Cancer Chemotherapy and Pharmacology最新文献

{"title":"Trends in renal function following vascular endothelial growth factor inhibitor administration in patients with cancer and diabetes mellitus.","authors":"Yuma Shibutani, Miki Hayakawa, Mayu Ishizaka","doi":"10.1007/s00280-025-04793-6","DOIUrl":"https://doi.org/10.1007/s00280-025-04793-6","url":null,"abstract":"<p><strong>Background: </strong>Vascular endothelial growth factor (VEGF) inhibitors are associated with a high incidence of proteinuria. In patients with diabetes, increased proteinuria is closely associated with decreased renal function; however, the impact of increased proteinuria on renal function in patients with cancer and diabetes mellitus undergoing VEGF inhibitor therapy remains unknown.</p><p><strong>Methods: </strong>The incidence of proteinuria and renal function in patients with cancer and a history of diabetes who were treated with VEGF inhibitors at the National Cancer Center Hospital East between January 2018 and December 2019 was retrospectively investigated.</p><p><strong>Results: </strong>Among the 49 patients included, 21 (43%) developed proteinuria ≥ 3 + after VEGF inhibitor treatment. In all patients, a decreasing trend in the estimated glomerular filtration rate (eGFR) was observed beginning 2 years after treatment initiation. The decrease in eGFR from baseline was - 6.6% at 1 year, -11% at 2 years, and - 13% at 4 years. Patients who developed proteinuria ≤ 2 + showed no significant decrease in eGFR from baseline to either the end of treatment (p = 0.91) or the latest value during the observation period (p = 0.64). Similarly, no significant decrease in eGFR was observed in those with proteinuria ≥ 3+ (end of treatment, p = 0.91; latest value during the observation period, p = 0.18).</p><p><strong>Conclusions: </strong>In patients with cancer and diabetes mellitus, increased proteinuria after VEGF inhibitor therapy suggested that it was not associated with a significant decline in renal function.</p>","PeriodicalId":9556,"journal":{"name":"Cancer Chemotherapy and Pharmacology","volume":"95 1","pages":"69"},"PeriodicalIF":2.7,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144539088","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":"Pharmacokinetics, safety, and tolerability of fedratinib in adults with moderate and severe hepatic impairment: results from the phase 1 FEDR-CP-001 trial.","authors":"Yizhe Chen, Richard A Preston, Thomas Marbury, William B Smith, Massimo Attanasio, Mark Thomas, Michael Thomas, Bing He, Yongjun Xue, Atalanta Ghosh, Gopal Krishna, Ken Ogasawara","doi":"10.1007/s00280-025-04785-6","DOIUrl":"https://doi.org/10.1007/s00280-025-04785-6","url":null,"abstract":"<p><strong>Purpose: </strong>The FEDR-CP-001 (NCT03983161) trial evaluated the pharmacokinetics (PK) and safety of a single dose of fedratinib in adults with moderate or severe hepatic impairment (HI) compared with matched healthy participants with normal hepatic function.</p><p><strong>Methods: </strong>This was a non-randomized, open-label, multicenter, phase 1 trial. Participants were aged 18-75 years and had a BMI of 18-40 kg/m². HI was determined by Child-Pugh score. Participants were placed into 1 of the following groups: group 1, moderate HI; group 2, healthy participants matched to group 1; group 3, severe HI; and group 4, healthy participants matched to group 3. Participants received a single dose of fedratinib 300 mg (groups 1 and 2) or 200 mg (groups 3 and 4) and were followed for 21 days.</p><p><strong>Results: </strong>All participants (N = 38; groups 1, 3, and 4 [n = 8 each], group 2 [n = 14]) completed the trial. Peak and total fedratinib exposures (C_max, AUC_0-∞) were similar between moderate HI versus matched healthy participants. In participants with severe HI, there were lower total exposures compared to the matched healthy participants where the ratios of geometric means for C_max, and AUC_0-∞ were 0.897 and 0.660, respectively, and with large inter-participant variability. Ten participants experienced a treatment-emergent adverse event (all were considered mild), which were evenly distributed across groups.