scanning densitometry, the percentage inhibition relative to vehicle control is calculated, and the IC50 value is calculated as for the in vitro determinations.(Only for Reference)

Storage & Handling

• Storage: store at low temperature,keep away from moisture | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice/Shipping at ambient temperature.
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

Alternative Names

inhibit, KU55933, KU-55933, KU 55933, mTOR, Inhibitor, DNA-PK, DNAPK, Autophagy, ATR, Ataxia telangiectasia mutated, ATM/ATR, ATM and RAD3 related, ATM Kinase Inhibitor, ATM, PI3K

Compound Identifiers

PubChem CID

5278396