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Sutent (Sunitinib Malate)
Sunitinib inhibits multiple receptor tyrosine kinases implicated in tumor growth, angiogenesis, and metastatic progression.
Sunitinib malate is a multi-targeted tyrosine kinase inhibitor approved for GIST, advanced RCC, adjuvant RCC, and pancreatic neuroendocrine tumors. The drug demonstrates potent inhibition of multiple RTKs involved in tumor growth and angiogenesis with oral bioavailability and manageable pharmacokinetics. Key risks include QTc prolongation and significant drug interactions via CYP3A4 metabolism requiring dose adjustments. Clinical utility is established across multiple cancer indications with dose modifications needed for concomitant enzyme inhibitors or inducers.
At a glance
| Generic name | Sunitinib Malate |
|---|---|
| Sponsor | Pfizer |
| Drug class | Small molecule kinase inhibitor |
| Target | Receptor tyrosine kinases (RTKs): PDGFRα, PDGFRβ, VEGFR1, VEGFR2, VEGFR3, KIT, FLT3, CSF-1R, RET |
| Modality | Small molecule |
| Therapeutic area | Oncology |
| Phase | FDA-approved |
| First approval | 2006 |
Mechanism of action
Sunitinib is a small molecule that inhibits multiple receptor tyrosine kinases implicated in tumor growth, pathologic angiogenesis, and metastatic progression of cancer. The drug was evaluated against over 80 kinases and identified as an inhibitor of platelet-derived growth factor receptors (PDGFRα and PDGFRβ), vascular endothelial growth factor receptors (VEGFR1, VEGFR2, and VEGFR3), stem cell factor receptor (KIT), Fms-like tyrosine kinase-3 (FLT3), colony stimulating factor receptor Type 1 (CSF-1R), and the glial cell-line derived neurotrophic factor receptor (RET). Sunitinib inhibition of these RTKs has been demonstrated in biochemical and cellular assays, with inhibition of function shown in cell proliferation assays. The primary metabolite exhibits similar potency compared to sunitinib in biochemical and cellular assays. In vivo studies demonstrated inhibition of tumor growth or tumor regression and/or inhibited metastases in experimental cancer models. Sunitinib demonstrated the ability to inhibit growth of tumor cells expressing dysregulated target RTKs (PDGFR, RET, or KIT) in vitro and to inhibit PDGFRβ- and VEGFR2-dependent tumor angiogenesis in vivo.
Approved indications
- Gastrointestinal stromal tumor
- Pancreatic Neuroendocrine Tumor
- Renal cell carcinoma
Boxed warnings
- WARNING: HEPATOTOXICITY Hepatotoxicity may be severe, and in some cases, fatal. Monitor hepatic function and interrupt, dose reduce, or discontinue SUTENT as recommended [see Warnings and Precautions (5.1) ] . WARNING: HEPATOTOXICITY See full prescribing information for complete boxed warning. Hepatotoxicity may be severe, and in some cases fatal. Monitor hepatic function and interrupt, dose reduce, or discontinue SUTENT as recommended [see Warnings and Precautions (5.1) ].
Common side effects
- Diarrhea
- Mucositis/stomatitis
- Constipation
- Anorexia
- Asthenia
- Skin discoloration
- Rash
- Hand-foot syndrome
- Altered taste
- Hypertension
- Myalgia/limb pain
- Oral pain
Drug interactions
- Strong CYP3A4 inhibitors
- Strong CYP3A4 inducers
- Drugs that prolong QT interval
Primary sources
Every claim on this page is sourced from regulatory or scientific primary sources. See our editorial policy for full methodology.
| Source | Used for |
|---|---|
| FDA label | Mechanism, indications, dosing, boxed warnings, drug interactions |
Competitive intelligence
For the full competitive landscape — auto-detected comparators, recent regulatory actions across the set, upcoming PDUFA, patent timeline, sponsor landscape:
- Sutent CI brief — competitive landscape report
- Sutent updates RSS · CI watch RSS
- Pfizer portfolio CI