Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (756 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
An indole and pyrrole derivative that inhibits vegfr-2 and pdgfr beta receptor tyrosine kinases. It is used as an antineoplastic agent for the treatment of gastrointestinal stromal tumors, and for treatment of advanced or metastatic renal cell carcinoma.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: 5-(5-Fluoro-2-oxo-1,2-dihydroindolylidenemethyl)-2,4-dimethyl-1H-pyrrole-3-carboxylic acid (2-diethylaminoethyl)amide; SU 11248; SU11248; SU-11248; SU 011248; SU-011248; SU011248; Sunitinib Malate.
Where it fits in the MeSH classification
- Broader topics
- Pyrroles; Indoles
Related concepts
- Vegfr-2
- Pdgfr Beta Receptor Tyrosine Kinases
- Gastrointestinal Stromal Tumors
- Renal Cell Carcinoma
Research landscape
PubMed indexes 4,543 records tagged with the MeSH heading “Sunitinib” (counts retrieved 2026-10-31). 995 of them (21.9%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 2,889 records.
Reviews account for 702 records (15.5%) and meta-analyses for 77. Randomized controlled trials number 241 (5.3%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 0 |
| 2000-2009 | 735 |
| 2010-2019 | 2,889 |
| 2020 onward | 995 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 702 | 15.5% |
| Meta-analyses | 77 | 1.7% |
| Randomized controlled trials | 241 | 5.3% |
Method: PubMed query "Sunitinib"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
RRM2 Regulates Sensitivity to Sunitinib and PD-1 Blockade in Renal Cancer by Stabilizing ANXA1 and Activating the AKT Pathway [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Renal cell carcinoma (RCC) is a malignant tumor of the kidneys.
- Closing excerpt
- Collectively, these results suggest that aberrantly expressed RRM2 may be a promising therapeutic target for RCC.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (199 words)
Renal cell carcinoma (RCC) is a malignant tumor of the kidneys. Approximately 70% of RCC cases are clear cell renal cell carcinoma with von Hippel-Lindau (VHL) gene mutation and activation of the vascular endothelial growth factor (VEGF) pathway. Tyrosine kinase inhibitors (TKIs) targeting VEGF have emerged as promising agents for RCC treatment. Apart from primary resistance, acquired resistance to TKIs after initial tumor regression is common in RCC. Recently, immune checkpoint inhibition, including PD-1/PD-L1 blockade, alone or in combination with TKIs has improved the overall survival of patients with RCC. Ribonucleotide reductase subunit M2 (RRM2) has been reported in many types of cancer and has been implicated in tumor progression. However, the role of RRM2 in TKIs resistance in RCC remains unclear. In this study, the authors have demonstrated that RRM2 is upregulated in sunitinib-resistant RCC cells and patient tissues. They also find that RRM2 stabilizes ANXA1 and activates the AKT pathway independent of its ribonucleotide reductase activity, promoting sunitinib resistance in RCC. Moreover, RRM2 regulated antitumor immune responses, and knockdown of RRM2 enhance the anti-tumor efficiency of PD-1 blockade in renal cancer. Collectively, these results suggest that aberrantly expressed RRM2 may be a promising therapeutic target for RCC.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34319001 · DOI · PMC8456228
N6-methyladenosine-modified TRAF1 promotes sunitinib resistance by regulating apoptosis and angiogenesis in a METTL14-dependent manner in renal cell carcinoma [2]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundSunitinib resistance can be classified into primary and secondary resistance.
