Anti-cancer agents in medicinal chemistry最新文献

{"title":"Novel PD-L1 Small-Molecule Inhibitors Advancing Cancer Immunotherapy.","authors":"Annoor Awadasseid, Mengda Wu, Feng Zhang, Yanhua Song, Yanling Wu, Wen Zhang","doi":"10.2174/0118715206393267250912114756","DOIUrl":"https://doi.org/10.2174/0118715206393267250912114756","url":null,"abstract":"<p><strong>Introduction: </strong>The emergence of immune checkpoint inhibitors has revolutionized the treatment of cancer. Among these, the programmed cell death protein-1 (PD-1)/programmed death-ligand 1 (PD-L1) axis remains a critical target. However, resistance to current biologics necessitates the development of novel Small- Molecule Inhibitors (SMIs) with distinct mechanisms and improved pharmacological profiles. This review provides a comprehensive analysis of recent progress in PD-L1-targeting SMIs, including original compounds from our laboratory.</p><p><strong>Methods: </strong>We conducted a structured literature review using electronic databases such as PubMed, Scopus, and Web of Science. Articles published between 2015 and 2025 were included based on relevance to small-molecule PD-L1 inhibitors in cancer immunotherapy. Key data were extracted and synthesized regarding molecular design strategies, mechanisms of action, pharmacokinetics, and therapeutic efficacy. Compounds synthesized in our laboratory (Compounds 5-10 [A56]) were evaluated using in vitro assays, including PD-L1/PD-1 binding inhibition, cancer cell viability assays, and gene expression profiling.</p><p><strong>Results: </strong>Recent SMIs exhibit diverse functional profiles: direct blockade of PD-1/PD-L1 interaction, intracellular PD-L1 modulation, and transcriptional downregulation. Notably, Compound 7 demonstrated significant suppression of PD-L1 mRNA expression, while Compounds 9 and 10 (A56) achieved nanomolar-level binding affinity. These findings reflect innovative approaches to overcoming immune resistance and enhancing antitumor responses.</p><p><strong>Discussions: </strong>Our findings underscore a trend toward multifunctional PD-L1-targeting SMIs that operate through both extracellular and intracellular mechanisms. Compounds from our laboratory represent potential leads for further optimization and clinical translation. However, challenges remain regarding oral bioavailability, metabolic stability, and immune-related adverse events.</p><p><strong>Conclusion: </strong>Small-molecule PD-L1 inhibitors offer a promising avenue for expanding cancer immunotherapy. Our review highlights key advances and introduces novel small-molecule PD-L1 inhibitors with strong potential for future development, particularly in combination regimens.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145231438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting TGF-βR1 Signaling Pathway in Pancreatic Cancer: A Potential Approach with Synthetic Flavanols.","authors":"Rachel Cordeiro, Milind Bhitre, Shivam Varma, Sumit Waragade, Shubham Varma","doi":"10.2174/0118715206388963250901091741","DOIUrl":"https://doi.org/10.2174/0118715206388963250901091741","url":null,"abstract":"<p><strong>Introduction: </strong>Pancreatic adenocarcinoma is a highly aggressive cancer with a poor prognosis and a five-year survival rate of just 13%. Its asymptomatic onset, rapid progression, and resistance to therapy make it challenging to treat. Transforming Growth Factor-β (TGF-β) signaling, particularly through TGF-β Receptor 1 (TGF-βR1/ALK-5), plays a major role in tumor progression by inducing Epithelial-Mesenchymal Transition (EMT), immune evasion, and apoptosis resistance. Targeting ALK-5 is a promising strategy for therapeutic intervention.</p><p><strong>Methods: </strong>Twenty-nine synthetic flavonols were designed to inhibit ALK-5 and docked using Schrodinger's Glide XP. The compounds were synthesized via a green, one-pot method and characterized using 1H-NMR, 13CNMR, Mass Spectrometry, CHN analysis, and IR spectroscopy. The anti-cancer activity was evaluated against MiAPaCa-2 pancreatic cancer cells by measuring GI50, TGI, and LC50. ALK-5 inhibition was quantified using the ADP-Glo® Kinase Assay, assessing ATP transfer.</p><p><strong>Results: </strong>RFL-1 showed the strongest binding affinity (-9.38 kcal/mol) at ALK-5's active site and the highest kinase inhibition (ATP transfer: 3.67%), outperforming quercetin (9.22%). It also demonstrated an IC50 of 14.92 ± 3.54 μM. Ten flavonols exhibited strong cytotoxicity (GI50 < 10 μM), while four others showed moderate activity (GI50 = 23-26 μM).</p><p><strong>Discussion: </strong>RFL-1 and related flavonols (RFL-12, RFL-20, RFL-25, RFL-28) effectively inhibited ALK-5 and suppressed the growth of pancreatic cancer cells. Their dual activity supports further development as targeted anti-cancer agents.</p><p><strong>Conclusion: </strong>Synthetic flavonols, particularly RFL-1, show promise as ALK-5 inhibitors and potential therapies for pancreatic adenocarcinoma, warranting further in vivo validation.