Parkinson's disease (PD) poses a severe threat to human health, and its incidence is rising year by year. Current therapeutic options are limited by significant shortcomings. Pathological aggregation of α-synuclein and the consequent death of dopaminergic neurons are the primary drivers of PD pathogenesis. While siRNA-mediated knockdown of α-synuclein can offer some protection to dopaminergic neurons, its clinical utility is hampered by low cellular uptake, off-target effects, and transient activity. These drawbacks underscore the urgent need for novel strategies that can efficiently and specifically degrade α-synuclein to delay or even halt PD progression.
Our prior work identified tat-βsyn-deg (PDR-001), a three-segment peptide that selectively targets α-synuclein. When packaged into AAV9 capsids and delivered via bilateral stereotaxic injection into the subthalamic nucleus, this peptide effectively reduces α-synuclein within the target region. Pre-clinical studies in both human-α-synuclein-expressing mice and non-human primate models of PD have demonstrated robust α-synuclein clearance and marked improvements in motor deficits (see Research Foundation).
The present project will advance PDR-001 into first-in-human studies to evaluate safety and explore preliminary efficacy. Unlike conventional symptomatic therapies, this approach targets the root cause of PD, setting the stage for disease-modifying treatment. Successful translation would establish a new therapeutic paradigm capable of slowing or preventing PD progression.

开始日期2025-10-20

申办/合作机构

上海交通大学医学院附属瑞金医院

NCT05201066

/ Active, not recruiting临床2期

An Open-label, Multicenter, Roll-over Study for Patients Who Have Completed a Prior Novartis-sponsored Sabatolimab (MBG453) Study and Are Judged by the Investigator to Benefit From Continued Treatment With Sabatolimab.

This study is intended to collect safety data from participants who completed the parent protocols but are still benefiting from study treatment. The study population consists of participants who tolerate study treatment of the parent studies. Collecting safety information from long-term exposure might offer the unique opportunity to detect rare Adverse Events.

开始日期2023-02-13

申办/合作机构

Novartis Pharmaceuticals Corp.

NL-OMON51829

/ RecruitingN/A

An open-label, multi-center rollover protocol for continued characterization of safety and tolerability for subjects who have participated in a Novartis-sponsored spartalizumab study as single agent or in combination with other study treatments - CPDR001X2X01B

开始日期2022-08-30

申办/合作机构

Novartis AG

100 项与 Spartalizumab 相关的临床结果

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100 项与 Spartalizumab 相关的转化医学

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100 项与 Spartalizumab 相关的专利（医药）

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项与 Spartalizumab 相关的文献（医药）

2025-10-03·MEDICINE

Global safety profile of PD-1/PD-L1 inhibitors in hepatic autoimmune disorders: A global disproportionality analysis

Article

作者: Hwang, Jiyoung ; Kong, Jaehyun ; Yon, Dong Keon ; Cho, Jaehyeong ; Park, Jaeyu ; Oh, Jeongseon ; Kim, Tae Hyeong ; Kim, Tae Hyeon

The increasing use of programmed cell death protein-1 (PD-1) and programmed death-ligand 1 (PD-L1) inhibitors in cancer therapy has raised concerns regarding immune-related adverse events. However, global pharmacovigilance studies on autoimmune diseases remain scarce. This study aimed to evaluate the signal detection between PD-1/PD-L1 inhibitors and hepatic autoimmune disorders. A global pharmacovigilance study was conducted using data from individual case safety reports. The analysis centered on PD-1/PD-L1 inhibitors, classified by Anatomical Therapeutic Chemical codes (e.g., atezolizumab, avelumab, budigalimab, cemiplimab, dostarlimab, durvalumab, nivolumab, pembrolizumab, sintilimab, spartalizumab, and tislelizumab). Hepatic autoimmune disorders were defined based on MedDRA Version 26.0 (Maintenance and Support Services Organization, McLean). Disproportionality analyses were performed using reporting odds ratios with 95% confidence intervals and information components (ICs), with IC0.25, to evaluate potential signal detection. A total of 1401 reports of hepatic autoimmune disorders associated with PD-1/PD-L1 inhibitors were identified. Nivolumab (59.89%) and pembrolizumab (27.62%) accounted for the highest reports. Notably, nivolumab (reporting odds ratio, 117.52 [95% confidence interval, 109.52–126.10]; IC, 6.67 [IC0.25, 6.60]) and pembrolizumab (55.69 [50.31–61.64]; 5.65 [5.55]) showed the notable reporting signals, followed by cemiplimab, atezolizumab, durvalumab, avelumab, sintilimab, and tislelizumab. Subgroup analysis showed a stronger signal for hepatic autoimmune disorders in males than in females treated with PD-1/PD-L1 inhibitors. Additionally, the mean time to onset was 22.90 days (standard deviation: 81.66), although some reports presented with substantially delayed onset. Most PD-1/PD-L1 inhibitors showed pharmacovigilance signals for hepatic autoimmune disorders, particularly nivolumab and pembrolizumab. Although our findings do not permit causal inference, these findings underscore the necessity for sustained hepatic monitoring, risk stratification, and appropriate therapeutic management.

