Sunitinib

SKU: orb1310675

Description

Sunitinib

Research Area

Cardiovascular Research, Cell Biology, Signal Transduction

Key Properties

• CAS Number: 557795-19-4
• MW: 398.47
• Purity: 99.67%
• Formula: C₂₂H₂₇FN₄O₂
• SMILES: C(=C\1/C=2C(NC1=O)=CC=C(F)C2)\C3=C(C)C(C(NCCN(CC)CC)=O)=C(C)N3
• Target: VEGFR,Autophagy,PDGFR,FLT,c-Kit,IRE1,Apoptosis,Mitophagy
• Solubility: Ethanol:< 1 mg/mL (insoluble or slightly soluble);H2O:< 1 mg/mL (insoluble or slightly soluble);10% DMSO+40% PEG300+5% Tween 80+45% Saline:1.25 mg/mL (3.14 mM);DMSO:25 mg/mL (62.74 mM)

Bioactivity

• Target IC50:
  VEGFR2:80 nM|PDGFRβ:2 nM
• In Vivo:
  METHODS: To assay antitumor activity in vivo, Sunitinib (1-40 mg/kg in a citrate-buffered solution (pH 3.5)) was administered by gavage to athymic nu/nu mice harboring human leukemia tumors MV4;11 once a day until the tumors regressed. RESULTS: Sunitinib demonstrated dose-dependent efficacy when administered at 4 0 and 20 mg/kg/d and regressed established large subcutaneous tumors. METHODS: To assay antitumor activity in vivo, Sunitinib (40-80 mg/kg in CMC) was administered by gavage to athymic nu/nu mice injected with breast cancer cells MDA-MB-435/HAL once a day for twenty-one days. RESULTS: Sunitinib treatment of hormonal mice resulted in a significant reduction in serum PYD levels, confirming the in vivo inhibitory effect of osteolysis. Using BLI, Sunitinib showed 64% inhibition of bone tumor growth at 40 mg/kg/day for 21 days of treatment and 89% inhibition at 80 mg/kg/day.
• In Vitro:
  METHODS: FLT3-ITD cell line MV4;11 and FLT3-WT cell line OC1-AML5 were treated with Sunitinib (0.001-10 µM) for 48 h, and cell viability was assayed using Alamar blue assay. RESULTS: Sunitinib significantly inhibited the proliferation of MV4;11 and OC1-AML5 cells in a dose-dependent manner, with IC50s of 8 nM and 14 nM, respectively. METHODS: GIST-T1 gastrointestinal mesenchymal stromal tumor cells were treated with Sunitinib (10-40 nM) for 48 h, and the expression levels of target proteins were detected by Western Blot. RESULTS: Sunitinib inhibited the autophosphorylation of c-KIT in a dose-dependent manner, and effectively blocked the phosphorylation of the downstream effectors of c-KIT, Akt and ERK, without affecting the phosphorylated forms of STAT3 and STAT5.
• Cell Research:
  Cells are starved overnight in medium containing 0.1% FBS prior to addition of Sunitinib and FL (50 ng/mL; FLT3-WT cells only). Proliferation is measured after 48 hours of culture using the Alamar Blue assay or trypan blue cell viability assays. Apoptosis is measured 24 hours after Sunitinib addition by Western blotting to detect cleavage of poly (ADP-ribose) polymerase (PARP) or levels of caspase-3. (Only for Reference)

Storage & Handling

• Storage: 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

Apoptosis, Autophagy, cKit, c-Kit, inhibit, IRE1, Platelet-derived growth factor receptor, Mitophagy, Mitochondrial Autophagy, Inositol requiring enzyme 1, Inhibitor, FLT3, SU 11248, SU11248, SU-11248, Sunitinib, PDGFR, PDGFRβ, VEGFR2, VEGFR, Vascular endothelial growth factor receptor

Compound Identifiers

PubChem CID

5329102

Ryan Tsz-Hei Tse 1, Christine Yim-Ping Wong 1, Xiaofan Ding 2, Carol Ka-Lo Cheng 1, Chit Chow 3, Ronald Cheong-Kin Chan 3, Joshua Hoi-Yan Ng 4, Victor Wai-Lun Tang 4, Peter Ka-Fung Chiu 1, Jeremy Yuen-Chun Teoh 1, Nathalie Wong 2, Ka-Fai To 3, Chi-Fai Ng The establishment of kidney cancer organoid line in drug testing Cancer Med, (2024)

PubMed: 38923304

Applications

Cell Culture