- Closing excerpt
- Targeting TRAF1 and its pathways may be a novel pharmaceutical intervention for sunitinib-treated patients.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (194 words)
BackgroundSunitinib resistance can be classified into primary and secondary resistance. While accumulating research has indicated several underlying factors contributing to sunitinib resistance, the precise mechanisms in renal cell carcinoma are still unclear.MethodsRNA sequencing and m6A sequencing were used to screen for functional genes involved in sunitinib resistance. In vitro and in vivo experiments were carried out and patient samples and clinical information were obtained for clinical analysis.ResultsWe identified a tumor necrosis factor receptor-associated factor, TRAF1, that was significantly increased in sunitinib-resistant cells, resistant cell-derived xenograft (CDX-R) models and clinical patients with sunitinib resistance. Silencing TRAF1 increased sunitinib-induced apoptotic and antiangiogenic effects. Mechanistically, the upregulated level of TRAF1 in sunitinib-resistant cells was derived from increased TRAF1 RNA stability, which was caused by an increased level of N6-methyladenosine (m6A) in a METTL14-dependent manner. Moreover, in vivo adeno-associated virus 9 (AAV9) -mediated transduction of TRAF1 suppressed the sunitinib-induced apoptotic and antiangiogenic effects in the CDX models, whereas knockdown of TRAF1 effectively resensitized the sunitinib-resistant CDXs to sunitinib treatment.ConclusionsOverexpression of TRAF1 promotes sunitinib resistance by modulating apoptotic and angiogenic pathways in a METTL14-dependent manner. Targeting TRAF1 and its pathways may be a novel pharmaceutical intervention for sunitinib-treated patients.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 35538475 · DOI · PMC9087993
Long noncoding RNA SNHG12 promotes tumour progression and sunitinib resistance by upregulating CDCA3 in renal cell carcinoma [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Renal cell carcinoma (RCC) is one of the most frequently observed malignant tumours in the urinary system and targeted drug resistance is quite common in RCC.
- Closing excerpt
- Our study revealed that the lncRNA SNHG12/SP1/CDCA3 axis promoted RCC progression and sunitinib resistance, which could provide a new therapeutic target for sunitinib-resistant RCC.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (164 words)
Renal cell carcinoma (RCC) is one of the most frequently observed malignant tumours in the urinary system and targeted drug resistance is quite common in RCC. Long noncoding RNA SNHG12 (lncRNA SNHG12) has emerged as a key molecule in numerous human cancers, but its functions in renal cell carcinoma (RCC) sunitinib resistance remain unclear. In this study, we found SNHG12 was highly expressed in RCC tissues and in sunitinib-resistant RCC cells and was associated with a poor clinical prognosis. SNHG12 promoted RCC proliferation, migration, invasion and sunitinib resistance via CDCA3 in vitro. Mechanically, SNHG12 bound to SP1 and prevented the ubiquitylation-dependent proteolysis of SP1. Stabilised SP1 bound to a specific region in the promoter of CDCA3 and increased CDCA3 expression. Furthermore, in vivo experiments showed that SNHG12 increased tumour growth and that knocking down SNHG12 could reverse RCC sunitinib resistance. Our study revealed that the lncRNA SNHG12/SP1/CDCA3 axis promoted RCC progression and sunitinib resistance, which could provide a new therapeutic target for sunitinib-resistant RCC.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32641718 · DOI · PMC7343829
Folic Acid-Modified Ginger-Derived Exosome-Like Nanoparticles Co-Delivering Sunitinib Suppress Renal Cell Carcinoma via PI3K-Akt Pathway Inhibition, P-gp Downregulation, and Macrophage Reprogramming [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Renal cell carcinoma (RCC) is a malignant tumor with highly recurrent and metastatic capability.
- Closing excerpt
- This study integrates network pharmacology with targeted delivery strategies, elucidating the mechanisms by which FPD-GELNs/Su inhibits RCC progression through multiple pathways, providing new insights for the development of precise and low-toxicity nano-therapies.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (199 words)
