Acta Pharmaceutica Sinica. B最新文献

{"title":"Targeting senescent cells with dipeptidyl peptidase 4-CAR-NK cells alleviates liver fibrosis and reverses metabolic dysfunction","authors":"Rui Hua, Kang Xu, Huan Peng, Kunda Liu, Nan Long, Chenye Zeng, Yida Wang, Yannan Guo, Zhao Wang","doi":"10.1016/j.apsb.2026.06.054","DOIUrl":"10.1016/j.apsb.2026.06.054","url":null,"abstract":"","PeriodicalId":6906,"journal":{"name":"Acta Pharmaceutica Sinica. B","volume":"16 9","pages":"Pages 6286-6291"},"PeriodicalIF":14.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148940584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The ADP-ribosyltransferases 3 (ART3) is a novel suppressor of pathological cardiac hypertrophy by ribosylating ITGA7","authors":"Yilei Meng,&nbsp;Sangyu Hu,&nbsp;Fang Lin,&nbsp;Yuping Zhu,&nbsp;Yingying Xiong,&nbsp;Yizhuo Sun,&nbsp;Qin Lin,&nbsp;Mingxing Lu,&nbsp;Na Yi,&nbsp;Tao Xiao,&nbsp;Hanrui Wang,&nbsp;Jie Sheng,&nbsp;Ye Xu,&nbsp;Chenyu Li,&nbsp;Cuimei Zhao,&nbsp;Haojie Lu,&nbsp;Agapios Sachinidis,&nbsp;Li Li,&nbsp;Luying Peng","doi":"10.1016/j.apsb.2026.06.053","DOIUrl":"10.1016/j.apsb.2026.06.053","url":null,"abstract":"<div><div>Pathological cardiac hypertrophy and heart failure remain mechanistically incompletely defined despite their clinical significance in cardiovascular disease. While ADP-ribosyltransferase cholera toxin-like (ARTC) enzymes modulate membrane protein function and downstream signaling <em>via</em> post-translational modifications, their role in cardiac pathology remains unexplored. Herein, we investigated the regulatory involvement of ADP-ribosyltransferase 3 (ART3) in myocardial remodeling. Cardiomyocyte-specific ART3 knockdown and overexpression murine models were established using adeno-associated virus serotype 9 (AAV9), with RNA-sequencing employed to profile ART3-dependent transcriptional responses in pathological cardiac hypertrophy. Functional validation was performed in complementary <em>in vitro</em> and <em>in vivo</em> hypertrophy models, complemented by immunoprecipitation-coupled mass spectrometry to identify ART3 substrates. ART3 was found to be cardiomyocyte-enriched and transcriptionally downregulated during progressive myocardial remodeling and heart failure. Cardiomyocyte-specific ART3 knockdown 3 accelerated the decompensatory transition of cardiac hypertrophy, whereas ART3 overexpression exerted significant anti-hypertrophic and anti-remodeling effects. Mechanistically, ART3 preserved cardiomyocyte mono-ADP-ribosyltransferase activity, catalyzing the site-specific mono-ADP-ribosylation (mADPr) of Integrin Subunit Alpha 7 (ITGA7) at residue R129. This post-translational modification was requisite for integrin signaling pathway activation, which mediated the observed cardioprotective effects. Collectively, these findings establish ART3 as a novel regulator of pathological cardiac hypertrophy by modulating ITGA7 <em>via</em> mADPr, highlighting its therapeutic potential as a target for heart failure intervention.</div></div>","PeriodicalId":6906,"journal":{"name":"Acta Pharmaceutica Sinica. B","volume":"16 9","pages":"Pages 5944-5960"},"PeriodicalIF":14.