Vasiyani Hitesh, Wadhwa Bhumika
Department of Pharmacology and Toxicology, Virginia Commonwealth University, Richmond, VA-23284, USA.
Department of Biochemistry, Faculty of Science, The Maharaja Sayajirao University of Baroda, Vadodara 390002, Gujarat, India.
Cell Signal. 2025 Apr;128:111647. doi: 10.1016/j.cellsig.2025.111647. Epub 2025 Feb 6.
In current immunotherapy cGAS (cyclic GMP-AMP synthase)-STING (stimulator of interferon genes) pathway considered as most focused area after CAR-T cell. Exploitation of host immunity against cancer using STING agonists generates the most interest as a therapeutic target. Classically cGAS activation through cytoplasmic DNA generates 2'3'cGAMP that is naturally identified STING agonist. Activation of STING leads to activation of type-1 interferon response and pro-inflammatory cytokines through TBK/IRF-3, TBK/NF-κB pathways. Pro-inflammatory cytokines attract immune cells to the tumor microenvironment and type-1 interferon exposes tumor antigens to T cells and NK cells, which leads to the activation of cellular immunity against tumor cells and eliminates tumor cells. Initially bacterial-derived c-di-AMP and c-di-GMP were identified as CDNs (Cyclic-dinucleotide) STING agonists. Moreover, chemically modified CDNs and completely synthetic STING agonists have been developed. Even though the breakthrough preclinical development none of the STING agonists were approved the by FDA for cancer therapy. All identified natural CDNs have poor pharmacokinetic properties due to high hydrophilicity and negative charge. Moreover, phosphodiester bonds in CDNs are most vulnerable to enzymatic degradation. Synthetic STING agonists have an off-target effect that generates autoimmunity and cytokine storm. STING agonist needs to improve for pharmacokinetics, efficacy, and safety. In this scenario delivery systems can overcome the challenges associated with STING agonists. Here, we highlight the ways of STING agonisms as direct and indirect, and further, we also discuss the existing STING agonists associated challenges and ongoing efforts for delivery of STING agonists in the tumor microenvironment (TME) via different non-targeted carriers like Nanoparticle, Hydrogel, Micelle, Liposome. We also discussed the most advanced targeted deliveries of ADC (Antibody-drug conjugate) and aptamers-based delivery.
在当前的免疫疗法中,cGAS(环鸟苷单磷酸腺苷合酶)-STING(干扰素基因刺激因子)通路被认为是继嵌合抗原受体T细胞(CAR-T细胞)之后最受关注的领域。利用STING激动剂开发宿主抗癌免疫作为一种治疗靶点引起了极大的兴趣。经典地,通过细胞质DNA激活cGAS会产生2'3'cGAMP,它是天然的STING激动剂。STING的激活会通过TBK/IRF-3、TBK/NF-κB通路导致1型干扰素反应和促炎细胞因子的激活。促炎细胞因子将免疫细胞吸引到肿瘤微环境中,而1型干扰素将肿瘤抗原呈递给T细胞和自然杀伤细胞(NK细胞),从而导致针对肿瘤细胞的细胞免疫激活并消除肿瘤细胞。最初,细菌衍生的环二腺苷酸(c-di-AMP)和环二鸟苷酸(c-di-GMP)被鉴定为环二核苷酸(CDN)类STING激动剂。此外,已经开发出了化学修饰的CDN和完全合成的STING激动剂。尽管在临床前开发方面取得了突破,但尚无一种STING激动剂获得美国食品药品监督管理局(FDA)批准用于癌症治疗。所有已鉴定的天然CDN由于高亲水性和负电荷而具有较差的药代动力学性质。此外,CDN中的磷酸二酯键极易受到酶促降解。合成的STING激动剂具有产生自身免疫和细胞因子风暴的脱靶效应。STING激动剂需要在药代动力学、疗效和安全性方面加以改进。在这种情况下,递送系统可以克服与STING激动剂相关的挑战。在此,我们重点介绍STING激动作用的直接和间接方式,此外,我们还讨论了现有STING激动剂相关的挑战以及通过纳米颗粒、水凝胶、胶束、脂质体等不同非靶向载体在肿瘤微环境(TME)中递送STING激动剂的持续努力。我们还讨论了抗体药物偶联物(ADC)和基于适配体的递送等最先进的靶向递送方式。