</p><p><strong>Conclusion: </strong>These data indicate that reducing fedratinib starting doses is not necessary for patients with moderate or severe HI, and support clinicians in regular monitoring of patients with HI taking fedratinib.</p>","PeriodicalId":9556,"journal":{"name":"Cancer Chemotherapy and Pharmacology","volume":"95 1","pages":"65"},"PeriodicalIF":2.7,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144539087","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":"Pazopanib and antacids: insights from the WHO pharmacovigilance database.","authors":"Kazuki Nishida, Yao Liang, Osamu Maeda, Angélique Da Silva, Yuichi Ando, Basile Chrétien","doi":"10.1007/s00280-025-04792-7","DOIUrl":"https://doi.org/10.1007/s00280-025-04792-7","url":null,"abstract":"<p><p>Pazopanib, a multi-targeted tyrosine kinase inhibitor, is used for advanced renal cell carcinoma and soft tissue sarcoma. However, it is associated with dose-dependent adverse events (AEs), including hypertension, and gastrointestinal issues. Antacids like proton pump inhibitors (PPIs) and histamine-2 receptor antagonists (H2RAs) are often co-administered, raising concerns about potential drug interactions. Pazopanib's solubility and absorption are pH-dependent, with increased gastric pH potentially reducing its bioavailability. In this study, we analyzed VigiBase^® data using multivariate logistic regression models and found significant interactions between pazopanib and antacids (PPIs, H2RAs, and others), suggesting reduced serious AE reporting, possibly due to lower pazopanib exposure. A secondary analysis of CYP3A4 inhibitors showed a non-significant trend for higher serious AEs, aligning with expected pharmacokinetic effects. These findings emphasize the need for caution when combining antacids with pazopanib, as it may reduce both toxicity and efficacy.</p>","PeriodicalId":9556,"journal":{"name":"Cancer Chemotherapy and Pharmacology","volume":"95 1","pages":"66"},"PeriodicalIF":2.7,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144539085","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 insulin-like growth factor-1 (IGF-1) by using metformin in non-diabetic metastatic breast cancer female patients: a randomized controlled trial.","authors":"Hager Salah, Hoda Rabea, Mostafa S Sheemy, Alshaimaa Ibrahim Rabie, Hebatallah Ahmed Mohamed Moustafa, Ahmed A Elberry, Ahmed Hassan","doi":"10.1007/s00280-025-04791-8","DOIUrl":"10.1007/s00280-025-04791-8","url":null,"abstract":"<p><strong>Purpose: </strong>Insulin-like growth factor-1 (IGF-1) may play a role in breast cancer (BC) development. Metformin was found to exert anti-cancer function in several studies, partly by interference with the IGF-1 signaling pathway and reducing its blood levels. Therefore, our study aimed primarily to find out how metformin affected both IGF-1 levels and clinical outcomes in metastatic breast cancer patients (MBC) and secondarily to identify the correlation between post-treatment IGF-1 decline rates and BC prognosis and metastasis.</p><p><strong>Methods: </strong>Fifty MBC female patients were randomly assigned to either the control group (who were administered conventional chemotherapy) and the intervention group (treated with metformin plus chemotherapy). An enzyme-linked immunosorbent assay (ELISA) was used to detect IGF-1 levels at baseline and three months post-treatment.</p><p><strong>Results: </strong>IGF-1 levels in the metformin group were significantly lower than in the control group (p = 0.011). Furthermore, the percentage of post-treatment drop in IGF-1 levels differed significantly between the control and metformin groups (p = 0.001). Patients whose IGF-1 levels increased after treatment had a statistically significant occurrence of progressive disease (disease progression) in the control group higher than in the metformin group (92.9% versus 87.5%).</p><p><strong>Conclusion: </strong>The co-administration of metformin with chemotherapy significantly inhibited the IGF-1 signaling pathway, which reduced progressive diseases and reduced mortality in non-diabetic MBC patients. However, while metformin exerts a robust IGF-1 lowering effect, combination chemotherapy and low metastasis burden may further enhance this effect.