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148940647","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"APRIL-driven BCMA/TACI dual-targeted ligand–drug conjugates for selective and potent therapy of multiple myeloma","authors":"Linling Zhou,&nbsp;Yanping Sun,&nbsp;Jie Bi,&nbsp;Jiaqi Zhao,&nbsp;Yinli Xia,&nbsp;Jun He,&nbsp;Jisheng Wang,&nbsp;Liqiang Pan","doi":"10.1016/j.apsb.2026.02.001","DOIUrl":"10.1016/j.apsb.2026.02.001","url":null,"abstract":"<div><div>B-cell maturation antigen (BCMA) is highly expressed on malignant plasma cells and has emerged as an ideal therapeutic target in multiple myeloma (MM). However, the efficacy of BCMA-targeted therapies is often limited by antigen downregulation and tumor escape. Here, we report the design of a dual-targeted ligand–drug conjugate (LDC) leveraging a proliferation-inducing ligand (APRIL), the natural ligand for both BCMA and transmembrane activator and calcium-modulator and cyclophilin ligand interactor (TACI). This dual-targeting strategy enables enhanced binding breadth and mitigates antigen-loss-mediated resistance. Compared to conventional antibodies, APRIL-based fusion proteins (APRILFc) exhibited markedly faster internalization in MM cells (∼25% within 30 min), facilitating efficient intracellular drug delivery. LDCs conjugated with monomethyl auristatin E (MMAE) or SN-38 demonstrated potent cytotoxicity across diverse MM cell lines, outperforming corresponding antibody–drug conjugates (ADCs). Notably, LDCs maintained strong antitumor activity in BCMA-knockout models, highlighting their capacity to overcome BCMA escape. In both subcutaneous and intratibial MM mouse models, LDC-MMAE significantly suppressed tumor growth, including in the context of BCMA shedding. These findings establish APRIL-based LDCs as a promising, mechanistically distinct modality for MM therapy, capable of addressing key limitations of current BCMA-targeted approaches.</div></div>","PeriodicalId":6906,"journal":{"name":"Acta Pharmaceutica Sinica. B","volume":"16 9","pages":"Pages 5540-5552"},"PeriodicalIF":14.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148949548","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SIRT6 activator MDL-800 alleviates periodontal inflammation by inhibiting AIM2 pathway","authors":"Peilei Shi,&nbsp;Rui Ma,&nbsp;Xiaobing Lan,&nbsp;Li Feng,&nbsp;Kun Xue,&nbsp;Runnan Dai,&nbsp;Xudong Xie,&nbsp;Chunmei Xu,&nbsp;Tao Pang,&nbsp;Jun Wang,&nbsp;Jian Zhang","doi":"10.1016/j.apsb.2026.07.021","DOIUrl":"10.1016/j.apsb.2026.07.021","url":null,"abstract":"<div><div>Periodontitis is an infectious and inflammatory disease. The inability to control clinical inflammation significantly contributes to unsuccessful periodontal treatment. As a key regulator of epigenetics, Sirtuin 6 is one of the NAD⁺-dependent histone deacetylase family members and has recently gained considerable interest in the context of inflammation. While MDL-800 has been demonstrated as an activator of SIRT6, its function in treating periodontitis remains unknown. In this study, animal experiments revealed that MDL-800 reduced alveolar bone resorption in ligature-induced periodontitis, particularly <em>via</em> reducing inflammation and inhibiting osteoclast production in a SIRT6-dependent manner. Furthermore, human gingival fibroblasts (HGFs) were exposed to lipopolysaccharide (LPS) to mimic periodontal inflammation <em>in vitro</em>. We noted that MDL-800 remarkably reduced expressions of pro-inflammatory cytokines in LPS-induced HGFs, which was neutralized by inhibiting SIRT6. Besides, MDL-800 could also reduce oxidative stress damage under inflammatory conditions. The suppression of AIM2 inflammasome activation was associated with the significant anti-inflammatory properties of MDL-800, as demonstrated by RNA sequencing and validation experiments. In conclusion, these findings suggest that MDL-800 was effective in reducing periodontal inflammation, partly by inhibiting AIM2 pathway in a SIRT6-dependent manner, demonstrating significant promise for enhancing therapeutic outcomes in periodontitis.</div></div>","PeriodicalId":6906,"journal":{"name":"Acta Pharmaceutica Sinica. B","volume":"16 9","pages":"Pages 6066-6079"},"PeriodicalIF":14.