Sunitinib

RTK inhibitor CAS# 557795-19-4

Sunitinib

Catalog No. BCC4064----Order now to get a substantial discount!

Product Name & Size Price Stock
Sunitinib: 5mg $35 In Stock
Sunitinib: 10mg Please Inquire In Stock
Sunitinib: 20mg Please Inquire Please Inquire
Sunitinib: 50mg Please Inquire Please Inquire
Sunitinib: 100mg Please Inquire Please Inquire
Sunitinib: 200mg Please Inquire Please Inquire
Sunitinib: 500mg Please Inquire Please Inquire
Sunitinib: 1000mg Please Inquire Please Inquire
Related Products

Quality Control of Sunitinib

Number of papers citing our products

Chemical structure

Sunitinib

3D structure

Chemical Properties of Sunitinib

Cas No. 557795-19-4 SDF Download SDF
PubChem ID 5329102 Appearance Powder
Formula C22H27FN4O2 M.Wt 398.47
Type of Compound N/A Storage Desiccate at -20°C
Synonyms SU 11248
Solubility DMSO : 25 mg/mL (62.74 mM; Need ultrasonic and warming)
Chemical Name N-[2-(diethylamino)ethyl]-5-[(Z)-(5-fluoro-2-oxo-1H-indol-3-ylidene)methyl]-2,4-dimethyl-1H-pyrrole-3-carboxamide
SMILES CCN(CC)CCNC(=O)C1=C(NC(=C1C)C=C2C3=C(C=CC(=C3)F)NC2=O)C
Standard InChIKey WINHZLLDWRZWRT-ATVHPVEESA-N
Standard InChI InChI=1S/C22H27FN4O2/c1-5-27(6-2)10-9-24-22(29)20-13(3)19(25-14(20)4)12-17-16-11-15(23)7-8-18(16)26-21(17)28/h7-8,11-12,25H,5-6,9-10H2,1-4H3,(H,24,29)(H,26,28)/b17-12-
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of Sunitinib

DescriptionSunitinib is an oral, multi-targeted and small-molecule inhibitor of receptor tyrosine kinase (RTK).
TargetsVEGFR-1VEGFR-2VEGFR3PDGFRαPDGFRβc-kit
IC50 4 nM 69 nM39 nM1-10 nM   

Protocol

Cell experiment: [1]

Cell lines

Human 786-O and RCC4 cells, murine Renca cells

Preparation method

The solubility of this compound in DMSO is >10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 °C for 10 minutes and/or shake it in the ultrasonic bath for a while.Stock solution can be stored below -20°C for several months.

Reacting condition

10 μM, 24 hours

Applications

Sunitinib induced RCC tumor cell apoptosis in all three tumor cell lines. It also inhibited cell proliferation in a dose-dependent manner. For concentrations at which sunitinib caused effective tumor cell death; there were corresponding increases in cleaved PARP. Sunitinib treatment (24 h) of 786-O, RCC4 and Renca tumor cells reduced expression of several key anti-apoptotic and pro-proliferation genes, including Cyclin E, Cyclin D1 and Survivin.

Animal experiment: [1]

Animal models

Female BALB/c mice injected with Renca cells

Dosage form

Oral administration, 40, 20, 10 mg/kg body weight, daily

Application

Sunitinib induced tumor cell apoptosis in vivo as early as 1 day post treatment, which occurred in the presence of apparently intact tumor vessels. There appeared to be more apoptosis in the tumor on days 3 and 11 post treatment, with greater disruption of the tumor vasculature. Sunitinib treatment reduced Stat3 activity and induced tumor cell death as early as one day post treatment.

Other notes

Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.

References:

[1] Xin H, Zhang C, Herrmann A, et al. Sunitinib inhibition of Stat3 induces renal cell carcinoma tumor cell apoptosis and reduces immunosuppressive cells. Cancer research, 2009, 69(6): 2506-2513.

Sunitinib Dilution Calculator

Concentration (start)
x
Volume (start)
=
Concentration (final)
x
Volume (final)
 
 
 
C1
V1
C2
V2

calculate

Sunitinib Molarity Calculator

Mass
=
Concentration
x
Volume
x
MW*
 
 
 
g/mol

calculate

Preparing Stock Solutions of Sunitinib

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.5096 mL 12.548 mL 25.096 mL 50.192 mL 62.74 mL
5 mM 0.5019 mL 2.5096 mL 5.0192 mL 10.0384 mL 12.548 mL
10 mM 0.251 mL 1.2548 mL 2.5096 mL 5.0192 mL 6.274 mL
50 mM 0.0502 mL 0.251 mL 0.5019 mL 1.0038 mL 1.2548 mL
100 mM 0.0251 mL 0.1255 mL 0.251 mL 0.5019 mL 0.6274 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

Organizitions Citing Our Products recently

 
 
 