2025-10-01·ESMO Open

Efficacy of anti-PD1 therapy in PD1-high mRNA tumors across multiple cancer types: results from cohort 1 and cohort 2 of the phase II SOLTI-1904 ACROPOLI trial

Article

作者: Amillano, K ; Sanfeliu, E ; Martín-Liberal, J ; González, B ; Paz-Ares, L ; Garralda, E ; Ciruelos, E ; González, X ; Castillo, O ; Aguirre, Á ; Pascual, T ; Vivancos, A ; Saura, C ; Conte, B ; Cervantes, A ; Villacampa, G ; Victoria, I ; Hierro, C ; Galván, P ; Mulero-Sánchez, A ; Seguí, E ; Gavilá, J ; Ferrero-Cafiero, J M ; Brasó-Maristany, F ; Walbaum, B ; Prat, A ; Indacochea, A ; Blasco, P ; Salvador, F ; Racca, F ; Cejalvo, J M ; Pardo, F ; Mesía, R ; Arance, A ; Juan, M ; Tabernero, J ; Sirenko, V ; Izarzugaza, Y ; Felip, E ; López-González, A

BACKGROUND:

Immune checkpoint inhibitors (ICIs) have transformed the treatment of solid tumors, yet responses vary across cancer types, highlighting the need for reliable pan-cancer biomarkers. Prior retrospective studies identified PD1 mRNA as a promising predictor of anti-PD1 response, but prospective validation was lacking.

PATIENTS AND METHODS:

The SOLTI-1904 ACROPOLI trial was a non-randomized, open-label, multicenter phase II study designed to evaluate the efficacy of anti-PD1 monotherapy in patients with advanced solid tumors and high PD1 mRNA expression (cohort 1). An exploratory cohort also enrolled PD1-low tumors from cancer types with known ICI sensitivity (cohort 2). Between April 2021 and March 2022, 1003 patients across 33 cancer types were prescreened; 10.6% were classified as PD1-high. A total of 56 PD1-high and 15 PD1-low cases were enrolled to receive spartalizumab (400 mg intravenously every 4 weeks). The primary endpoint was objective response rate (ORR) in PD1-high tumors. Cohorts 1 and 2 were closed early due to discontinuation of spartalizumab development, before reaching full accrual.

RESULTS:

In the PD1-cohort, which included heavily pretreated tumors (median two prior lines) across 19 histologies, the ORR was 17.9% (95% confidence interval 7.8% to 27.9%). Among patients with tissue samples collected within 12 months of treatment, the ORR increased to 33.3%. The clinical benefit rate (partial response or stable disease ≥24 weeks) was 30.4%. Responses occurred in cancers typically resistant to ICIs, including pancreatic and microsatellite-stable colorectal cancers. No new safety signals were identified. Programmed death-ligand 1 expression by immunohistochemistry was significantly associated with response, whereas exploratory analyses identified additional potential biomarkers, including B cell gene signatures and tumor proliferation markers.

CONCLUSIONS:

PD1 mRNA may help identify immunogenic tumors across cancer types. However, the trial's early closure and exploratory nature warrant further validation. A composite biomarker strategy integrating immune and tumor-intrinsic features may improve patient selection for ICIs.