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148940234","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development of galectin-3 targeted radioimmunoligands for cancer theranostics","authors":"Siqi Zhang,&nbsp;Qichen Hu,&nbsp;Qingshuang Lu,&nbsp;Jiang Wu,&nbsp;Zhen Li,&nbsp;Yanjun Wan,&nbsp;Hongyi Huang,&nbsp;Xueyao Chen,&nbsp;Can Liu,&nbsp;Hao Tian,&nbsp;Jieting Shen,&nbsp;Shuo Jiang,&nbsp;Quan Zuo,&nbsp;Xin Gao,&nbsp;Zhifei Cao,&nbsp;Xiushuang Yuan,&nbsp;Bing Cui,&nbsp;Feng Wang,&nbsp;Junfeng Wang,&nbsp;Ming-Rong Zhang,&nbsp;Kuan Hu","doi":"10.1016/j.apsb.2025.12.028","DOIUrl":"10.1016/j.apsb.2025.12.028","url":null,"abstract":"<div><div>Galectin-3 is associated with aggression, proliferation, and metastasis in various refractory cancers. Although galectin-3 targeted positron emission tomography (PET) tracers have shown considerable promise for cancer diagnosis, the therapeutic potential of galectin-3-directed radiopharmaceutical therapy for refractory or untreatable malignancies remains largely unexplored. This study aimed to develop novel galectin-3-targeted radioimmunoligands and verify their radiotheranostic potential in multiple tumor models. Two novel galectin-3 targeted monoclonal antibodies (QMAb-1 and QMAb-2) were labeled with both ⁸⁹Zr and ¹⁷⁷Lu. PET/CT imaging of [⁸⁹Zr]Zr-DFO-QMAb-1 and [⁸⁹Zr]Zr-DFO-QMAb-2 were evaluated in mouse tumor models with varying galectin-3 expression levels. Besides, the therapeutic efficacy of [¹⁷⁷Lu]Lu-DTPA-QMAb-1 and [¹⁷⁷Lu]Lu-DTPA-QMAb-2 was also investigated. The superior tumor uptake and retention time of [⁸⁹Zr]Zr-DFO-QMAb-1 was observed. Notably, [⁸⁹Zr]Zr-DFO-QMAb-1 demonstrated minimal off-target accumulation and rapid clearance from the bloodstream and major organs. Furthermore, [¹⁷⁷Lu]Lu-DTPA-QMAb-1 showed potent anti-tumor efficacy without inducing hematotoxicity and major organ damage, highlighting its therapeutic potential and safety profile. This study expands the repertoire of the galectin-3 radiopharmaceutical toolbox by harnessing high affinity mAbs as ligands, offering a new modality for the diagnosis and treatment of galectin-3-positive cancers. In addition, the favorable performance of [⁸⁹Zr]Zr-DFO-QMAb-1 and [¹⁷⁷Lu]Lu-DTPA-QMAb-1 theranostic pair in triple-negative breast cancer models further supports their clinical application potential across a range of refractory malignancies.</div></div>","PeriodicalId":6906,"journal":{"name":"Acta Pharmaceutica Sinica. B","volume":"16 9","pages":"Pages 5553-5565"},"PeriodicalIF":14.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147908324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular architecture responsible for specific inhibition of oncogenic PI3Kα mutants by RLY-2608 and STX-478","authors":"Xiao Liu,&nbsp;Yanyan Chen,&nbsp;Guanyi Li,&nbsp;Anqi Chen,&nbsp;Qingtong Zhou,&nbsp;Ming-Wei Wang","doi":"10.1016/j.apsb.2026.07.003","DOIUrl":"10.1016/j.apsb.2026.07.003","url":null,"abstract":"<div><div>Hotspot mutations in phosphoinositide 3-kinase alpha (PI3K<em>α</em>), such as H1047R, E542K, and E545K, drive tumorigenesis across multiple cancer types. Orthosteric PI3K<em>α</em> inhibitors are effective but have toxicity against wild-type PI3K<em>α</em>, the emergence of resistance, and a narrow therapeutic index. Allosteric inhibitors such as RLY-2608 and STX-478 offer a promising path toward mutant-specific suppression, yet the structural basis for their selectivity and mechanisms of action remain elusive. Here, we report high-resolution cryogenic electron microscopy structures of RLY-2608- and STX-478-bound H1047R, E542K, and E545K, revealing a shared cryptic allosteric pocket, accessible only through a major conformational rearrangement of the activation loop that is stabilized in oncogenic mutants. While both inhibitors occupy this pocket, they have distinct interaction networks and propagate divergent allosteric activities: RLY-2608 induces large-scale remodeling of catalytic and membrane-interacting elements, whereas STX-478 reinforces autoinhibitory interfaces between p110<em>α</em> and p85<em>α</em> subunits. Comparative analysis provides structural insights into their differentiated potency and selectivity.