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 (638 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
A niacinamide and phenylurea derivative that inhibits multiple intracellular and cell surface kinases thought to be involved in angiogenesis, including raf kinases and vegf receptors. It is used in the treatment of advanced renal cell carcinoma and hepatocellular carcinoma, and for treatment of thyroid carcinoma refractory to radioactive iodine therapy.
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: BAY 43-9006; BAY 439006; BAY 43 9006; Sorafenib Tosylate; 4-(4-(3-(4-Chloro-3-trifluoromethylphenyl)ureido)phenoxy)pyridine-2-carboxylic acid methyamide-4-methylbenzenesulfonate; Nexavar; BAY 545-9085; BAY 5459085.
Where it fits in the MeSH classification
- Broader topics
- Phenylurea Compounds; Niacinamide
Related concepts
- Angiogenesis
- Raf Kinases
- Vegf Receptors
- Renal Cell Carcinoma
- Hepatocellular Carcinoma
- Thyroid Carcinoma
Research landscape
PubMed indexes 7,406 records tagged with the MeSH heading “Sorafenib” (counts retrieved 2026-10-31). 2,587 of them (34.9%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 4,191 records.
Reviews account for 1,064 records (14.4%) and meta-analyses for 158. Randomized controlled trials number 319 (4.3%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 0 |
| 2000-2009 | 738 |
| 2010-2019 | 4,191 |
| 2020 onward | 2,587 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 1,064 | 14.4% |
| Meta-analyses | 158 | 2.1% |
| Randomized controlled trials | 319 | 4.3% |
Method: PubMed query "Sorafenib"[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.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| The mechanisms of sorafenib resistance in hepatocellular carcinoma: theoretical basis and therapeutic aspects | 2020 | Review article Design not recorded in structured metadata | 913 | cc by PMID 32532960 · DOI · PMC7292831 |
| Targeted therapy for hepatocellular carcinoma | 2020 | Review article Design not recorded in structured metadata | 594 | cc by PMID 32782275 · DOI · PMC7419547 |
| CircRNA-SORE mediates sorafenib resistance in hepatocellular carcinoma by stabilizing YBX1 | 2020 | Research article Design not recorded in structured metadata | 385 | cc by PMID 33361760 · DOI · PMC7762756 |
| CD147-positive migrasome macropinocytosis promotes HCC sorafenib resistance via inducing vasculogenic mimicry triggered by PI3K/AKT/TWIST1 signaling | 2026 | Research article Design not recorded in structured metadata | 0 | cc by PMID 42297770 · DOI · PMC13500725 |
The mechanisms of sorafenib resistance in hepatocellular carcinoma: theoretical basis and therapeutic aspects [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Sorafenib is a multikinase inhibitor capable of facilitating apoptosis, mitigating angiogenesis and suppressing tumor cell proliferation.
- Closing excerpt
- This study summarizes discoveries achieved recently in terms of the principles of sorafenib resistance and outlines approaches suitable for improving therapeutic outcomes for HCC 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 (108 words)
Sorafenib is a multikinase inhibitor capable of facilitating apoptosis, mitigating angiogenesis and suppressing tumor cell proliferation. In late-stage hepatocellular carcinoma (HCC), sorafenib is currently an effective first-line therapy. Unfortunately, the development of drug resistance to sorafenib is becoming increasingly common. This study aims to identify factors contributing to resistance and ways to mitigate resistance. Recent studies have shown that epigenetics, transport processes, regulated cell death, and the tumor microenvironment are involved in the development of sorafenib resistance in HCC and subsequent HCC progression. This study summarizes discoveries achieved recently in terms of the principles of sorafenib resistance and outlines approaches suitable for improving therapeutic outcomes for HCC patients.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32532960 · DOI · PMC7292831
Targeted therapy for hepatocellular carcinoma [2]
Abstract reading summary — source excerpts
- Opening excerpt
- The last 3 years have seen the emergence of promising targeted therapies for the treatment of hepatocellular carcinoma (HCC).
- Closing excerpt
- Work continues to develop additional novel therapeutic agents which could potentially augment the presently available options and understand the underlying mechanisms responsible for drug resistance, with the goal of improving the survival of patients with HCC.