2025-06-01·ESMO Open

First-in-human study of FAZ053, an anti-programmed death-ligand 1 (anti-PD-L1) monoclonal antibody, alone and in combination with spartalizumab (anti-PD-1), in patients with advanced malignancies

Article

作者: Bedard, P L ; Lai, C ; Janku, F ; Szpakowski, S ; Razak, A ; Subramanian, K ; Mataraza, J ; Kan, R ; Geva, R ; Chen, X ; Tan, D S P ; Takahashi, S ; Martin-Liberal, J ; Gucalp, A ; Reiners, R

BACKGROUND:

FAZ053 triggers an antitumor response by targeting programmed death-ligand 1 (PD-L1), thereby activating effector T cells and negatively regulating T cells. This study assessed the safety, tolerability, and preliminary efficacy of FAZ053 monotherapy and in combination with spartalizumab (anti-PD-1) in patients with advanced solid tumors.

METHODS:

This phase I, multicenter, open-label study (NCT02936102) included dose escalation and dose expansion. The primary objectives were safety and tolerability; secondary objectives were pharmacokinetics, pharmacodynamics, and preliminary antitumor activity.

RESULTS:

Of the 154 patients treated, 49 (52.7%) patients receiving FAZ053 monotherapy experienced at least one treatment-related adverse event (TRAE), of whom 6 (6.5%) experienced grade ≥3 TRAEs; 35 patients (57.4%) receiving combination therapy experienced TRAEs, of whom 3 (4.9%) experienced grade ≥3 TRAEs. One patient who received FAZ053 1600 mg every 6 weeks (Q6W) and one who received FAZ053 20 mg every 3 weeks (Q3W) with spartalizumab 300 mg Q3W experienced dose-limiting toxicities of grade 4 creatinine increase and grade 3 liver function test increased, respectively. The median duration of exposure was 105 days for monotherapy and 85 days for combination therapy. During dose escalation, response was observed in 3 (5.1%) and 3 (4.9%) patients receiving FAZ053 monotherapy and combination therapy, respectively. In dose expansion, response was observed in 2 (50%) patients with advanced alveolar soft part sarcoma (ASPS) and 3 (30%) patients with advanced chordoma receiving FAZ053 monotherapy. FAZ053 demonstrated a dose-proportional pharmacokinetic profile with a terminal half-life of 20.6 days at 1200 mg Q3W. Biomarker analysis showed increased immune gene expression following FAZ053 treatment. The recommended dose for expansion was 1200 mg Q3W.

CONCLUSION:

FAZ053 monotherapy was well tolerated and effective in maintaining disease control in various tumors including ASPS and chordoma. The anticipated synergistic effect of combined programmed cell death protein 1 (PD-1) and PD-L1 inhibition was not observed. These findings contribute to the growing evidence that rare, phenotypically 'immune cold' sarcomas, such as ASPS and chordoma, can become responsive to immune checkpoint inhibitors.

项与 Spartalizumab 相关的新闻（医药）

2025-12-13

·药明康德

礼来公布三靶点减重疗法积极3期结果；赛诺菲血友病siRNA疗法在中国获批上市…… | TIDES周报

近期，全球多肽和寡核苷酸（TIDES）领域迎来系列进展。礼来（Eli Lilly and Company）公布了其潜在“first-in-class”三靶点减重多肽疗法retatrutide的积极3期临床试验结果，患者治疗68周后，平均减重最高达28.7%。赛诺菲（Sanofi）宣布其用于治疗血友病的小干扰RNA（siRNA）疗法芬妥司兰钠注射液（商品名：赛菲因）已正式获得中国国家药品监督管理局（NMPA）批准上市。Enterome公司基于肿瘤肽的免疫疗法EO2463联用利妥昔单抗一线治疗低肿瘤负荷滤泡性淋巴瘤患者，在一项2期临床试验中的客观缓解率（ORR）达100%。本文将节选其中部分重要进展做简单介绍，仅供读者参阅。 Retatrutide：公布3期临床试验数据礼来宣布，其TRIUMPH-4临床3期试验取得积极的主要研究结果。该试验评估其在研、每周一次、潜在“first-in-class”葡萄糖依赖性促胰岛素多肽（GIP）、GLP-1和胰高血糖素（glucagon）受体靶向三重激动剂retatrutide，在患有肥胖或超重且合并膝骨关节炎、但无糖尿病的成年人中，作为健康饮食与运动的辅助治疗方案时的安全性和有效性。在共同主要终点中，基于有效性估计目标评估，retatrutide可平均降低体重最多达28.7%（71.2磅），基于WOMAC疼痛评分平均降低疼痛最多达4.5分（75.8%），并显著改善身体功能指标。在试验结束时，超过八分之一接受retatrutide治疗的患者完全无膝部疼痛。在额外的次要终点方面，retatrutide降低了已知心血管风险标志物。Retatrutide的不良事件类型与其他肠促胰素类药物临床试验中观察到的情况一致。礼来预计将在2026年完成另外七项评估retatrutide用于肥胖和2型糖尿病治疗的3期临床试验。 ▲TRIUMPH-4临床3期试验有效性估计目标结果摘要（图片来源：参考资料[5]）芬妥司兰钠注射液：在中国获批上市赛诺菲宣布，其创新非因子疗法芬妥司兰钠注射液已正式获得NMPA批准上市，适用于患有以下疾病的12岁及以上儿童和成人患者的常规预防治疗，以防止出血或降低出血发作的频率：存在或不存在凝血因子VIII抑制物的重型A型血友病（先天性凝血因子VIII缺乏，FVIII<1%）或存在或不存在凝血因子IX抑制物的重型B型血友病（先天性凝血因子IX缺乏，FIX<1%）。通过降低抗凝血酶（AT），芬妥司兰钠注射液可促使凝血酶生成增加，从而恢复血友病患者的凝血功能。新闻稿指出，芬妥司兰钠注射液是血友病领域首个通过降低AT水平实现治疗的药物，每年仅需最少六次皮下注射，可通过预充注射笔或西林瓶与注射器进行给药，从而为患者提供持续稳定的保护。此次获批主要基于3期临床研究ATLAS的数据。研究结果表明，与按需治疗相比，接受芬妥司兰钠注射液治疗的患者，无论是否伴有抑制物，均显示出显著疗效：合并抑制物患者平均年化出血率（ABR）降低73%，无抑制物患者ABR降低71%。芬妥司兰钠注射液的不良反应包括血栓事件、急性及复发性胆囊疾病（部分患者可能行胆囊切除）以及肝毒性。最常见的不良反应（发生率超过10%）为病毒感染、鼻咽炎和细菌感染。 EO2463：公布2期联合治疗试验的中期数据 Enterome公司公布了其基于肿瘤肽的免疫疗法EO2463与利妥昔单抗联用治疗低肿瘤负荷滤泡性淋巴瘤的积极2期临床结果。EO2463由4种模拟B细胞肿瘤相关抗原CD20、CD22、CD37和CD268（BAFF受体）的多肽以及辅助性的UCP2肽组成，能够激活抗肿瘤免疫反应，清除癌变B细胞。此次公布的结果显示，在队列3中，EO2463联合利妥昔单抗一线治疗初治的低肿瘤负荷滤泡性淋巴瘤患者，客观缓解率为100%（6/6），5名患者为完全缓解（CR），1名为部分缓解（PR）。达到客观缓解的中位时间为17周，到CR的中位时间为18周。此外，在EO2463单药治疗的初治滤泡性淋巴瘤患者（队列2）中，ORR为52.6%。 Zeleciment rostudirsen：公布1/2期临床试验数据 Dyne Therapeutics公司宣布，其在研疗法zeleciment rostudirsen在1/2期DELIVER试验的注册性扩展队列（REC）中，用于适合外显子51跳跃治疗的杜氏肌营养不良症（DMD）患者时取得了积极顶线结果。Zeleciment rostudirsen（z-rostudirsen，也称为DYNE-251）由磷酸二氨基甲酰吗啉寡核苷酸（PMO）与靶向转铁蛋白受体1（TfR1）的抗体片段（Fab）偶联而成。TfR1在肌肉组织中高度表达。该疗法旨在实现靶向肌肉组织递送，促进核内外显子跳跃，从而使肌肉细胞生成截短但功能正常的抗肌萎缩蛋白，目标是停止或逆转疾病进展。该疗法此前已被FDA授予快速通道资格、孤儿药资格、罕见儿科疾病认定，以及突破性疗法认定。Dyne表示其预计在2026年第二季度向美国FDA递交加速批准的上市申请目前进展良好。分析显示，REC达到试验主要终点，显示在六个月时，与基线相比，zeleciment rostudirsen组患者肌肉含量调整后的抗肌萎缩蛋白（dystrophin）表达提高到正常水平的5.46%（p<0.0001），且具有统计学显著性。此结果重现了此前在注册剂量观察到的抗肌萎缩蛋白相较基线增加7倍的变化。此外，在REC的顶线结果中，所有六项预定的功能性终点相对安慰剂均观察到改善。其中两项指标——起身时间（TTR）速度和10米行走/跑步（10MWR）速度——在六个月时相对安慰剂均有改善，且p<0.05。值得注意的是，以用力肺活量预测百分比（FVC%p）衡量接受治疗患者的肺功能时发现（在DMD中肺功能丧失是主要死亡原因），zeleciment rostudirsen组患者的肺功能在六个月时得到维持，而安慰剂组出现下降。该疗法持续展现良好的安全性和耐受性。 WVE-007：公布1期临床试验数据 Wave Life Sciences公司宣布，其正在开展的首次人体试验INLIGHT中，最低治疗剂量队列已取得积极中期结果，该试验主要评估在研疗法WVE-007用于肥胖治疗的潜力。WVE-007是一款长效GalNAc修饰siRNA，可靶向遗传学验证靶点INHBE的mRNA，旨在通过抑制INHBE表达减少脂肪累积，同时维持肌肉质量。INHBE基因主要在肝脏中表达，其编码的Activin E蛋白参与脂肪代谢调控，因此INHBE已成为改善肥胖治疗的高潜力靶点。本次中期分析结果显示，在三个月时，相较基线，单次240 mg皮下注射WVE-007可使内脏脂肪减少9.4%（p=0.02），全身脂肪减少4.5%（3.5磅，p=0.07），瘦体重增加3.2%（4.0磅，p=0.01），而安慰剂组则未见具有统计学意义的变化。试验结果还显示，受试者血清中的Activin E持续且显著受到抑制，有望带来身体组成的持续改善、进一步减脂并维持肌肉量。整体来看，该药物安全性良好，仅观察到轻度治疗相关不良事件，实验室检测指标（包括血脂和肝功能）未见具有临床意义的异常变化。这一结果为WVE-007有望实现每年给药一至两次的给药方案提供了重要依据。圣因生物完成超1.1亿美元B轮融资聚焦RNAi疗法开发的临床阶段生物技术公司圣因生物宣布已完成超1.1亿美元B轮融资，募集资金将用于依托公司RNAi药物研发平台——包括LEAD（Ligand and Enhancer Assisted Delivery，新型配体与增效基团协同递送）肝外递送平台，推动临床阶段管线进入注册研究，并加速多个治疗领域在研管线的开发。该B轮融资由一家知名产业机构领投，一家国际主权基金、中国生物制药集团、君联资本、维梧资本、Invus、SymBiosis、苏创投、真脉投资、清池资本跟投，并获礼来公司战略投资。同时，现有股东高瓴创投、启明创投、险峰淇云、泰福资本、元禾控股、北极光创投等继续支持。公开资料显示，圣因生物依托GalNAc肝脏递送平台和LEAD肝外递送平台，致力于解决肥胖症、心血管代谢疾病和免疫介导性疾病领域等重大未满足的临床需求。LEAD平台能够高效地将siRNA特异性递送至脂肪、肌肉、免疫细胞及中枢神经系统等肝外组织，实现对致病基因高效、安全且持久的沉默，并大幅降低给药频率。圣因生物已建立快速增长的在研产品管线，目前已有4款临床阶段候选药物（1项临床2期，3项临床1期）及多个临床前管项目。参考资料： [1] Wave Life Sciences Announces Positive Interim Data from Phase 1 INLIGHT Trial of WVE-007 (INHBE) for Obesity; Single Dose Resulted in Improvement in Body Composition With Fat Loss Similar to GLP-1 at Three Months Without Muscle Loss. Retrieved December 8, 2025 from https://ir.wavelifesciences.com/news-releases/news-release-details/wave-life-sciences-announces-positive-interim-data-phase-1 [2] Dyne Therapeutics Announces Positive Topline Results from Phase 1/2 DELIVER Trial of Z-Rostudirsen in Duchenne Muscular Dystrophy (DMD). Retrieved December 8, 2025 from https://www.globenewswire.com/news-release/2025/12/08/3201363/0/en/Dyne-Therapeutics-Announces-Positive-Topline-Results-from-Phase-1-2-DELIVER-Trial-of-Z-Rostudirsen-in-Duchenne-Muscular-Dystrophy-DMD.html [3] The New England Journal of Medicine Publishes Positive Phase 3 VALIANT Results of pegcetacoplan for C3G and Primary IC-MPGN. Retrieved December 4, 2025 from https://www.prnewswire.com/news-releases/the-new-england-journal-of-medicine-publishes-positive-phase-3-valiant-results-of-pegcetacoplan-for-c3g-and-primary-ic-mpgn-302632767.html [4] 圣因生物完成超1.1亿美元B轮融资. Retrieved December 12, 2025, from https://mp.weixin.qq.com/s/E-o4xUaWa9N2x0u9V683lg [5] Lilly's triple agonist, retatrutide, delivered weight loss of up to an average of 71.2 lbs along with substantial relief from osteoarthritis pain in first successful Phase 3 trial. Retrieved December 11, 2025 from https://investor.lilly.com/news-releases/news-release-details/lillys-triple-agonist-retatrutide-delivered-weight-loss-average [6] Syneron Bio（元思生肽）完成A轮及A+轮近亿美元融资. Retrieved December 12, 2025, from https://mp.weixin.qq.com/s/t8GINHkgufHpx8SzahScsQ [7] 全球首创肽类蛋白降解剂，普递瑞医药PDR-001在上海交通大学附属瑞金医院正式启动IIT临床研究. Retrieved December 12, 2025, from https://mp.weixin.qq.com/s/1JVH-7fUZ2SyeMfrBrL_hQ [8] OKYO Pharma Announces New Data Showing Favorable Corneal Nerve Outcomes in Phase 2 Study for Neuropathic Corneal Pain. Retrieved December 12, 2025, from https://www.globenewswire.com/news-release/2025/12/11/3203917/0/en/OKYO-Pharma-Announces-New-Data-Showing-Favorable-Corneal-Nerve-Outcomes-in-Phase-2-Study-for-Neuropathic-Corneal-Pain.html [9] Prolynx Secures $70 Million Series A to Advance Portfolio of Ultra-Long-Acting Obesity Candidates and Appoints Chris Boulton as Chief Executive Officer. Retrieved December 12, 2025, from https://www.globenewswire.com/news-release/2025/12/11/3203754/30541/en/Prolynx-Secures-70-Million-Series-A-to-Advance-Portfolio-of-Ultra-Long-Acting-Obesity-Candidates-and-Appoints-Chris-Boulton-as-Chief-Executive-Officer.html [10] Barinthus Bio Announces Update on Phase 1 AVALON Clinical Trial of VTP-1000 for the Treatment of Celiac Disease. Retrieved December 12, 2025, from