</div></div>","PeriodicalId":6906,"journal":{"name":"Acta Pharmaceutica Sinica. B","volume":"16 9","pages":"Pages 5884-5900"},"PeriodicalIF":14.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148949554","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metrnl in mitigating radiation enteritis via label-retaining cells protection by modulating the c-KIT-WNT pathway","authors":"Sailong Zhang,&nbsp;Simin Chen,&nbsp;Bingjie Guo,&nbsp;Qisheng Ling,&nbsp;Shuling Wang,&nbsp;Zhuwei Miao,&nbsp;Zhi Wang,&nbsp;Yuchen Wei,&nbsp;Sili Zheng,&nbsp;Zhiyong Li,&nbsp;An-Qiang Feng,&nbsp;Feng-Hua Qian,&nbsp;Chao-Yu Miao","doi":"10.1016/j.apsb.2026.06.026","DOIUrl":"10.1016/j.apsb.2026.06.026","url":null,"abstract":"<div><div>Currently, there exists no definitive standardized therapy for radiation enteritis. This study unveils Metrnl as a pivotal regulator of intestinal radioprotection through multi-dimensional single-cell profiling and mechanistic dissection. We first demonstrate that radiation dynamically reprograms Metrnl expression in a time-dependent manner, revealing its role as a radiation-responsive mediator. Crucially, Metrnl confers potent protection against radiation-induced intestinal injury through double mechanisms; Metrnl safeguards label-retaining cells (LRCs) rather than conventional Lgr5⁺ intestinal stem cells, and activates a novel c-KIT-WNT signaling axis <em>via</em> ERK/GSK3<em>β</em>-mediated pathway crosstalk, both revitalizing intestinal epithelial regeneration. Therapeutically, recombinant Metrnl emerges as a potential biotherapeutic, effectively attenuating radiation enteritis. These findings establish Metrnl as a key mediator bridging radiation biology and regenerative medicine, offering a transformative potential for radiation injury management.</div></div>","PeriodicalId":6906,"journal":{"name":"Acta Pharmaceutica Sinica. B","volume":"16 9","pages":"Pages 6129-6144"},"PeriodicalIF":14.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148940131","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dual-modal tumor-selective benzofuran tracer integrating real-time imaging and anticancer effects","authors":"Ho Jin Han,&nbsp;Min Su Yim,&nbsp;Gwi Ja Hwang,&nbsp;Junyeol Han,&nbsp;Sumin Kim,&nbsp;Yerim Choi,&nbsp;Min Ju Kim,&nbsp;Kyeong-Ryoon Lee,&nbsp;Junhye Kwon,&nbsp;Uisup Shin,&nbsp;Eun Young Shin,&nbsp;Jeong Kyu Bang,&nbsp;Eun Kyoung Ryu,&nbsp;Bo Yeon Kim,&nbsp;Nak-Kyun Soung","doi":"10.1016/j.apsb.2026.06.012","DOIUrl":"10.1016/j.apsb.2026.06.012","url":null,"abstract":"<div><div>Microtubule-targeting agents remain a cornerstone of cancer therapy; however, few compounds can simultaneously visualize intratumoral distribution and correlate pharmacodynamics with therapeutic response. Here, we describe BF-04, a Benzofuran-derived microtubule destabilizer that circumvents multidrug resistance and integrates anticancer efficacy with dual-modality imaging. Chemical conjugation with the Cyanine 5 fluorescent dye (Cy5) and Zirconium-89 (89Zr) provided high-contrast, real-time fluorescence and Positron emission tomography (PET) signals without the need for antibody or nanoparticle carriers, enabling direct monitoring of drug distribution and retention in tumors. Importantly, BF-04 exhibited