</p><p><strong>Trail registration: </strong>Our trial was registered at clinicaltrials.gov (ID no. NCT04143282).</p>","PeriodicalId":9556,"journal":{"name":"Cancer Chemotherapy and Pharmacology","volume":"95 1","pages":"64"},"PeriodicalIF":2.7,"publicationDate":"2025-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144511602","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":"Potential anticancer effects of sodium-glucose cotransporter protein 2 (SGLT2) inhibitors Canagliflozin and Dapagliflozin.","authors":"Weiyu Dong, Yanyan Wang, Shaohua Fan","doi":"10.1007/s00280-025-04788-3","DOIUrl":"https://doi.org/10.1007/s00280-025-04788-3","url":null,"abstract":"<p><p>The use of sodium-glucose cotransporter protein 2 (SGLT2) inhibitors, specifically canagliflozin and dapagliflozin, has expanded from diabetes treatment to promising anticancer applications. Epidemiological links between diabetes and certain cancers highlight the potential of these agents in oncology, as SGLT2 is highly expressed in various tumor types. By inhibiting glucose uptake, canagliflozin and dapagliflozin disrupt glycolysis-dependent tumor growth, promoting apoptosis and reducing proliferation across multiple cancer models, including liver, prostate, and lung cancers. Key pathways involved in these effects include PI3K/AKT, mTOR, and AMPK signaling. Importantly, the combination of SGLT2 inhibitors with chemotherapy or radiotherapy has been shown to enhance antitumor efficacy and reduce treatment resistance, underscoring their potential as adjunctive therapies. However, adverse effects, such as increased risk of infection, and the need for more comprehensive mechanistic studies limit current applications. Future research should focus on expanding the understanding of these mechanisms, evaluating efficacy in additional tumor types, and optimizing combination therapies to mitigate side effects. SGLT2 inhibitors thus represent a novel class of metabolic modulators with potential for significant impact in cancer therapeutics.</p>","PeriodicalId":9556,"journal":{"name":"Cancer Chemotherapy and Pharmacology","volume":"95 1","pages":"63"},"PeriodicalIF":2.7,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144494743","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":"Clinical relevance of Nectin-4 downregulation and biological changes caused by cytotoxic chemotherapy in bladder cancer.","authors":"Makito Miyake, Takuya Owari, Kota Iida, Sayuri Onishi, Nobutaka Nishimura, Tomomi Fujii, Cynthia N Jinno, Hideki Furuya, Yuki Oda, Tatsuki Miyamoto, Mitsuru Tomizawa, Takuto Shimizu, Kenta Onishi, Shunta Hori, Yosuke Morizawa, Daisuke Goto, Yasushi Nakai, Nobumichi Tanaka, Noriyoshi Miura, Tadahiko Kikugawa, Takashi Saika, Charles Rosser, Kiyohide Fujimoto","doi":"10.1007/s00280-025-04783-8","DOIUrl":"https://doi.org/10.1007/s00280-025-04783-8","url":null,"abstract":"<p><strong>Introduction: </strong>Mechanism underlying resistance to enfortumab vedotin (EV) and prognostication of Nectin-4 expression in muscle-invasive bladder cancer (MIBC) remains unclear.</p><p><strong>Methods: </strong>We generated gemcitabine-resistant HT-1376 and cisplatin-resistant HT-1376 cells generated from parental HT1376 cells (derived from MIBC). Transcriptome analysis was conducted to explore the biological function of differentially expressed genes detected in chemoresistant HT-1376 cells compared to parental HT-1376. In 70 patients with MIBC undergoing radical cystectomy, unsupervised hierarchical clustering was performed using immunohistochemical staining pattern with GATA3, KRT20, KRT5/6, KRT14, and Nectin-4 expression derived from the gene expression-based Nectin-4-modified NanoString molecular classification: Luminal-Nec4-High, Luminal-Nec4-Low, Basal-Nec4-High, and Basal-Nec4-Low subgroups.