Apatinib is effective as third-line and more treatment of advanced metastatic non-small-cell lung cancer

Abstract

No standard methods are recommended for patients with advanced metastatic non-small-cell lung cancer (NSCLC) experiencing progression after 2 or more lines treatment now. The aim of this retrospective study was to assess the efficacy and safety of apatinib in metastatic NSCLC patients after second-line or more treatments failure in a real-world setting.A total of 52 advanced NSCLC patients who experienced progression after second-line and more treatments and received apatinib from March 2016 to February 2018 were retrospectively reviewed. Patients were treated with oral apatinib 500 mg QD (take the medicine once a day), every 4 weeks for a cycle. Responding and stable patients continued the treatment until progression or intolerable toxicity. The overall survival (OS), progression-free survival (PFS), objective remission rate (ORR) and disease control rate (DCR), and side effects of the drug were collected and reviewed.The ORR and the DCR were 6.9% and 67.4%. The median PFS and median OS of all patients were 3.8 months and 5.8 months, respectively. The Eastern Cooperative Oncology Group score was the independent influencing factor of PFS and OS for the advanced NSCLC patients who were treated with apatinib after second-line and above standard regimens (PFS: hazard ratio [HR] = 4.446, 95% confidence interval [CI]: 1.185–16.678, P = .027 and OS: HR = 8.149, 95% CI: 1.173–56.596, P = .034). The most common adverse events apatinib-related included hypertension (19.2%), hand-foot syndrome (11.5%), and mucous membrane reaction (17.3%). And treatment-related grade 3/4 toxicities were low.Apatinib showed favorable efficacy and safety and could be a treatment option in patients with advanced NSCLC experiencing progression after second-line and more treatment.

Comparison of the Therapeutic Efficacies of Topical Rivoceranib and Topical Bevacizumab in a Murine Model of Corneal Neovascularization

“…Rivoceranib has been approved in China for use as a single or combination therapy for various end-stage solid cancers including stomach, colorectal, liver, and adenoid cyst carcinoma [18,20,22]. This small-molecule receptor TKI can block the phosphorylation of VEGFR-2 by binding its intracellular adenosine triphosphate sites [18,19,20].…”

“…Rivoceranib has been approved in China for use as a single or combination therapy for various end-stage solid cancers including stomach, colorectal, liver, and adenoid cyst carcinoma [18,20,22]. This small-molecule receptor TKI can block the phosphorylation of VEGFR-2 by binding its intracellular adenosine triphosphate sites [18,19,20]. Hence, rivoceranib can restrain several signaling pathways as follows: the Raf/MEK/Erk pathway, which results in the proliferation of endothelial cells; the p38-MAPK pathway, which stimulates the migration of endothelial cells; and the PI3K/AKT/mTOR pathway, which enhances vascular permeability [18,19,20].…”

“…This small-molecule receptor TKI can block the phosphorylation of VEGFR-2 by binding its intracellular adenosine triphosphate sites [18,19,20]. Hence, rivoceranib can restrain several signaling pathways as follows: the Raf/MEK/Erk pathway, which results in the proliferation of endothelial cells; the p38-MAPK pathway, which stimulates the migration of endothelial cells; and the PI3K/AKT/mTOR pathway, which enhances vascular permeability [18,19,20]. Recently, many studies have shown that rivoceranib could directly act on the process of inhibiting the PI3K/AKT signaling pathway associated with other VEGF-independent compensatory mechanisms [19,21].…”

“…The effectiveness of rivoceranib has already been proven in metastatic solid cancer, including gastric, colorectal, hepatocellular, and lung cancer [18,20,22]. Thus, we thought that rivoceranib could be a potential therapeutic agent in CNV.…”

“…Rivoceranib, a novel and selective potent VEGFR-2 tyrosine kinase inhibitor (TKI), can restrain several signaling pathways of VEGFR-2 such as the Raf/MEK/Erk, p38-MAPK, and PI3K/AKT/mTOR pathways, which results in vascular angiogenesis [18,19,20]. Recently, several studies have shown that rivoceranib could directly inhibit the PI3K/AKT signaling pathway, which was associated with a VEGF-independent compensatory pathway in angiogenesis [19,21].…”