声动力疗法
内质网
癌症研究
小分子
免疫原性细胞死亡
细胞毒性
活性氧
医学
全身给药
转移
细胞内
翻译(生物学)
化学
癌症
癌细胞
癌症治疗
光热治疗
免疫疗法
体内
未折叠蛋白反应
细胞生物学
抗体
免疫原性
光动力疗法
程序性细胞死亡
联合疗法
HMGB1
全身疗法
药理学
原位
作者
Jinrong Li,Kun Shao,Lin Cheng,Guanyi Zhang,Jianlong Su,Yiming Liu,Yang Wang,Chengdong Wang,Zhihao Wu,Xu Wang,Yuxuan Zhang,Bohua Yan,Lei Wang,Guangzhe Li
摘要
ABSTRACT Unimolecule‐mediated sonodynamic therapy (SDT) offers a promising approach to combat tumors systemically by enabling synergistic sono‐triggered cytotoxicity and in situ vaccine‐like effects within tumors. Although chlorin‐based sensitizers have achieved clinical success in phototherapy, their translation to SDT has been impeded by inadequate ultrasound (US)‐triggered reactive oxygen species (ROS) generation, leading to suboptimal immunogenic cell death (ICD) and compromised antitumor immunity. To address this, we designed two organic sonosensitizers based on the natural product‐derived scaffold, Chenghai pyropheophorbide‐a (CHPpa). CHPpa‐er was constructed by appending a p ‐toluenesulfonamide group for specific endoplasmic reticulum (ER) targeting. Its analogue, CHPpa‐er‐Asp, was additionally functionalized with aspartic acid to modulate molecular polarity. Remarkably, despite differing by only one pharmacophore, the two compounds exhibited profoundly distinct profiles in target protein (K ATP channel) engagement and intracellular trafficking, highlighting the critical impact of rational molecular design. As the lead candidate, CHPpa‐er elicited precise, intraluminal ROS bursts under US, inducing severe ER stress and robust ICD. In two preclinical tumor models, CHPpa‐er‐mediated SDT effectively suppressed both primary tumor growth and metastasis by provoking potent systemic antitumor immunity. This work introduced a unimolecular sonosensitizer strategy that transformed SDT from a localized modality into a systemic intervention, offering a translatable platform for comprehensive cancer therapy.
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