- 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 (167 words)
The last 3 years have seen the emergence of promising targeted therapies for the treatment of hepatocellular carcinoma (HCC). Sorafenib has been the mainstay of treatment for a decade and newer modalities were ineffective and did not confer any increased therapeutic benefit until the introduction of lenvatinib which was approved based on its non-inferiority to sorafenib. The subsequent success of regorafenib in HCC patients who progress on sorafenib treatment heralded a new era of second-line treatment and was quickly followed by ramucirumab, cabozantinib, and the most influential, immune checkpoint inhibitors (ICIs). Over the same period combination therapies, including anti-angiogenesis agents with ICIs, dual ICIs and targeted agents in conjunction with surgery or other loco-regional therapies, have been extensively investigated and have shown promise and provided the basis for exciting clinical trials. Work continues to develop additional novel therapeutic agents which could potentially augment the presently available options and understand the underlying mechanisms responsible for drug resistance, with the goal of improving the survival of patients with HCC.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32782275 · DOI · PMC7419547
CircRNA-SORE mediates sorafenib resistance in hepatocellular carcinoma by stabilizing YBX1 [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Sorafenib is the first-line chemotherapeutic therapy for advanced hepatocellular carcinoma (HCC).
- Closing excerpt
- Our study provides a proof-of-concept demonstration for a potential strategy to overcome sorafenib resistance in HCC patients by targeting circRNA-SORE or YBX1.
- 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 (169 words)
Sorafenib is the first-line chemotherapeutic therapy for advanced hepatocellular carcinoma (HCC). However, sorafenib resistance significantly limits its therapeutic efficacy, and the mechanisms underlying resistance have not been fully clarified. Here we report that a circular RNA, circRNA-SORE (a circular RNA upregulated in sorafenib-resistant HCC cells), plays a significant role in sorafenib resistance in HCC. We found that circRNA-SORE is upregulated in sorafenib-resistant HCC cells and depletion of circRNA-SORE substantially increases the cell-killing ability of sorafenib. Further studies revealed that circRNA-SORE binds the master oncogenic protein YBX1 in the cytoplasm, which prevents YBX1 nuclear interaction with the E3 ubiquitin ligase PRP19 and thus blocks PRP19-mediated YBX1 degradation. Moreover, our in vitro and in vivo results suggest that circRNA-SORE is transported by exosomes to spread sorafenib resistance among HCC cells. Using different HCC mouse models, we demonstrated that silencing circRNA-SORE by injection of siRNA could substantially overcome sorafenib resistance. Our study provides a proof-of-concept demonstration for a potential strategy to overcome sorafenib resistance in HCC patients by targeting circRNA-SORE or YBX1.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33361760 · DOI · PMC7762756
CD147-positive migrasome macropinocytosis promotes HCC sorafenib resistance via inducing vasculogenic mimicry triggered by PI3K/AKT/TWIST1 signaling [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Sorafenib is a widely used targeting drug for hepatocellular carcinoma (HCC) patients; however, sorafenib resistance poses a significant clinical challenge.
- Closing excerpt
- Conclusively, our findings uncover a novel sorafenib resistance mechanism induced by CD147+-hypo-Migs, and highlight dual-targeting of macropinocytosis and VM as a promising strategy to overcome the sorafenib resistance in HCC.
