Most cancer cells that do not respond to a single immune checkpoint inhibitor escape through the innate immune escape mechanism, allowing them to grow and survive. Different from the inherent resistance mechanism, some patients who initially responded to immune checkpoint inhibitors developed disease progression after a period of treatment and follow-up, suggesting acquired resistance. Therefore, clinical strategies continue to be applied to overcome inherent and acquired resistance to improve the clinical efficacy of immune checkpoint inhibitors. Combining an immune checkpoint inhibitor with another drug that has both immune regulation and anti-tumor properties can enhance the anti-tumor efficacy of any one drug when used alone. Studies have shown that tumor angiogenesis participates in anti-tumor immune regulation and will aggravate the tumor immunosuppressive microenvironment, and anti-angiogenesis therapy can normalize the abnormal vascular structure and function of tumors, and help the recruitment and infiltration of effector T cells. , Reduce the accumulation of immunosuppressive regulatory T cells, relieve the immunosuppressive state, thereby improving the efficacy of immunotherapy. The combination of anti-angiogenic drugs and immune checkpoint inhibitors has become a promising treatment strategy.
The combination of immunocheckpoint inhibitors and anti-angiogenesis therapy has synergistic anti-tumor effect and is a reasonable method to improve the prognosis of patients. Therefore, in this study, it is hoped that antinib hydrochloride combined with Sinidilizumab can overcome immunotherapy resistance, improve the efficacy of immunotherapy, and further improve the survival of patients, so as to provide more clinical evidence for the treatment of advanced NSCLC patients with negative driver gene after first-line treatment with anti-PD-1 antibody.