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.
- 1. Nicole A Muench, Heather M Schmitt, et al. "Preservation of Murine Whole Eyes With Supplemented UW Cold Storage Solution: Anatomical Considerations." Transl Vis Sci Technol. 2024 Nov 4;13(11):24 PMID: 39560629
- 2. Zixuan Chen, Xing Jia, et al. "AUY922 Improves Sensitivity to Sunitinib in Clear Cell Renal Cell Carcinoma Based on Network Pharmacology and in Vitro Experiments." Heliyon. 2024 Jul 18;10(14):e34834 PMID: 39149033
- 3. Marieke Van Daele, Laura E Kilpatrick, et al. "Characterisation of tyrosine kinase inhibitor-receptor interactions at VEGFR2 using sunitinib-red and nanoBRET." Biochem Pharmacol. 2023 Aug;214:115672. PMID: 37406966
- 4. Jia-Qi Guo, Chang-Dong Wang, et al. "PDGF‐BB/PDGFRβ Promotes Epithelial‐Mesenchymal Transition by Affecting PI3K/AKT/mTOR‐Driven Aerobic Glycolysis in Wilms' tumor G401 Cells." Cell Biol Int. 2022 Feb 14. PMID: 35165984
- 5. Bhola PD, Ahmed E, et al. "High-throughput dynamic BH3 profiling may quickly and accurately predict effective therapies in solid tumors." Sci Signal. 2020;13(636):eaay1451. PMID:32546544
| Physical Appearance | A solid |
| Storage | Store at -20°C |
| M.Wt | 398.47 |
| Cas No. | 557795-19-4 |
| Formula | C22H27FN4O2 |
| Solubility | insoluble in H2O; ≥19.9 mg/mL in DMSO with gentle warming; ≥3.16 mg/mL in EtOH with gentle 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 |
| SDF | Download SDF |
| Canonical SMILES | CCN(CC)CCNC(=O)C1=C(NC(=C1C)C=C2C3=C(C=CC(=C3)F)NC2=O)C |
| Shipping Condition | Small Molecules with Blue Ice, Modified Nucleotides with Dry Ice. |
| General tips | We do not recommend long-term storage for the solution, please use it up soon. |
| Cell experiment: [1] | |
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Cell lines |
Human 786-O and RCC4 cells, murine Renca cells |
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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. |
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Reaction Conditions |
10 μM, 24 hours |
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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] | |
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Animal models |
Female BALB/c mice injected with Renca cells |
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Dosage form |
Oral administration, 40, 20, 10 mg/kg body weight, daily |
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Applications |
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. |
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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. |
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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. |
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| Description | Sunitinib is an oral, multi-targeted and small-molecule inhibitor of receptor tyrosine kinase (RTK). | |||||
| Targets | VEGFR-1 | VEGFR-2 | VEGFR3 | PDGFRα | PDGFRβ | c-kit |
| IC50 | 4 nM | 69 nM | 39 nM | 1-10 nM | ||
Quality Control & MSDS
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Chemical structure
Related Biological Data