- 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)
Sorafenib is a widely used targeting drug for hepatocellular carcinoma (HCC) patients; however, sorafenib resistance poses a significant clinical challenge. Hypoxia and extracellular vesicles (EVs) induce vasculogenic mimicry (VM) which is linked to sorafenib resistance in HCC. Migrasomes (Migs), the newly discovered large EVs, foster HCC malignant phenotypes by facilitating the intercellular transfer of functional molecules. Despite these advancements, the precise mechanism by which Migs cause sorafenib resistance is still unknown. In this study, we found that hypoxia upregulates the Migs release and CD147 expression on Migs surface, which is related to sorafenib resistance in HCC. Further investigations revealed that hypoxia-induced migrasomes (hypo-Migs) induce VM formation, thereby promoting sorafenib resistance in HCC. Notably, hypo-Migs are internalized into HCC cells through macropinocytosis, which depends on the expression of lysophosphatidic acid receptor 6 (LPAR6). Mechanistically, CD147-positive (CD147+) hypo-Migs activate the PI3K/AKT/TWIST1 signaling pathway, subsequently inducing VM formation and promoting sorafenib resistance. Importantly, dual blockade of CD147+-hypo-Migs macropinocytosis and VM formation enhances the sorafenib-killing efficacy to HCC. Conclusively, our findings uncover a novel sorafenib resistance mechanism induced by CD147+-hypo-Migs, and highlight dual-targeting of macropinocytosis and VM as a promising strategy to overcome the sorafenib resistance in HCC.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42297770 · DOI · PMC13500725
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 The Role of Angiogenesis in Hepatocellular Carcinoma [5]
- Research article Molecular therapies for HCC: Looking outside the box [6]
- Research article Sorafenib resistance in hepatocarcinoma: role of hypoxia-inducible factors [7]
- Research article The microenvironmental and metabolic aspects of sorafenib resistance in hepatocellular carcinoma [8]
- Research article Current status of sorafenib nanoparticle delivery systems in the treatment of hepatocellular carcinoma [9]
- Research article Ten years of sorafenib in hepatocellular carcinoma: Are there any predictive and/or prognostic markers? [10]
References
- Tang W, Chen Z, Zhang W, Cheng Y, Zhang B, Wu F, et al.. The mechanisms of sorafenib resistance in hepatocellular carcinoma: theoretical basis and therapeutic aspects. . 2020. PMID 32532960 · DOI · PMC7292831
- Huang A, Yang XR, Chung WY, Dennison AR, Zhou J. Targeted therapy for hepatocellular carcinoma. . 2020. PMID 32782275 · DOI · PMC7419547
- Xu J, Ji L, Liang Y, Wan Z, Zheng W, Song X, et al.. CircRNA-SORE mediates sorafenib resistance in hepatocellular carcinoma by stabilizing YBX1. . 2020. PMID 33361760 · DOI · PMC7762756
- Qian L, Chen P, Wang B, Zhang Q, Guo Y, Cui J, et al.. CD147-positive migrasome macropinocytosis promotes HCC sorafenib resistance via inducing vasculogenic mimicry triggered by PI3K/AKT/TWIST1 signaling. . 2026. PMID 42297770 · DOI · PMC13500725
- Morse MA, Sun W, Kim R, He AR, Abada PB, Mynderse M, et al.. The Role of Angiogenesis in Hepatocellular Carcinoma. Clin Cancer Res. 2019. PMID 30274981 · DOI
- Faivre S, Rimassa L, Finn RS. Molecular therapies for HCC: Looking outside the box. J Hepatol. 2020. PMID 31954496 · DOI
- Méndez-Blanco C, Fondevila F, García-Palomo A, González-Gallego J, Mauriz JL. Sorafenib resistance in hepatocarcinoma: role of hypoxia-inducible factors. Exp Mol Med. 2018. PMID 30315182 · DOI · PMC6185986
- Xia S, Pan Y, Liang Y, Xu J, Cai X. The microenvironmental and metabolic aspects of sorafenib resistance in hepatocellular carcinoma. EBioMedicine. 2020. PMID 31918403 · DOI · PMC7000339
- Kong FH, Ye QF, Miao XY, Liu X, Huang SQ, Xiong L, et al.. Current status of sorafenib nanoparticle delivery systems in the treatment of hepatocellular carcinoma. Theranostics. 2021. PMID 33859758 · DOI · PMC8039945
- Marisi G, Cucchetti A, Ulivi P, Canale M, Cabibbo G, Solaini L, et al.. Ten years of sorafenib in hepatocellular carcinoma: Are there any predictive and/or prognostic markers?. World J Gastroenterol. 2018. PMID 30271080 · DOI · PMC6158485
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.
See how EvidenceLib is built. Spotted an error? Email support@evidencehelix.com.
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.