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145231112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Induction of Apoptosis and Activation of Endoplasmic Reticulum Stress by SJ6986 in Diffuse Large B-cell Lymphoma.","authors":"Chenxing Zhang, Bangxue Jiang, Xiaomei Liang, Yinting Chen, Zhaozheng Li, Minyi Zhao, Dongjun Lin","doi":"10.2174/0118715206407523250902055051","DOIUrl":"https://doi.org/10.2174/0118715206407523250902055051","url":null,"abstract":"<p><strong>Introduction: </strong>Diffuse large B-cell lymphoma (DLBCL) is one of the most prevalent hematological malignancies with high mortality. G1 to S phase transition 1 (GSPT1), a key translation termination factor involved in protein synthesis, has been implicated in tumor progression. This study aimed to investigate the effectiveness and underlying mechanisms of the GSPT1 degrader SJ6986 in DLBCL.</p><p><strong>Methods: </strong>The TCGA and GTEx datasets were utilized to assess the expression of GSPT1 in DLBCL. The viability and proliferation of DLBCL cells were detected using the Cell Counting Kit-8 (CCK-8) assay. Cell apoptosis was detected via flow cytometry. The expression of GSPT1 was evaluated using qRT-PCR and Western blot. Xenograft mouse models were employed to explore the in vivo therapeutic potential of SJ6986. RNA sequencing was used to explore the potential mechanism of SJ6986 in DLBCL.</p><p><strong>Results: </strong>This study first identified that GSPT1 is highly expressed in DLBCL and demonstrated that its genetic knockdown significantly suppressed the activity of DLBCL cells. Furthermore, it was found that SJ6986 effectively reduced the proliferation of DLBCL cells, induced cell apoptosis, and inhibited tumor growth in vivo without significant toxicity. Mechanistically, RNA sequencing analysis showed that the endoplasmic reticulum (ER) stress was significantly triggered following SJ6986 treatment, and SJ6986 was found to activate the ER stress-related apoptosis in DLBCL cells.</p><p><strong>Discussion: </strong>Our findings suggested that SJ6986 exerts its anti-tumor effects in DLBCL and activates the ER stress-related apoptotic signaling. These results supported SJ6986 as a viable anticancer drug for treating DLBCL. Future studies should further investigate its mechanism and evaluate its clinical application value.</p><p><strong>Conclusions: </strong>This study validated the efficacy and safety of SJ6986 in treating DLBCL and discovered its role in inducing ER stress and subsequent apoptosis, offering a promising therapeutic option for DLBCL patients.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145197534","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PRR22: A Novel Prognostic Indicator and Therapeutic Target for Prostate Cancer.","authors":"Wenxia Chen, Guodong Ding, Yuantang Zhong, Meiting Lao, Qing Zhang, Dongbing Li, Wangdong Deng, Yiwen Chen","doi":"10.2174/0118715206415552250910202624","DOIUrl":"https://doi.org/10.2174/0118715206415552250910202624","url":null,"abstract":"<p><strong>Introduction: </strong>Prostate cancer (PRAD) remains a leading malignancy with limited prognostic biomarkers and therapeutic targets. PRR22, a proline-rich protein-coding gene, has a role in PRAD that remains undefined. This study is the first to systematically investigate the clinical relevance and mechanistic implications of PRR22 in PRAD.</p><p><strong>Methods: </strong>PRR22 expression was analyzed in TCGA-PRAD (n = 501), GSE55945, and the Human Protein Atlas datasets. Prognostic value was assessed via Kaplan-Meier and multivariate Cox analyses. Mechanistic insights were derived from GSEA, immune infiltration profiling, MSI/mRNA-si correlations, and drug sensitivity analysis. Experimental validation was performed via qRT-PCR in PRAD cell lines.</p><p><strong>Results: </strong>PRR22 was significantly upregulated in PRAD tissues compared to normal tissues (p < 0.001) and independently predicted shorter progression-free survival (HR = 1.82, p = 0.009). Novel associations were identified between PRR22 and TGF-β signaling, immune evasion (e.g., LAG3 upregulation), microsatellite instability (MSI), and stemness (mRNA-si). High PRR22 correlated with resistance to multiple drugs (e.g., bicalutamide, vorinostat).</p><p><strong>Discussion: </strong>PRR22 overexpression in PRAD is linked to poor prognosis and immune regulation, suggesting its potential as a prognostic biomarker and therapeutic target. Future research should focus on clinical validation and on exploring the molecular mechanisms underlying PRR22's role in PRAD.</p><p><strong>Conclusion: </strong>PRR22 is a novel, independent prognostic biomarker and actionable therapeutic target in PRAD, linking tumor aggressiveness to immune microenvironment remodeling and drug resistance. These findings establish PRR22 as a candidate for clinical implementation in risk stratification and targeted therapy.