Calcutta University

University of Minnesota

University of Maryland School of Medicine

University of Illinois at Chicago

The Ohio State University

University of Zurich

Harvard University

Colorado State University

Auburn University

Yale University

Worcester Polytechnic Institute

Washington State University

Stanford University

University of Leipzig

Universidade da Beira Interior

The Institute of Cancer Research

Heidelberg University

University of Amsterdam

University of Auckland
TsingHua University
TsingHua University
The University of Michigan
The University of Michigan
Miami University
Miami University
DRURY University
DRURY University
Jilin University
Jilin University
Fudan University
Fudan University
Wuhan University
Wuhan University
Sun Yat-sen University
Sun Yat-sen University
Universite de Paris
Universite de Paris
Deemed University
Deemed University
Auckland University
Auckland University
The University of Tokyo
The University of Tokyo
Korea University
Korea University

Background on Sunitinib

Sunitinib is an oral, multi-targeted and small-molecule inhibitor of receptor tyrosine kinase (RTK) [1].

Sunitinib is a RTK inhibitor against vascular endothelial growth factor receptors (VEGFR1-3), platelet-derived growth factor receptors (PDGFRα and PDGFRβ ), stem cell factor receptor (c-kit), glial cell-line derived neurotrophic factor receptor(RET). Sunitinib has been reported to inhibit the growth in five NPC cell lines (HK1, CNE-2, HON E-1, CNE-1 and C666-1) with the IC50 values of 2.06 ± 0.29μM, 3.45 ± 0.11μM, 4.07 ± 1.07μM, 2.60 ± 0.38 and 7.57 ± 1.74μM, respectively. Apart from these, Sunitinib has been observed to induce apoptosis in NPC cells as well as induce cell cycle arrest at the G0 /G1 phase in HONE-1 and CNE-2 cells. In vivo, Sunitinib treatment could induce a significant reduction in MVD in CNE2 NPC xenograft [1].

References:
[1]Hui EP1, Lui VW, Wong CS, Ma BB, Lau CP, Cheung CS, Ho K, Cheng SH, Ng MH, Chan AT. Preclinical evaluation of sunitinib as single agent or in combination with chemotherapy in nasopharyngeal carcinoma. Invest New Drugs. 2011 Dec;29(6):1123-31.

Featured Products
New Products
 

References on Sunitinib

Comprehensive insight into the binding of sunitinib, a multi-targeted anticancer drug to human serum albumin.[Pubmed:28376387]

Spectrochim Acta A Mol Biomol Spectrosc. 2017 Jun 15;181:254-263.

Binding studies between a multi-targeted anticancer drug, Sunitinib (SU) and human serum albumin (HSA) were made using fluorescence, UV-vis absorption, circular dichroism (CD) and molecular docking analysis. Both fluorescence quenching data and UV-vis absorption results suggested formation of SU-HSA complex. Moderate binding affinity between SU and HSA was evident from the value of the binding constant (3.04x10(4)M(-1)), obtained at 298K. Involvement of hydrophobic interactions and hydrogen bonds as the leading intermolecular forces in the formation of SU-HSA complex was predicted from the thermodynamic data of the binding reaction. These results were in good agreement with the molecular docking analysis. Microenvironmental perturbations around Tyr and Trp residues as well as secondary and tertiary structural changes in HSA upon SU binding were evident from the three-dimensional fluorescence and circular dichroism results. SU binding to HSA also improved the thermal stability of the protein. Competitive displacement results and molecular docking analysis revealed the binding locus of SU to HSA in subdomain IIA (Sudlow's site I). The influence of a few common ions on the binding constant of SU-HSA complex was also noticed.

Sunitinib-induced hypothyroidism predicts progression-free survival in metastatic renal cell carcinoma patients.[Pubmed:28343336]

Med Oncol. 2017 Apr;34(4):68.

Sunitinib is a tyrosine kinase inhibitor (TKI) used in treatment of metastatic renal cell carcinoma (mRCC), gastrointestinal stromal tumors and pancreatic neuroendocrine tumors. One of the most common side effects related to Sunitinib is hypothyroidism. Recent trials suggest correlation between the incidence of hypothyroidism and treatment outcome in patients treated with TKI. This study evaluates whether development of hypothyroidism is a predictive marker of progression-free survival (PFS) in patients with mRCC treated with Sunitinib. Twenty-seven patients diagnosed with clear cell mRCC, after nephrectomy and in 'good' or 'intermediate' MSKCC risk prognostic group, were included in the study. All patients received Sunitinib as a first-line treatment on a standard schedule (initial dose 50 mg/day, 4 weeks on, 2 weeks off). The thyroid-stimulating hormone serum levels were obtained at the baseline and every 12 weeks of treatment. In statistic analyses, we used Kaplan-Meier method for assessment of progression-free survival; for comparison of survival, we used log-rank test. In our study, the incidence of hypothyroidism was 44%. The patients who had developed hypothyroidism had better median PFS to patients with normal thyroid function 28,3 months [95% (CI) 20.4-36.2 months] versus 9.8 months (6.4-13.1 months). In survival analysis, we perceive that thyroid dysfunction is a predictive factor of a progression-free survival (PFS). In the unified group of patients, the development of hypothyroidism during treatment with Sunitinib is a positive marker for PFS. During that treatment, thyroid function should be evaluated regularly.