</p><p><strong>Results: </strong>We found significant downregulation of Nectin-4 expression along with epithelial-to-mesenchymal transition in chemoresistant HT-1376 cells. Exogenous expression of NECTIN4 in chemoresistant HT-1376 cells partially restored sensitivity to EV. RNA seq identified differentially expressed genes, including Nectin-4 and small proline-rich proteins, downregulated in chemoresistant HT-1376 cells. Over-representation analysis using GO and KEGG revealed upregulation of gene sets enriched for ribosome biogenesis-related pathways in chemoresistant HT-1376 cells. Nectin-4-modified molecular subtype resulted in better stratification of survival-the Luminal-Nec4-High subgroup had the best and the Basal-Nec4-Low subgroup had the worst prognosis. Comparing molecular subtypes of MIBC cells between transurethral resection specimens and matched radical cystectomy specimens revealed that 43% of neoadjuvant chemotherapy-treated patients with luminal subtype tumors showed a marked shift to the basal subtype in the cystectomy specimens.</p><p><strong>Conclusion: </strong>The clinical utility of Nection-4, associated molecules, and Nectin-4-modified molecular subtype need to be studied for better management strategies for MIBC.</p>","PeriodicalId":9556,"journal":{"name":"Cancer Chemotherapy and Pharmacology","volume":"95 1","pages":"62"},"PeriodicalIF":2.7,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144483220","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":"Novel desensitization protocol utilizing conventional formulations to mitigate Temozolomide-Related skin hypersensitivity.","authors":"Morgan E Cantley, Clyde Coleman, Rachael M Morgan, Niharika Reddy, Sarah A Sertich, John L Villano","doi":"10.1007/s00280-025-04782-9","DOIUrl":"10.1007/s00280-025-04782-9","url":null,"abstract":"","PeriodicalId":9556,"journal":{"name":"Cancer Chemotherapy and Pharmacology","volume":"95 1","pages":"61"},"PeriodicalIF":2.7,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144332513","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":"From predictive biomarker to therapeutic target: the dual role of SLFN11 in chemotherapy sensitivity.","authors":"Yue Feng, Yingze Li, Zhenhao Zhang, Yuxuan Dai, Xingchun Gou, Kejing Lao, Running Zhang","doi":"10.1007/s00280-025-04781-w","DOIUrl":"https://doi.org/10.1007/s00280-025-04781-w","url":null,"abstract":"<p><p>SLFN11, a DNA/RNA helicase implicated in replication stress response, has recently emerged as a pivotal determinant of chemotherapy sensitivity across multiple cancer types. The expression level of SLFN11 in various cancers is significantly positively correlated with the sensitivity of cancer cell DNA damage agents. SLFN11 exerts its chemosensitizing effects by RPA-coated single-stranded DNA (ssDNA) at stressed replication forks at stalled replication forks, thereby potentiating the cytotoxicity of platinum agents, topoisomerase inhibitors, and PARP inhibitors. Its roles in inhibiting ATR translation, mediating p53-independent apoptosis, sensitizing towards IFN-γ and enhancing chromatin accessibility also remain investigational. The down-regulation of SLFN11 expression is associated with epigenetic silencing including promoter methylation, histone deacetylation, and the histone methylation. In this paper, we reviewed the recent progress of SLFN11 as predictive biomarker and therapeutic target in multiple cancers including medulloblastoma, prostate cancer, breast cancer, ovarian cancer, lung cancer, head and neck cancer, esophageal carcinoma, gastric carcinoma and colorectal cancer. We also summarized 10 active clinical trials conducting molecular analyses to assess SLFN11's role. By bridging mechanistic understanding with translational opportunities, this review provides a roadmap for leveraging SLFN11 to overcome chemoresistance and advance precision oncology.</p>","PeriodicalId":9556,"journal":{"name":"Cancer Chemotherapy and Pharmacology","volume":"95 1","pages":"60"},"PeriodicalIF":2.7,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144324584","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":"Effect of Metformin on vascular endothelial injury in patients with non-small cell lung cancer treated with chemotherapy combined with bevacizumab.","authors":"Hongyan Li, Zhenye Pu, Jin Fang","doi":"10.1007/s00280-025-04780-x","DOIUrl":"10.1007/s00280-025-04780-x","url":null,"abstract":"<p><strong>Objective: </strong>This paper aimed to unravel the effect of metformin on vascular endothelial injury in patients with non-small cell lung cancer (NSCLC) treated with chemotherapy combined with bevacizumab.