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145197485","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Apoptosis-Mediated Anticancer Activity of Zinc Oxide Nanoparticles Derived and Characterized from Halophila beccarii.","authors":"Jayasheela Sarilla, Vani Mathakala, Uma Maheswari Devi Palempalli","doi":"10.2174/0118715206413187250923055621","DOIUrl":"https://doi.org/10.2174/0118715206413187250923055621","url":null,"abstract":"<p><strong>Introduction: </strong>Recent advancements in nanomedicine have drawn attention to the use of zinc oxide nanoparticles as apoptotic agents to address triple-negative breast cancer. Halophila beccarii-mediated zinc oxide nanoparticles (Hb-ZnONPs) were fabricated using zinc acetate dihydrate as the precursor.</p><p><strong>Methods: </strong>The fabricated nanoparticles were characterized based on morphological, structural, and elemental composition using SEM and XRD. The antiproliferative potential of Hb-ZnONPs was studied using the BT-549 cell line as an in vitro model, employing the MTT assay and Annexin V-FITC/PI-based flow cytometry analysis.</p><p><strong>Results: </strong>The Hb-ZnONPs exhibited characteristic absorption maxima at 367 nm with a particle size of 35 nm and -44.7 mV stability. XRD confirmed the hexagonal wurtzite structure with an elemental composition of 62.3% Zn and 25.79% Oxygen. The Hb-ZnONPs demonstrated significant cytotoxicity against BT-549 cells, with 35.26% apoptosis at 5 μg/ml and 38.25% apoptosis at 10 μg/ml. However, cells in the late apoptosis stage increased from 14.48% at 5 μg/ml to 28.16% at 10 μg/ml, indicating a nearly twofold increase with the higher concentration.</p><p><strong>Conclusion: </strong>Hb-ZnONPs may act as promising apoptotic inducers in the chemotherapy of breast cancer.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145197494","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rosmarinic Acid as a Potential Therapeutic Agent against Neuroblastoma: Anticancer Activity and Molecular Docking Insights.","authors":"Pınar Yumrutaş, Demet Taşdemir, Önder Yumrutaş","doi":"10.2174/0118715206406705250911103628","DOIUrl":"https://doi.org/10.2174/0118715206406705250911103628","url":null,"abstract":"<p><strong>Introduction: </strong>Rosmarinic acid (RA) is a phenolic acid known for its important biological activities. Although it has been shown to inhibit various cancer cell types, its effects on the suppression and induction of apoptosis in neuroblastoma cells remain unclear. In this study, the antiproliferation and apoptosis-inducing effects of various concentrations of rosmarinic acid on neuroblastoma cells (SH-SY5Y) were investigated. Additionally, molecular docking analysis was conducted to examine the interaction between rosmarinic acid and the antiapoptotic protein BCL2.</p><p><strong>Methods: </strong>SH-SY5Y cells were treated with rosmarinic acid at concentrations of 50, 100, 150, and 200 μg/ml for 24 hours. The percentages of apoptotic and necrotic cells in cultures treated with the lowest and highest concentrations were assessed using the Annexin V/PI staining method. Furthermore, the interaction between rosmarinic acid and BCL2 protein was analyzed using molecular docking techniques.</p><p><strong>Results: </strong>The viability of rosmarinic acid-treated SH-SY5Y cells decreased. In SH-SY5Y cells, the percentage of late apoptotic cells increased to 40%. Molecular docking results showed that the benzene ring of rosmarinic acid formed pi-alkyl interactions with PHE71 and van der Waals interactions with SER64, ALA72, SER75, and VAL115 of BCL2. The lowest binding energy was calculated as -7.2 kcal/mol.</p><p><strong>Discussion: </strong>RA demonstrated a suppressive effect on SH-SY5Y cells by targeting the antiapoptotic protein BCL2, suggesting a potential mechanism of action through the induction of apoptosis.</p><p><strong>Conclusion: </strong>RA inhibited neuroblastoma SH-SY5Y cell proliferation and induced apoptotic cell death. It inhibited the proliferation of neuroblastoma SH-SY5Y cells and promoted apoptotic cell death, potentially through interaction with the BCL2 protein.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147442","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Review of the Anticancer Properties of Cedrol and its Molecular Mechanisms.","authors":"Ali Mohammad Pourbagher Shahri, Sajad Sahab Negah, Meysam Moghbeli, Ehsan Saburi, Fatemeh Forouzanfar","doi":"10.2174/0118715206389915250911110114","DOIUrl":"https://doi.org/10.2174/0118715206389915250911110114","url":null,"abstract":"<p><p>Despite decades of research on promising new therapies, cancer remains a leading cause of morbidity and mortality. Over the years, extensive research has been conducted on the potential anticancer effects of various medicinal plants. One extremely promising agent or adjuvant that may be utilized for the prevention/ treatment of several malignancies is cedrol, a naturally occurring sesquiterpene. Cedrol modulates multiple molecular pathways involved in the protracted carcinogenesis process, including the generation of reactive oxygen species, activation of pro-death autophagy, inhibition of survival signals, promotion of apoptosis, and inhibition of minichromosome maintenance proteins. This review suggests that cedrol might be a unique medication for the treatment of glioblastoma, lung cancer, and colorectal cancers. Further in-depth investigations of cedrol's anticancer mechanisms are needed.