Renal cell carcinoma (RCC) is a malignant tumor with highly recurrent and metastatic capability. The current therapies for RCC are limited by drug resistance and toxic side effects. This study introduces an innovative approach that combines ginger-derived exosome-like nanoparticles (GELNs) with sunitinib (Su) and folic acid-polyethylene glycol (FA-PEG, FPD) in an active-passive targeting strategy to explore its multi-mechanism and synergistic therapeutic effects on RCC. GELNs are extracted via differential centrifugation combined with sucrose gradient ultracentrifugation. Metabolomics and network pharmacology predicted that GELNs may exert their anticancer efficacy via the PI3K-Akt signaling pathway, which is subsequently validated through in vitro experiments. By loading Su and modifying it with FPD, FPD-GELNs/Su is constructed. The FPD modification significantly enhanced tumor targeting and amplified the Su sensitivity by reducing ABCB1/P-gp expression induced by GELNs. In vivo experiments revealed that FPD-GELNs/Su promoted M1 macrophage polarization and increased immune T-cell infiltration by remodeling the tumor microenvironment, leading to significant inhibition of tumor growth and lung metastasis without causing notable liver or kidney toxicity. This study integrates network pharmacology with targeted delivery strategies, elucidating the mechanisms by which FPD-GELNs/Su inhibits RCC progression through multiple pathways, providing new insights for the development of precise and low-toxicity nano-therapies.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41243691 · DOI · PMC12866827
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Sunitinib in the Treatment of Thyroid Cancer [5]
- Research article Drug-Induced Hypertension Caused by Multikinase Inhibitors (Sorafenib, Sunitinib, Lenvatinib and Axitinib) in Renal Cell Carcinoma Treatment [6]
- Research article Sunitinib for Metastatic Renal Cell Carcinoma: A Systematic Review and Meta-Analysis of Real-World and Clinical Trials Data [7]
- Research article Overview of Current and Future First-Line Systemic Therapy for Metastatic Clear Cell Renal Cell Carcinoma [8]
- Research article Systemic therapy in the management of localized and locally advanced renal cell carcinoma: Current state and future perspectives [9]
- Research article Chordoma: a case series and review of the literature [10]
References
- Xiong W, Zhang B, Yu H, Zhu L, Yi L, Jin X. RRM2 Regulates Sensitivity to Sunitinib and PD-1 Blockade in Renal Cancer by Stabilizing ANXA1 and Activating the AKT Pathway. . 2021. PMID 34319001 · DOI · PMC8456228
- Chen Y, Lu Z, Qi C, Yu C, Li Y, Huan W, et al.. N6-methyladenosine-modified TRAF1 promotes sunitinib resistance by regulating apoptosis and angiogenesis in a METTL14-dependent manner in renal cell carcinoma. . 2022. PMID 35538475 · DOI · PMC9087993
- Liu Y, Cheng G, Huang Z, Bao L, Liu J, Wang C, et al.. Long noncoding RNA SNHG12 promotes tumour progression and sunitinib resistance by upregulating CDCA3 in renal cell carcinoma. . 2020. PMID 32641718 · DOI · PMC7343829
- Xu H, Hu D, Liu S, Yang L, Li J, Bai Y, et al.. Folic Acid-Modified Ginger-Derived Exosome-Like Nanoparticles Co-Delivering Sunitinib Suppress Renal Cell Carcinoma via PI3K-Akt Pathway Inhibition, P-gp Downregulation, and Macrophage Reprogramming. . 2026. PMID 41243691 · DOI · PMC12866827
- Ferrari SM, Centanni M, Virili C, Miccoli M, Ferrari P, Ruffilli I, et al.. Sunitinib in the Treatment of Thyroid Cancer. Curr Med Chem. 2019. PMID 28990511 · DOI
- Bæk Møller N, Budolfsen C, Grimm D, Krüger M, Infanger M, Wehland M, et al.. Drug-Induced Hypertension Caused by Multikinase Inhibitors (Sorafenib, Sunitinib, Lenvatinib and Axitinib) in Renal Cell Carcinoma Treatment. Int J Mol Sci. 2019. PMID 31547602 · DOI · PMC6801695
- Moran M, Nickens D, Adcock K, Bennetts M, Desscan A, Charnley N, et al.. Sunitinib for Metastatic Renal Cell Carcinoma: A Systematic Review and Meta-Analysis of Real-World and Clinical Trials Data. Target Oncol. 2019. PMID 31301015 · DOI · PMC6684538
- Gill DM, Hahn AW, Hale P, Maughan BL. Overview of Current and Future First-Line Systemic Therapy for Metastatic Clear Cell Renal Cell Carcinoma. Curr Treat Options Oncol. 2018. PMID 29368125 · DOI
- Berquist SW, Yim K, Ryan ST, Patel SH, Eldefrawy A, Cotta BH, et al.. Systemic therapy in the management of localized and locally advanced renal cell carcinoma: Current state and future perspectives. Int J Urol. 2019. PMID 30943578 · DOI
- Alan O, Akin Telli T, Ercelep O, Tanrikulu Simsek E, Basoglu Tuylu T, Mutis A, et al.. Chordoma: a case series and review of the literature. J Med Case Rep. 2018. PMID 30145982 · DOI · PMC6109974
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.