1. Protein Tyrosine Kinase/RTK
    Autophagy
  2. VEGFR
    PDGFR
    Autophagy

Sunitinib (Synonyms: SU 11248)

Cat. No.: HY-10255A Purity: 99.56%
Data Sheet SDS Handling Instructions

Sunitinib is a potent tyrosine kinase inhibitor targeting VEGFR2 and PDGFRβ with IC50 of 80 nM and 2 nM, respectively.

For research use only. We do not sell to patients.
Sunitinib Chemical Structure

Sunitinib Chemical Structure

CAS No. : 557795-19-4

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Other Forms of Sunitinib:

    Sunitinib purchased from MCE. Usage Cited in: Int J Clin Exp Pathol. 2015 Apr 1;8(4):3871-81.

    The relationship between SOX9 and Raf/MEK/ERK signaling pathway. Co-treatment of si-SOX9-1 and Sorafenib (10uM, 15uM)/Sunitinib (2 uM, 3 uM) significantly decreases expression of MEK1 and its phosphorylated protein (p-MEK1/2, p-ERK1/2) as assayed by Western blot (with GAPDH as internal control).

    Sunitinib purchased from MCE. Usage Cited in: Int J Clin Exp Pathol. 2015 Apr 1;8(4):3871-81.

    The relationship between SOX9 and Raf/MEK/ERK signaling pathway. Co-treatment of si-SOX9-1 and Sorafenib (10uM, 15uM)/Sunitinib (2 uM, 3 uM) significantly decreases expression of MEK1 and its phosphorylated protein (p-MEK1/2, p-ERK1/2) as assayed by RT-PCR (with β-actin as internal control).

    Sunitinib purchased from MCE. Usage Cited in: J Med Chem. 2016 Sep 22;59(18):8456-72.

    Effect of compounds 1 (Imatinib), 2 (Sunitinib), and 35 on cKIT mediated signaling pathways in GIST-T1 and GIST-5R cancer cell lines.
    • Biological Activity

    • Protocol

    • Technical Information

    • Purity & Documentation

    • References

    Description

    Sunitinib is a potent tyrosine kinase inhibitor targeting VEGFR2 and PDGFRβ with IC50 of 80 nM and 2 nM, respectively.

    IC50 & Target

    IC50: 2 nM (PDGFRβ), 80 nM (VEGFR2)[1]

    In Vitro

    Sunitinib Malate is also a good inhibitor of KIT and FLT-3[1]. In biochemical assays, Sunitinib (SU11248) exhibits competitive inhibition (with regard to ATP) against Flk-1 and PDGFRβ with Ki values of 9 nM and 8 nM, respectively. Sunitinib is also a competitive, albeit less potent, inhibitor of FGFR1 tyrosine kinase activity, with a Ki value of 0.83 μM. In addition to these three structurally related split kinase domain RTKs, the activity of Sunitinib has also been evaluated against a broad panel of additional tyrosine and serine/threonine kinases. In these biochemical assays, the IC50 values for Sunitinib are generally at least 10-fold higher than those for Flk-1 and PDGFR (e.g., IC50values of: >10 μM for EGFR and Cdk2; 4 μM for Met; 2.4 μM for IGFR-1; 0.8 μM for Abl; and 0.6 μM for Src)[2]. In RS4;11 cells (FLT3-WT), treatment with Sunitinib (SU11248) inhibits FLT3-WT phosphorylation in a dose-dependent manner with IC50 of approximately 250 nM. In MV4;11 cells that express FLT3-ITD, Sunitinib inhibits FLT3-ITD phosphorylation in a dose-dependent manner with an IC50 of 50 nM following a 2-hour treatment[3].