</p><p><strong>Methods: </strong>We recruited 120 NSCLC patients and then classified into A and B groups (n = 60 cases). A group was treated with chemotherapy + bevacizumab + metformin, and B group was treated with chemotherapy + bevacizumab. The efficacy, pro-inflammatory factors, immune factors, and markers of vascular endothelial injury before and after treatment were compared between the two groups. The incidence of adverse reactions and prognostic 1-year survival status during the treatment period in both groups were counted.</p><p><strong>Results: </strong>Higher ORR and DCR were observed in Group A relative to Group B. TNF-α, IL-2, IL-12, ET-1, TM, and vWF were elevated in both groups after treatment, but were lower in Group A than in Group B. CD³⁺, CD4⁺, and CD⁴⁺/CD⁸⁺ were reduced in both groups after treatment, but were higher in Group A than in Group B. OS and DFS were higher in Group A than in Group B.</p><p><strong>Conclusion: </strong>Metformin has some anti-inflammatory and immunoprotective effects on NSCLC patients treated with chemotherapy combined with bevacizumab, which may help to attenuate the vascular endothelial injury induced by chemotherapy and bevacizumab treatment and further improve the prognosis.</p>","PeriodicalId":9556,"journal":{"name":"Cancer Chemotherapy and Pharmacology","volume":"95 1","pages":"59"},"PeriodicalIF":2.7,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144301176","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":"Phase 1 studies of the indenoisoquinolines LMP776 and LMP744 in patients with solid tumors and lymphomas.","authors":"Geraldine O'Sullivan Coyne, Shivaani Kummar, Larry V Rubinstein, Deborah Wilsker, Nancy Moore, Murielle Hogu, Richard Piekarz, Joe Covey, Jan H Beumer, Katherine V Ferry-Galow, Liza C Villaruz, Melinda G Hollingshead, Julianne L Holleran, Joshua J Deppas, Yves Pommier, Brian Ko, Barry C Johnson, Ralph E Parchhment, Percy Ivy, James H Doroshow, Alice P Chen","doi":"10.1007/s00280-025-04778-5","DOIUrl":"10.1007/s00280-025-04778-5","url":null,"abstract":"<p><strong>Purpose: </strong>Indenoisoquinolines are a class of topoisomerase I (TOP1) inhibitors designed to overcome clinical limitations of camptothecins. Three indenoisoquinolines (LMP400, LMP776, and LMP744) demonstrated activity in murine models and a comparative canine lymphoma study. Clinical data for LMP400 were previously reported (NCT01051635). The maximum tolerated dose (MTD), safety, and clinical data from phase 1 studies of LMP776 (NCT01051635) and LMP744 (NCT03030417) are reported herein.</p><p><strong>Methods: </strong>Patients ≥ 18 years of age with advanced, refractory solid tumors or lymphomas received either LMP776 (n = 34) or LMP744 (n = 35) intravenously following a Simon accelerated titration design. Both LMP776 and LMP744 were administered daily for 5 days (QDx5) in 28-day cycles. Adverse events and clinical responses were evaluated according to CTCAE and RECIST v1.1 criteria, respectively. Pharmacokinetic and pharmacodynamic changes were evaluated.</p><p><strong>Results: </strong>The MTD of LMP776 was 12 mg/m²/day and that of LMP744 was 190 mg/m²/day. Dose-limiting toxicities (DLTs) for LMP776 included hypercalcemia, anemia, and hyponatremia; DLTs for LMP744 included hypokalemia, anemia, and weight loss. There was 1 confirmed partial response (cPR) among 35 patients receiving LMP744 (overall response rate 3%) and no objective responses in patients receiving LMP776. Tumor biopsies from the patient with cPR demonstrated high baseline expression of SLFN11 and a unique pattern of pharmacodynamic responses, including increased RAD51, phosphorylated KAP1 (pKAP1), γH2AX, and cleaved caspase-3 (cCasp3).</p><p><strong>Conclusion: </strong>MTDs and safety profiles are reported for LMP776 and LMP744. Target engagement by an indenoisoquinoline was measured for the first time in human samples.</p>","PeriodicalId":9556,"journal":{"name":"Cancer Chemotherapy and Pharmacology","volume":"95 1","pages":"58"},"PeriodicalIF":2.7,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12122562/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144172534","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}