Characteristics of early-onset hematotoxicity of sunitinib in Japanese patients with renal cell carcinoma.[Pubmed:28335742]

BMC Cancer. 2017 Mar 23;17(1):214.

BACKGROUND: A high incidence of severe hematological adverse events during Sunitinib treatment complicates decision making on dose and treatment cycle. We identified the characteristics of early-onset hematotoxicity of Sunitinib in Japanese patients with renal cell carcinoma (RCC). METHODS: Seventy-nine patients were treated with Sunitinib as 6-week cycles of "4-week on 2-week off" schedule. To evaluate early-onset hematotoxicity, we compared patients with dose reduction during the first cycle (dose-reduced group, n = 57) and those who maintained the initial dose (dose-maintained group, n = 22). ABCG2 and FLT3 genotypes were analyzed for association between hematotoxicity and reported gene polymorphisms. RESULTS: Mean relative dose intensity (RDI) was similar in the two groups during the first 2 weeks of dosing in the first cycle, but was significantly lower in the dose-reduced group during the last 2 weeks. Lymphocytopenia and thrombocytopenia were observed in the dose-reduced group within the first 2 weeks. Genetic analysis indicated a significantly higher frequency of FLT3 738 T/C polymorphism in the dose-reduced group, but no significant difference in the ABCG2 421 C/A polymorphism. CONCLUSIONS: This study showed a high incidence of Sunitinib-induced hematotoxicity in Japanese patients with RCC, many of whom need dose adjustment during the first cycle. Further studies should verify whether dose adjustment based on early-onset thrombocytopenia prolongs Sunitinib treatment.

Germline Genetic Biomarkers of Sunitinib Efficacy in Advanced Renal Cell Carcinoma: Results From the RENAL EFFECT Trial.[Pubmed:28330808]

Clin Genitourin Cancer. 2017 Oct;15(5):526-533.

BACKGROUND: Sunitinib, the vascular endothelial growth factor pathway inhibitor, is an established standard-of-care for advanced renal cell carcinoma (RCC). This study aimed to assess correlations between candidate germline single nucleotide polymorphisms (SNPs) and Sunitinib efficacy in patients from the RENAL EFFECT trial (NCT00267748), a randomized phase II study in patients with metastatic RCC comparing the 4-weeks-on/2-weeks-off schedule and a continuous daily dosing schedule. PATIENTS AND METHODS: Informed consent for pharmacogenetics research was obtained from 202 out of 289 treated patients in the trial. Associations between 9 SNP variants (CXCL8, LOXL2, CCDC26, SH3GL2, CLLU1, IL2RA, AURKB, and 2 SNPs on Chromosomes 7 and 12) and progression-free survival (PFS), objective response rate, and overall survival were assessed using Kaplan-Meier analysis, Cox proportional hazard model, and the Fisher exact test. RESULTS: CXCL8 rs1126647 A/A versus A/T (P = .004) or T/T (P < .0001) and SH3GL2 rs10963287 C/C versus C/T (P = .005) or T/T (P = .018) were associated with improved overall survival in all patients. CLLU1 rs525810 A/A genotype versus A/G (P = .014) or G/G (P = .048) was associated with improved PFS in the continuous daily dosing arm. IL2RA rs7893467 T/G versus T/T was associated with improved PFS (P = .034) in the 4-weeks-on/2-weeks-off arm and objective response rate (P = .034) in all patients. No significant associations between improved efficacy and genotype were found for other SNPs. CONCLUSION: Germline variants in CLLU1, IL2RA, CXCL8, and SH3GL2 warrant further retrospective study in independent cohorts of patients with metastatic RCC treated with vascular endothelial growth factor-class inhibitors, to test their biological significance and potential clinical fitness as biomarkers to guide treatment.

Description

Sunitinib (SU 11248) is a multi-targeted receptor tyrosine kinase inhibitor with IC50s of 80 nM and 2 nM for VEGFR2 and PDGFRβ, respectively. Sunitinib, an ATP-competitive inhibitor, effectively inhibits autophosphorylation of Ire1α by inhibiting autophosphorylation and consequent RNase activation.

Keywords:

Sunitinib,557795-19-4,SU 11248,Natural Products,PDGFR, buy Sunitinib , Sunitinib supplier , purchase Sunitinib , Sunitinib cost , Sunitinib manufacturer , order Sunitinib , high purity Sunitinib

Online Inquiry for:

      Fill out the information below

      • Size:Qty: - +

      * Required Fields

                                      Result: