米托蒽醌（MX）可以诱导肿瘤细胞的免疫原性死亡（ICD），并激活抗肿瘤免疫反应。然而，它也会在ICD期间引起色胺酸2,3-双加氧酶（IDO）的高表达，导致T细胞凋亡和免疫反应的减弱。一种IDO抑制剂，1-甲基色氨酸（1-MT），可以抑制MX引起的IDO活性，从而增强化疗免疫疗法。在这里，MX-1-MT通过酯键连接，该键可以在酸性肿瘤微环境中被断裂。MX-1-MT通过二硫键与聚乙二醇（PEG）结合，该键可以被在肿瘤中过表达的谷胱甘肽还原，从而加速药物在靶点处的释放。引入叶酸修饰的二十二烷基磷酸酰乙醇胺-聚乙二醇（DSPE-PEG-FA）形成靶向小分子聚集体。该小分子聚集体具有均匀的粒径、高稳定性和高响应性。它们可以被耐药的MCF-7 / ADR细胞吞噬，并表现出高的靶向能力和诱导增强的细胞毒性和ICD。由于添加了1-MT，小分子聚集体可以抑制IDO。体内研究表明，小分子聚集体可以在裸鼠的肿瘤组织中积累，从而导致增强的抗肿瘤效果和少量的副作用。

Mitoxantrone (MX) can induce the immunogenic-cell death (ICD) of tumor cells and activate anti-tumor immune responses. However, it can also cause high expression of indole amine 2, 3-dioxygenase (IDO) during ICD, leading to T-cell apoptosis and a weakened immune response. An IDO inhibitor, 1-methyl tryptophan (1-MT), can inhibit the activity of IDO caused by MX, resulting in enhanced chemo-immunotherapy. Here, MX-1-MT was connected by ester bond which could be broken in an acidic tumor microenvironment. MX-1-MT was combined with polyethylene glycol (PEG) via a disulfide bond which could be reduced by glutathione overexpressed in tumors, thereby accelerating drug release at target sites. Folic acid-modified distearoyl phosphoethanolamine-polyethylene glycol (DSPE-PEG-FA) was introduced to form targeting micelles. The micelles were of uniform particle size, high stability, and high responsiveness. They could be taken-up by drug-resistant MCF-7/ADR cells, displayed high targeting ability, and induced enhanced cytotoxicity and ICD. Due to 1-MT addition, micelles could inhibit IDO. In vivo studies demonstrated that micelles could accumulate in the tumor tissues of nude mice, resulting in an enhanced antitumor effect and few side-effects.