This is a multicenter, randomized-controlled, open-label, blinded endpoint clinical trial that aims to evaluate the efficacy and safety of hemoadsorption for severe ischemic stroke

开始日期2025-09-01

申办/合作机构

皖南医学院

[+2]

NCT07027774

/ Not yet recruiting临床4期IIT

A Multicenter, Prospective, Randomized, Controlled Study Evaluating the Progression of Renal Function in Patients With Late-Stage Chronic Kidney Disease Treated With Henagliflozin

This is a multicenter, prospective, randomized, controlled study that will enroll approximately 429 subjects. The screening period will last 4-8 weeks. Subjects will undergo pre-screening based on eGFR and urinary albumin-to-creatinine ratio (UACR). Only non-dialysis subjects meeting the following criteria confirmed by local laboratories within 6 months prior to screening will be eligible for central laboratory screening:
10 mL/min/1.73m² ≤ eGFR < 30 mL/min/1.73m² and 150 mg/g (16.95 mg/mmol) ≤ UACR < 5000 mg/g (565 mg/mmol).
Unless contraindicated due to intolerance, subjects with 20 mL/min/1.73m² ≤ eGFR < 30 mL/min/1.73m² must receive stable, maximally tolerated labeled daily doses of ACEi or ARB for at least 4 weeks prior to randomization. For subjects with 10 mL/min/1.73m² ≤ eGFR < 20 mL/min/1.73m², investigators will determine ACEi/ARB treatment based on patient condition per KDIGO guidelines. Other antihypertensive, lipid-lowering, and glucose-lowering therapies should be stabilized for approximately 4 weeks before randomization. Investigators are encouraged to maintain stability of medications known to affect serum creatinine levels during screening and approximately 2 weeks prior to any serum chemistry measurements throughout the study. Eligible subjects will be randomized in a 1:1:1 ratio to receive Henagliflozin (10 mg q.d., 5 mg q.d.) or conventional therapy.
Thereafter, subjects will undergo laboratory assessments, concomitant medication review, adverse event collection, and clinical endpoint ascertainment at Week 4 (Day 30), Week 12 (Day 90), and Week 24 (Day 180), followed by every 12-week intervals. Throughout the study, all subjects will receive glycemic, blood pressure (target SBP <140 mmHg and DBP <90 mmHg), and lipid management according to current guidelines. All subjects will complete an end-of-study visit. Subjects discontinuing study drug prematurely should continue all subsequent study visits.

开始日期2025-07-10

申办/合作机构

皖南医学院

[+1]

NCT06990295

/ Not yet recruitingN/AIIT

Effects of Focused Ultrasound Spleen Neuromodulation on Inflammatory Cytokine Levels in Patients With Septic Shock: A Randomized Controlled Pilot Trial

This study evaluates the safety and effectiveness of focused ultrasound spleen neuromodulation in patients with septic shock, a life-threatening condition characterized by excessive inflammation and organ dysfunction. The primary objective is to determine whether non-invasive, focused ultrasound stimulation of the spleen can reduce circulating inflammatory cytokine levels in this patient population.
Eligibility Criteria:
Adults aged 18 years or older Diagnosed with septic shock and admitted to the ICU within 24 hours Expected to require intensive care for at least 72 hours
Study Protocol:
Participants will be randomly assigned to one of two groups:
Intervention Group: Will receive standard septic shock care plus twice-daily focused ultrasound stimulation over the spleen for five days, using a portable device.
Control Group: Will receive standard septic shock care alone. Blood samples will be collected at baseline, Day 3, and Day 5 to measure inflammatory cytokine levels, including TNF-α, IL-1β, IL-6, and IL-10. Additional assessments will include lymphocyte subpopulations, organ function scores, ICU length of stay, 28-day mortality, and adverse events.
Outcome Measures:
Primary: Change in levels of inflammatory cytokines on Day 3 and Day 5. Secondary: Changes in organ function (SOFA score), ICU length of stay, 28-day survival, and safety/tolerability of the intervention.

开始日期2025-07-03

申办/合作机构

皖南医学院

100 项与皖南医学院相关的临床结果

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0 项与皖南医学院相关的专利（医药）

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3,919

项与皖南医学院相关的文献（医药）

2026-02-01·BIOMATERIALS

Hydroxyl-augmented gold nanorods via lactone ring-opening alleviate cisplatin nephrotoxicity through Nrf2 activation

Article

作者: Cai, Yueming ; Fang, Chunyan ; Cai, Ying ; Lu, Yong ; Wang, Xiaoyan ; He, Cui

Cisplatin-induced acute kidney injury (AKI) epitomizes a critical barrier and paradox in cancers, where dose-limiting nephrotoxicity propelled by oxidative cascades lacks targeted interventions. This pressing clinical dilemma underscores the paramount need for kidney injury mitigation, while existing therapeutic strategies fail to achieve it due to inadequate efficacy and specificity. Here, we introduce a lactone ring-opening chemistry approach to amplify hydroxyl-driven redox modulation on gold nanorods (Au-M NRs), addressing the unmet need for precision antioxidant delivery. Specifically, the sequential functionalization of gold nanorods with thiolated polyethylene glycol amine (HS-PEG₂₀₀₀-NH₂) and 5,8-dihydroxypsoralen (5,8-DHP) triggered a structural transformation, cleaving the six-membered lactone ring of 5,8-DHP and generating an additional phenolic hydroxyl group. In cisplatin-challenged HK-2 cells, hydroxyl-enriched Au-M markedly attenuated reactive oxygen species (ROS) level and activated Keap1/Nrf2 pathway, evidenced by upregulated SOD and antioxidant Nqo1 expression alongside suppressed MDA and prooxidant Nox2 levels. SiNrf2 transfection severely abrogated the cytoprotective effects of Au-M, while Nrf2 overexpression synergistically enhanced the anti-apoptotic efficacy of Au-M in renal tubular epithelial cells. Mirroring cellular outcomes, the Au-M nanosystem elicited potent renoprotection via Nrf2-orchestrated transcriptional reprogramming in vivo, concurrently preserving the integrity and safety of healthy tissues. Critically, Au-M NRs conferred sustained protection in chronic exposure models, exhibited biocompatibility upon repeated dosing, and accelerated renal recovery, affirming their long-term therapeutic viability. This lactone-to-phenol conversion strategy pioneers a topology-guided paradigm for redox homeostasis regulation beyond AKI, establishing a transformative platform to harness natural product derivatization in combating organ-specific oxidative injury.

2025-12-31·REDOX REPORT

MS-275 facilitates osseointegration in osteoporotic rats by mitigating oxidative stress via activation of the miR-200a/Keap1/Nrf2 signaling pathway

Article

作者: Yan, Junjie ; Chen, Yuhu ; Guan, Wengang ; Chen, Bin ; Jiang, Wenkai ; Gu, Qinsong ; Yang, Min ; Zhou, Zhi ; Li, Jianqiao

OBJECTIVES:

Osteoporosis, a prevalent metabolic bone disease affecting millions worldwide. Although MS-275 has been reported to inhibit oxidative stress, its ability to protect osteoblasts from oxidative stress damage has yet to be clarified. This study investigated whether MS-275 can inhibit oxidative stress and promote osteogenesis by activating the miRNA-200a/Keap1/Nrf2 signaling pathway.

METHODS:

In vitro, MC3T3-E1 cells underwent induction with carbonyl cyanide 3-chlorophenylhydrazone, leading to the establishment of an oxidative stress model, investigating the underlying mechanism. In vivo, using a rat model of ovariectomized osteoporosis, evaluating the effects of MS-275.

RESULTS:

In vitro, MS-275 treatment of oxidation-induced MC3T3-E1 cells resulted in up-regulation of osteoblast protein, increased expression of miRNA-200a, increased binding of miRNA-200a to Keap1 mRNA, decreased expression of Keap1 protein, and dissociation of Nrf2 from Keap1. The expressions of total Nrf2, nuclear Nrf2 and HO-1 were increased, mitochondrial function was enhanced, and oxidative damage was reduced. However, these effects were reversed after interference with miRNA-200a. In vivo,MS-275 effectively enhanced the microstructural features of distal femoral trabecular bone, increased the mineralization capacity of osteoblasts, and promoted bone formation.

DISCUSSION:

MS-275 can reverse oxidative stress-induced cell damage, promote bone healing, and improve osteoporosis by activating the miRNA-200a/Keap1/Nrf2 pathway.

2025-12-31·RENAL FAILURE

Fecal microbiota transplantation modulates myeloid-derived suppressor cells and attenuates renal fibrosis in a murine model

Article

作者: Chen, Yuye ; Cao, Yuhan ; Xiao, Zihao ; Wang, Yajie ; Fu, Cong ; Shi, Yuanhui

BACKGROUND:

Renal fibrosis is a hallmark of progressive chronic kidney disease (CKD), with emerging evidence linking gut microbiota dysbiosis to disease progression. Myeloid-derived suppressor cells (MDSCs) have demonstrated renoprotective effects, yet the impact of fecal microbiota transplantation (FMT) on MDSC-mediated modulation of renal fibrosis remains unclear.

METHODS:

C57BL/6J mice underwent unilateral ureteral obstruction (UUO) to induce renal fibrosis, followed by FMT administration via gavage. Flow cytometry was used to quantify granulocytic (G-MDSCs) and monocytic (M-MDSCs) MDSC populations in peripheral blood, kidney, and spleen. To elucidate the role of MDSCs in FMT-mediated effects, MDSCs were depleted or adoptively transferred in vivo. Renal fibrosis severity and inflammatory cytokine expression were subsequently analyzed.

RESULTS:

FMT altered MDSC distribution, increasing M-MDSC accumulation in the blood and kidney. This was associated with downregulation of proinflammatory cytokines and attenuation of renal fibrosis. Adoptive MDSC transfer similarly produced anti-inflammatory and antifibrotic effects, reinforcing their therapeutic role in FMT-mediated renal protection.

CONCLUSIONS:

FMT enhances M-MDSC-mediated immunomodulation, reducing inflammation and renal fibrosis in UUO-induced CKD. These findings suggest a potential therapeutic strategy targeting the gut-kidney axis in CKD management.

项与皖南医学院相关的新闻（医药）

2025-06-04

·Firstwordpharma

Ascletis' Sagimet-sourced oral FASN inhibitor hits all goals in pivotal acne study

Ascletis Pharma on Tuesday said its oral FASN inhibitor denifanstat — in-licensed from Sagiment Biosciences for Greater China rights — met all primary and secondary endpoints in a Phase III study for the treatment of moderate-to-severe acne vulgaris, paving the way for a marketing application in the country. The trial randomised 480 patients in China to receive either denifanstat once daily or placebo for 12 weeks. For the primary endpoint of treatment success — defined as an Investigator's Global Assessment score of 0 (clear) or 1 (almost clear) with at least a 2-point decrease from baseline at week 12 — the denifanstat group demonstrated a statistically significant 33.2% success rate over the placebo group’s 14.6%.Additional primary goals further corroborated denifanstat's efficacy versus placebo: reduction in total lesion count (57.4% vs 35.4%) and reduction in inflammatory lesion count (63.5% vs 43.2%). Moreover, a key secondary endpoint showed a significant 51.9% reduction in non-inflammatory lesion count for denifanstat versus 28.9% for placebo.“Denifanstat…demonstrated impressive efficacy beyond treatment success," said Jinzi Jason Wu, chief executive of Ascletis, adding that the drug will "soon" be submitted to the China National Medical Products Administration (NMPA).In terms of safety, denifanstat exhibited a favourable profile, with the incidence of treatment-emergent adverse events (AEs) comparable to placebo. All treatment-related AEs were mild or moderate, with no denifanstat-related Grade 3 or 4 events, serious AEs or deaths reported.Besides acne, denifanstat — also known as ASC40 — is being investigated for metabolic dysfunction-associated steatohepatitis (MASH), where it has delivered positive findings in a Phase IIb study, and is also undergoing late-stage testing in combination with bevacizumab for recurrent glioblastoma.

临床结果临床2期临床3期

2025-05-19

·今日头条

细胞衰老调控新发现！皖南医学院与南京医科大学合作研究为结直肠癌治疗提供新策略

【导读】 S100A11 的异常表达已在多种恶性肿瘤中被发现，但其在结直肠癌（CRC）中的功能作用及潜在机制尚未完全阐明。 5月15日，皖南医学院/南京医科大学研究团队合作共同在期刊《Cell Death&Disease》上发表了研究论文，题为“USP14/S100A11 axis promote colorectal cancer progression by inhibiting cell senescence”，本研究旨在探究 S100A11 在结直肠癌（CRC）中的表达及其功能意义，结果表明 S100A11 在 CRC 中显著上调，并与不良生存结局相关。功能研究显示，在 CRC 细胞系中敲低 S100A11 可抑制细胞增殖、侵袭和迁移，从而在体内降低肿瘤生长和转移。机制研究揭示，S100A11 通过抑制细胞衰老促进细胞增殖和侵袭。此外，USP14 与 S100A11 相互作用并介导其去泛素化。更重要的是，S100A11 的过表达能够部分抵消 USP14 敲低所导致的细胞增殖减少。总之，USP14 和 S100A11 构成的新型调控轴通过抑制细胞衰老来调节 CRC 细胞的恶性生物学行为，因此 USP14 与 S100A11 之间的相互作用在 CRC 治疗中具有潜在的应用价值。 https://www.nature.com/articles/s41419-025-07724-8#Sec10 背景知识 01 结直肠癌（CRC）是第三常见的癌症类型，在全球死亡率中占重要地位，其发病率和死亡率在亚洲迅速上升。导致结直肠癌发病和发展的遗传因素错综复杂且多种多样，包括体细胞突变、异常基因融合、缺失或扩增，以及表观遗传变化和肠道微生物群。因此，了解驱动结直肠癌发生和发展的分子机制有助于发现其诊断、预后和治疗选择的潜在生物标志物。近年来，几种靶向疗法已作为结直肠癌的有前景的治疗方法崭露头角。例如，西妥昔单抗和帕尼单抗这两种靶向表皮生长因子受体（EGFR）的单克隆抗体，已在 RAS 基因野生型肿瘤患者中得到广泛应用。此外，贝伐珠单抗这种抗血管内皮生长因子（VEGF）抗体，通过抑制血管生成与化疗联合使用时也显示出疗效。再者，瑞戈非尼这种多激酶抑制剂，已在标准疗法进展后的转移性结直肠癌患者中获批使用。这些例子突显了在结直肠癌治疗中探索的分子靶点的多样性。 S100A11 促进结直肠癌的增殖和侵袭 02 研究人员采用 SW620 和 HCT116 结直肠癌细胞系进行功能获得性实验，以确定 S100A11 的功能作用。蛋白质印迹分析证实了转染成功。S100A11 敲低显著抑制了 SW620 和 HCT116 细胞的增殖，并增加了细胞凋亡，同时上调了促凋亡蛋白 BAK 的表达，下调了抗凋亡蛋白 Bcl-2、FOXM1 和 survivin 的表达。S100A11 敲低还显著降低了细胞迁移和侵袭能力。在 HCT116 和 SW620 细胞中，与 si-NC 组相比，S100A11 敲低显著增加了 E-钙粘蛋白的表达，降低了 N-钙粘蛋白和 Snail 的水平。在 SW480 细胞中异位表达 S100A11 显著促进了细胞增殖，这通过集落形成、EdU、细胞生长曲线实验、细胞迁移和侵袭实验得以证实。这些结果表明 S100A11 在结直肠癌细胞中起着癌基因的作用。 S100A11 敲低对结直肠癌细胞增殖、凋亡、迁移和侵袭的影响结论 03 总之，本研究不仅证实了 S100A11 在结直肠癌中的关键作用，还引入了 S100A11 与 USP14 相互作用这一新的调控机制，该机制有望用于治疗。未来的研究应着重开发能特异性破坏这种相互作用的抑制剂，这可能为结直肠癌的治疗开辟新的途径。参考资料： https://www.nature.com/articles/s41419-025-07724-8#Sec10 【关于投稿】转化医学网（360zhyx.com）是转化医学核心门户，旨在推动基础研究、临床诊疗和产业的发展，核心内容涵盖组学、检验、免疫、肿瘤、心血管、糖尿病等。如您有最新的研究内容发表，欢迎联系我们进行免费报道（公众号菜单栏-在线客服联系），我们的理念：内容创造价值，转化铸就未来！转化医学网（360zhyx.com）发布的文章旨在介绍前沿医学研究进展，不能作为治疗方案使用；如需获得健康指导，请至正规医院就诊。责任声明：本稿件如有错误之处，敬请联系转化医学网客服进行修改事宜！微信号：zhuanhuayixue 热门推荐活动点击免费报名 🕓 上海｜2025年6月12-15日 ▶ 第七届上海国际癌症大会暨第十八届全国医学生物技术研讨会暨第六届中德双边论坛 🕓 上海｜2025年7月17-18日 ▶ 第四届长三角体外诊断产业高峰论坛 🕓 北京｜2025年9月19-20日 ▶ 第六届单细胞技术应用研讨会暨空间组学前沿研讨会 🕓 上海｜2025年11月14-15日 ▶ 第二届中国类器官转化医学大会点击对应文字查看详情

临床研究微生物疗法

2025-04-15

·Pharma CMC

君圣泰「熊去氧胆小檗碱」2型糖尿病III期临床试验达到主要终点，即将申报上市

4月14日，君圣泰医药发布公告，其自主研发的肠肝抗炎及代谢调节剂熊去氧胆小檗碱(HTD1801)在中国2型糖尿病(T2DM)患者中开展的两项3期临床试验SYMPHONY1和SYMPHONY2）达成主要疗效终点及多个次要疗效终点。基于此次发布的积极的临床试验数据，君圣泰医药计划于今年内向CDE递交HTD1801治疗T2DM适应症的新药上市申请(NDA)。SYMPHONY 1(NCT06350890)及SYMPHONY 2(NCT06353347)试验是两项多中心、随机、双盲、安慰剂平行对照的临床3期试验，旨在分别评估HTD1801在饮食及运动干预后血糖控制不佳（SYMPHONY1;N=407）和二甲双胍控制不佳（SYMPHONY2;N=549）的T2DM患者中的有效性和安全性。两项研究的主要疗终点为与安慰剂相比，HTD1801治疗24周后糖化血红蛋白(HbA1c)相对于基线的变化，次要终点包含达到HbA1c<7.0%的受试者百分比、空腹血糖(FPG)、低密度脂蛋白胆固醇(LDL-C)、γ－谷氨酰转移酶(GGT)和超敏C反应蛋白(hs-CRP)。SYMPHONY 1（单药治疗）：HTD1801治疗组第24周HbA1c自基线平均变化值为-1.3%，显著优于安慰剂组。HTD1801在高基线的严重患者人群中展示出更优的降低疗效：在基线HbA1c≥8.5%的患者中，HTD1801治疗组的HbA1c自基线平均变化值为-1.5%。SYMPHONY 2（与二甲双胍联合治疗）：HTD1801治疗组第24周HbA1c自基线平均变化值为-1.2%，显著优于安慰剂组HTD1801。在高基线的严重患者人群中展示出更优的降低疗效：在基线HbA1c≥8.5%的患者中，HTD1801治疗组的HbA1c自基线平均变化值为-1.6%。在这两项3期临床研究中，都观察到了治疗期内HTD1801治疗组的HbA1c随治疗时间呈现出持续下降的趋势，提示HTD1801可以持久改善T2DM患者的血糖代谢的潜力。在两项研究中，治疗24周后，HTD1801治疗组中达到HbA1c<7.0%的患者比例显著高于安慰剂组。与安慰剂相比，HTD1801可同时显著降低餐后血糖及空腹血糖。此外，HTD1801展现出糖脂同降能力，可显著降低低密度脂蛋白胆固醇(LDL-C)、非高密度脂蛋白胆固醇(non-HDL-C)。另外，HTD1801治疗能够降低与心血管事件及T2DM患者临床结局密切相关的炎症标记物γ－谷氨酰转移酶(GGT)和超敏C反应蛋白(hs-CRP)。熊脱氧胆小檗碱(HTD1801)是一种靶向肠－肝系统的口服抗炎及代谢调节剂，正在开发用于治疗代谢及消化系统疾病。HTD1801作为熊脱氧胆酸和小檗碱形成的离子盐，是一种具有独特双机制的新分子实体，通过激活AMPK及抑制NLRP3发挥其生物学活性。这两种关键机制与改善胰岛素抵抗、葡萄糖代谢、脂质代谢和肝脏炎症相关，为复杂代谢性疾病的治疗提供综合性解决方案。HTD1801针对多个适应症进行临床开发，除了T2DM，针对代谢相关脂肪性肝炎(MASH)的有效性已在临床2a期研究被验证，全球多中心2b期临床试验正在顺利推进，预计2025年公布试验结果。

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