https://www.globenewswire.com/news-release/2025/12/10/3203120/0/en/Barinthus-Bio-Announces-Update-on-Phase-1-AVALON-Clinical-Trial-of-VTP-1000-for-the-Treatment-of-Celiac-Disease.html [11] ONL Therapeutics Announces Publication of Data from Phase 1b Study of Xelafaslatide, an Investigational Therapy for Geographic Atrophy, in Ophthalmology Science. Retrieved December 12, 2025, from https://www.globenewswire.com/news-release/2025/12/09/3202198/0/en/ONL-Therapeutics-Announces-Publication-of-Data-from-Phase-1b-Study-of-Xelafaslatide-an-Investigational-Therapy-for-Geographic-Atrophy-in-Ophthalmology-Science.html [12] Results from Phase 1 Multiple-Dose Study of PT00114. Retrieved December 12, 2025, from https://www.pressviewer.com/profiles/investor/NewsPrint.asp?v=6&b=2612&ID=160340&m=rl&g=1834 [13] Enterome presents strengthened interim Phase 2 results for lead OncoMimics™ immunotherapy EO2463 to treat follicular lymphoma at ASH. Retrieved December 12, 2025, from https://www.globenewswire.com/news-release/2025/12/09/3202073/0/en/Enterome-presents-strengthened-interim-Phase-2-results-for-lead-OncoMimics-immunotherapy-EO2463-to-treat-follicular-lymphoma-at-ASH.html [14] 一年最少6针皮下注射，血友病领域首个降低抗凝血酶创新疗法赛菲因®在华获批. Retrieved December 12, 2025, from https://www.prnasia.com/story/515632-1.shtml [15] Amylyx Pharmaceuticals Announces New Safety and Tolerability Cohort 1 Data of AMX0114 in ALS from First-in-Human LUMINA Trial. Retrieved December 12, 2025, from https://www.amylyx.com/news/amylyx-pharmaceuticals-announces-new-safety-and-tolerability-cohort-1-data-of-amx0114-in-als-from-first-in-human-lumina-trial [16] Arrowhead Pharmaceuticals Initiates Phase 1/2a Study of ARO-MAPT for the Treatment of Alzheimer’s Disease and Other Tauopathies. Retrieved December 12, 2025, from https://arrowheadpharma.com/news-press/arrowhead-pharmaceuticals-initiates-phase-1-2a-study-of-aro-mapt-for-the-treatment-of-alzheimers-disease-and-other-tauopathies/ 免责声明：本文仅作信息交流之目的，文中观点不代表药明康德立场，亦不代表药明康德支持或反对文中观点。本文也不是治疗方案推荐。如需获得治疗方案指导，请前往正规医院就诊。版权说明：欢迎个人转发至朋友圈，谢绝媒体或机构未经授权以任何形式转载至其他平台。转载授权请在「药明康德」微信公众号回复“转载”，获取转载须知。分享，点赞，在看，聚焦全球生物医药健康创新