tumor-selective accumulation independent of labeling, confirming a scaffold-driven targeting mechanism with strong translational potential for image-guided therapy. Mechanistically, BF-04 induced microtubule depolymerization, mitotic arrest, and apoptosis across multiple cancer cell lines and patient-derived organoids (PDOs). <em>In vivo</em> studies demonstrated selective tumor uptake and robust growth suppression with minimal systemic toxicity. Collectively, these findings establish BF-04 as a promising theranostic platform that combines potent microtubule disruption with real-time imaging to facilitate precision cancer therapy.</div></div>","PeriodicalId":6906,"journal":{"name":"Acta Pharmaceutica Sinica. B","volume":"16 9","pages":"Pages 6221-6234"},"PeriodicalIF":14.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148940132","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum to “Ginsenoside Rg1 alleviates post-ischemic stroke neuroinflammation by inhibiting CKLF1-mediated suppression of dead/dying neuron clearance” [Acta Pharmaceutica Sinica B 16 (2026) 3632–3654]","authors":"Pinglong Fan,&nbsp;Yuan Ruan,&nbsp;Kaichao Hu,&nbsp;Hongyun Wang,&nbsp;Junrui Ye,&nbsp;Shasha Wang,&nbsp;Ruolan Yuan,&nbsp;Guangyi Yang,&nbsp;Fangmin Liu,&nbsp;Wenbin He,&nbsp;Gang Li,&nbsp;Xu Yan,&nbsp;Shifeng Chu,&nbsp;Zhao Zhang,&nbsp;Naihong Chen","doi":"10.1016/j.apsb.2026.07.015","DOIUrl":"10.1016/j.apsb.2026.07.015","url":null,"abstract":"","PeriodicalId":6906,"journal":{"name":"Acta Pharmaceutica Sinica. B","volume":"16 9","pages":"Page 6307"},"PeriodicalIF":14.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148940235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The polymeric nanovectors landscape for cancer immunotherapies towards advanced therapy medicinal products (ATMPs)","authors":"Ilaria Elena Palamà,&nbsp;Alessandra Invidia,&nbsp;Claudia De Stradis,&nbsp;Gabriella Leccese,&nbsp;Clara Baldari,&nbsp;Barbara Cortese,&nbsp;Clara Guido,&nbsp;Andrea Giglio,&nbsp;Concetta Quintarelli,&nbsp;Biagio De Angelis,&nbsp;Gabriele Maiorano,&nbsp;Franco Locatelli,&nbsp;Giuseppe Gigli","doi":"10.1016/j.apsb.2026.07.020","DOIUrl":"10.1016/j.apsb.2026.07.020","url":null,"abstract":"<div><div>Despite major advances in oncology, cancer remains one of the leading causes of mortality worldwide, underscoring the need for more effective and personalized therapeutic solutions. Advanced therapy medicinal products (ATMPs), including gene and cell-based therapies, have emerged as a promising frontier for immune cell engineering in oncology. However, current approaches still face several technical/safety issues, mainly associated with the delivery strategies used and their complex manufacturing processes. In this context, polymeric nanovectors (pNVs) have gained attention as a promising tool for developing efficient therapeutic delivery systems. The possibility of customizing pNVs’ composition/physicochemical properties, exploiting natural/synthetic polymers, enables more precise and controlled cargo delivery to immune cells, paving the way for the development of future ATMPs-oriented strategies for cancer immunotherapy. This review highlights the recent advancements in the application of pNVs for the editing of immune cells, focusing on innovative nanotechnology-based strategies to enhance the precision and efficacy of immunotherapy with a particular emphasis on their prospective role in next-generation ATMP development.</div></div>","PeriodicalId":6906,"journal":{"name":"Acta Pharmaceutica Sinica. B","volume":"16 9","pages":"Pages 5760-5784"},"PeriodicalIF":14.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148940648","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}