文章：

SH003作为一种氧化还原免疫调节植物药：从铁死亡诱导、外泌体串扰到转化肿瘤学的视角

SH003 as a Redox-Immune Modulating Phytomedicine: A Ferroptosis Induction, Exosomal Crosstalk, and Translational Oncology Perspective

原文发布日期：31 October 2025

DOI: 10.3390/cancers17213519

类型: Article

开放获取: 是

英文摘要：

Redox dysregulation, ferroptosis evasion, and immune suppression are major barriers in cancer therapy. SH003, a multi-herbal formulation standardized under GMP conditions and evaluated in early-phase clinical studies (NCT03081819; KCT0004770), demonstrated a favorable safety profile supporting its translational potential. Preclinical studies reveal that SH003 disrupts mitochondrial homeostasis, triggers endoplasmic reticulum stress apoptosis, and sensitizes resistant tumors to ferroptosis via suppression of the SLC7A11–GPX4 axis and NRF2 destabilization. In parallel, SH003 remodels tumor immunity by attenuating STAT3-driven PD-L1 signaling, promoting macrophage repolarization, and enhancing cytotoxic lymphocyte activity. Exosome-associated microRNAs further suggest SH003’s role in redox–immune communication, although functional validation is pending. Collectively, SH003 represents a clinically tested phytomedicine that integrates ferroptosis induction with immune modulation, offering a biomarker-informed approach to precision oncology.

摘要翻译： 

氧化还原失调、铁死亡逃逸和免疫抑制是癌症治疗的主要障碍。SH003是一种在GMP条件下标准化的多草药复方制剂，已在早期临床研究（NCT03081819；KCT0004770）中进行评估，显示出良好的安全性，支持其转化潜力。临床前研究表明，SH003通过抑制SLC7A11–GPX4轴和NRF2去稳定化，破坏线粒体稳态，触发内质网应激凋亡，并使耐药肿瘤对铁死亡敏感。同时，SH003通过减弱STAT3驱动的PD-L1信号传导、促进巨噬细胞复极化及增强细胞毒性淋巴细胞活性，重塑肿瘤免疫。外泌体相关微小RNA进一步提示SH003在氧化还原-免疫通讯中的作用，但其功能验证尚待完成。总体而言，SH003是一种经过临床验证的植物药，整合了铁死亡诱导与免疫调节功能，为精准肿瘤学提供了基于生物标志物的治疗策略。

原文链接：

SH003 as a Redox-Immune Modulating Phytomedicine: A Ferroptosis Induction, Exosomal Crosstalk, and Translational Oncology Perspective