    In Vivo

    Sunitinib Malate has very good oral bioavailability, is highly efficacious in a number of preclinical tumor models, and is well tolerated at efficacious doses[1]. Sunitinib (80 mg/kg/day) inhibits the growth of established SF763T and Colo205 tumor xenografts in athymic mice. Sunitinib (SU11248) treatment effectively inhibits the growth of established tumor xenografts[2]. Sunitinib malate is an inhibitor of VEGFR, PDGFR, FGFR, and is used in the treatment of advanced renal cell carcinoma and gastrointestinal stromal tumors. Sunitinib malate-treated rats display much lower levels of tumor growth than untreated rats, and their tumors have much smaller necrotic areas and lower vascular density[4].

    Clinical Trial
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    References
    Preparing Stock Solutions
    Concentration Volume Mass 1 mg 5 mg 10 mg
    1 mM 2.5096 mL 12.5480 mL 25.0960 mL
    5 mM 0.5019 mL 2.5096 mL 5.0192 mL
    10 mM 0.2510 mL 1.2548 mL 2.5096 mL
    Please refer to the solubility information to select the appropriate solvent.
    Kinase Assay
    [2]

    Biochemical assays to determine the activity of Sunitinib against different protein kinases are performed. Ki values for SU11248 against Flk-1, PDGFRβ, and FGFR1 are determined using glutathione S-transferase-fusion proteins containing the complete cytoplasmic domain of the RTK. Cellular assays to directly determine the ability of SU11248 to inhibit ligand-dependent RTK phosphorylation or cell proliferation and mitogenic responses are performed using serum-starved cells stimulated with 40 ng/mL VEGF165 (Flk-1/KDR), 0.5 μg/mL basic FGF (FGFR), or 50 ng/mL PDGF-AA (PDGFRα) or PDGF-BB (PDGFRβ)[2]. MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Cell Assay
    [3]

    Sunitinib (SU11248) is dissolved in DMSO and stored, and then diluted with appropriate media before use[3].

    RS4;11 and MV4;11 cell lines are starved overnight in medium containing 0.1% FBS prior to addition of SU11248 (1 nM, 5 nM, 10 nM, 25 nM, 75 nM, 100 nM, 250 nM, 500 nM) and FL (50 ng/mL; FLT3-WT cells only). Proliferation is measured after 48 hours of culture using the Alamar Blue assay in triplicate for each condition, as described by the manufacturer. Trypan blue cell viability assays are performed in parallel and yielded similar results[3]. MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Animal Administration
    [2][4]

    Sunitinib (SU11248) is prepared as a carboxymethyl cellulose suspension (Mice)[2].

    Mice[2]
    Female nu/nu mice (8-12 weeks old, 25 grams) are used. Briefly, 3-5×106 tumor cells are implanted s.c. into the hind flank region of mice on day 0. Daily treatment of tumor-bearing mice with oral administration of SU11248 as a carboxymethyl cellulose suspension or as a citrate buffered (pH 3.5) solution is initiated once the tumors reached the indicated average size. Tumor growth is evaluated based on twice-weekly measurement of tumor volume. Typically, studies are terminated when tumors in vehicle-treated animals reach an average size of 1000 mm3 or when the tumors are judged to adversely effect the well being of the animals.
    Rat[4]
    Adult male Wistar rats (325-349 g) are used. To validate the ability of the time-lapse imaging method to evaluate the anti-angiogenic effects for a given drug treatment, two drug studies are conducted. In the first study, mesenteric windows are harvested from adult male Wistar rats and cultured for 3 days according to the two experimental groups: 1) 10% serum (n=8 tissues from 4 rats), and 2) 10% serum+Sunitinib (5 μM; n=8 tissues from 4 rats). MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    References
    Molecular Weight

    398.47

    Formula

    C₂₂H₂₇FN₄O₂

    CAS No.

    557795-19-4

    Storage
    Powder -20°C 3 years
      4°C 2 years
    In solvent -80°C 6 months
      -20°C 1 month
    Shipping

    Room temperature in continental US; may vary elsewhere

    Solvent & Solubility

    DMSO: 25 mg/mL

    * "<1 mg/mL" means slightly soluble or insoluble. "≥" means soluble, but saturation unknown.

    Purity: 99.56%

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    Product Name:
    Sunitinib
    Cat. No.:
    HY-10255A
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