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147528","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nanosomal-Mediated Lipid Suspension Delivery of Docetaxel as a Promising Landscape to Enhance the Therapeutic Potential in Triple-Negative Breast Cancer","authors":"Pritya Jha, Varisha Anjum, Rabia Choudhary, Ammar Kadi, Faraat Ali, Irina Potoroko","doi":"10.2174/0118715206366378250519105734","DOIUrl":"10.2174/0118715206366378250519105734","url":null,"abstract":"<p><p>The challenging subtype of breast cancer known as Triple-Negative Breast Cancer (TNBC) is characterized by the absence of HER2 expression, progesterone receptors, and estrogen receptors. TNBC is linked to a harsh treatment trajectory, elevated rates of recurrence, and restricted therapeutic alternatives. The mainstay of treatment for TNBC has historically been conventional chemotherapy, especially taxanes like Docetaxel. However, the effectiveness of these drugs is frequently compromised by systemic toxicity and resistance mechanisms. The development of Nanosomal Docetaxel Lipid Suspension (NDLS) offers a promising alternative, designed to enhance Docetaxel's therapeutic index by improving solubility, reducing side effects, and optimizing tumor-targeted drug delivery. NDLS has potential as a delivery system for additional chemotherapy drugs or combination treatments. This study addresses the cellular and molecular causes of TNBC, emphasizes the drawbacks of traditional treatments, and offers a thorough examination of NDLS in preclinical and clinical settings. This review provides a thorough analysis of NDLS in TNBC, laying the groundwork for further studies and therapeutic applications.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144179717","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting the Lin28/let-7 Axis with Compounds to Regulate Transcriptional Control in Cancer.","authors":"Xingpeng Wang, Pham Kim Thuong Van, Bo Liu, Tingxiu Zhao, Yun-Shan Wu","doi":"10.2174/0118715206375441250901064006","DOIUrl":"https://doi.org/10.2174/0118715206375441250901064006","url":null,"abstract":"<p><p>Lin28 is a pivotal RNA-binding protein that regulates the biogenesis of let-7 microRNAs, which play a crucial role in the post-transcriptional regulation of oncogenes in cancer. The Lin28/let-7 axis is integral to the regulation of key cellular processes such as proliferation, differentiation, and apoptosis. Lin28 promotes the upregulation of oncogenes, including MYC, RAS, and HMGA2, by inhibiting the maturation of let-7, thereby facilitating tumor initiation, progression, and metastasis. Consequently, targeting the Lin28/let-7 interaction has emerged as a promising therapeutic strategy, particularly for malignancies that lack specific molecular targets. This approach holds potential for downregulating oncogene expression and inhibiting tumor progression. Through a comprehensive review of the literature, this article classifies Lin28/let-7 inhibitors into three categories: CSD/ZKD inhibitors, non-CSD/ZKD inhibitors, and let-7 restorers. CSD/ZKD inhibitors, such as TPEN and KCB3602, function by binding to the CSD or ZKD domains of Lin28, thereby inhibiting its activity. Non- CSD/ZKD inhibitors, including compounds like C1632 and Simvastatin, have been identified as molecules that can reduce Lin28 activity, though their binding sites remain unknown. Let-7 restorers, on the other hand, do not directly target Lin28 but instead work indirectly by modulating the activity of associated molecules, such as Zcchc11 and Zcchc6, thereby promoting the restoration of let-7 expression levels. Notable examples of these include IPA-3 and FPA124. This review summarizes recent advances in the development of Lin28/let-7 inhibitors and their therapeutic potential, providing an important reference for ongoing research on Lin28 inhibitors in cancer therapy.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145084651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PREFACE.","authors":"Simone Carradori","doi":"10.2174/0118715206442176250912055138","DOIUrl":"https://doi.org/10.2174/0118715206442176250912055138","url":null,"abstract":"","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145079508","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}