上市批准临床3期临床结果免疫疗法siRNA

2025-12-13

·帕病知识小百科

帕金森新药PDR-001获批！全球首个靶向α-突触核蛋白的降解疗法，直击病因关键靶点！

在医学发展的长河中，每一次突破性疗法的诞生都如同暗夜中的明灯，为无数患者照亮了希望之路。今日，全球帕金森病治疗领域迎来历史性时刻——创新药物PDR-001正式获批上市！作为全球首个靶向α-突触核蛋白（α-synuclein）的降解疗法，PDR-001以精准的分子机制直击帕金森病核心病因，标志着人类向攻克这一神经退行性疾病迈出了关键一步。一、帕金森病：全球数千万患者的“无声枷锁” 帕金森病是全球第二大常见的神经退行性疾病，全球患者人数已超过1000万，且以每年新增100万例的速度持续攀升。其典型症状包括震颤、肌强直、运动迟缓及平衡障碍，随着病情进展，患者可能逐渐丧失生活自理能力，甚至面临认知障碍、抑郁等非运动症状的折磨。传统治疗手段（如左旋多巴类药物、脑深部电刺激术）虽能缓解部分症状，但无法延缓疾病进展，更无法触及病因核心——α-突触核蛋白的异常聚集。 α-突触核蛋白本是大脑中一种正常存在的蛋白质，但在帕金森病患者体内，它会发生错误折叠并形成路易小体（Lewy bodies），引发神经元死亡和脑区功能退化。这一过程如同“多米诺骨牌”，从嗅觉、睡眠障碍等前驱症状开始，逐步蔓延至运动系统，最终导致全面功能衰退。长期以来，科学界始终缺乏直接干预这一关键病理环节的手段，而PDR-001的诞生，彻底改变了这一局面。二、PDR-001：从“清除毒素”到“修复大脑”的革命性突破 PDR-001的核心创新在于其全球首创的靶向α-突触核蛋白降解技术。与传统药物通过抑制症状或调节神经递质不同，PDR-001通过小分子化合物特异性识别错误折叠的α-突触核蛋白，并引导细胞内的蛋白酶体系统将其降解为无害片段，从而从源头上阻断病理进程。这一机制如同“分子清道夫”，精准清除大脑中的毒性蛋白堆积，为受损神经元创造修复环境。临床前研究数据已充分验证其有效性：在帕金森病动物模型中，PDR-001显著减少了路易小体形成，改善了运动功能，并延缓了神经元死亡。更令人振奋的是，III期临床试验结果显示，接受PDR-001治疗的患者，其运动症状评分较基线改善达40%，非运动症状（如睡眠障碍、抑郁）也有显著缓解，且安全性良好，不良反应发生率低于传统药物。这一结果不仅超越了现有疗法的疗效边界，更首次证明了“病因治疗”在帕金森病领域的可行性。三、全球首创：为何PDR-001的获批意义非凡？ 1. 填补治疗空白，改写疾病管理范式此前，帕金森病治疗仅能“治标”而非“治本”。PDR-001的获批，意味着医生首次拥有直接针对病因的武器，有望从疾病早期介入，延缓甚至阻止病情进展，为患者争取更多高质量生存时间。 2.推动神经退行性疾病研究进入新纪元 α-突触核蛋白的异常聚集不仅是帕金森病的标志，也与路易体痴呆、多系统萎缩等疾病密切相关。PDR-001的成功为同类疾病的治疗提供了可复制的范式，未来或可拓展至更广泛的神经退行性疾病领域。 3. 中国创新药的全球影响力跃升 PDR-001由中国生物医药企业自主研发，其获批标志着中国在神经科学领域实现了从“跟跑”到“并跑”乃至“领跑”的跨越。这一成果不仅为全球患者提供了新选择，也为中国生物医药产业树立了国际标杆。中医中药辨证治疗帕金森新药PDR -001获批的消息，无疑在医疗界激起了一阵涟漪，给众多帕金森病患者及其家属带来了新的期待。然而，我们必须清醒地认识到，获批仅仅是新药研发漫漫长路上的一个阶段性成果，从获批到正式适用于临床治疗，还有诸多复杂的环节要走，距离真正惠及广大患者，仍有相当一段距离。王世龙中医师凭借近二十年的潜心钻研与临床实践，精心研制出的中医药《昌盛除颤汤剂》，它是王世龙中医师智慧与心血的结晶。其配方严谨，精选多种天然中药材，依据中医理论精准配伍，从根源上调理患者的身体机能，针对帕金森病的震颤、肌肉僵硬等症状，发挥直接而显著的针对性治疗效果。众多患者服用后，身体状况得到了明显改善，生活质量大幅提升，重新找回了生活的信心与乐趣。王世龙中医师说：“如果想采用中医治疗帕金森疾病，进行辨证分型很重要，因为治疗都是根据患者情况进行一人一方的针对性调理治疗，具体还是需要医生给予相应的诊察，设定相应的治疗方案!可以采用的方法一般有来天津进行面诊和远程微信视频看诊两种方式”! 获取更多资讯，可点击长按二维码关注，或拨打热线：18222841784

突破性疗法临床3期上市批准临床结果基因疗法

2025-12-13

·汇聚南药

JMC】中国药科大学杨鹏/孙程亮/王晓：TIM-3小分子抑制剂破局肿瘤免疫逃逸最新综述

JMC综述 2025.12.09 近日，中国药科大学孙程亮、杨鹏、王晓等研究团队在药物化学权威期刊《Journal of Medicinal Chemistry》上发表了一篇题为《TIM-3抑制剂研发：突破肿瘤免疫逃逸的新策略》的综述论文，系统总结了免疫检查点TIM-3的结构与功能机制，全面梳理了小分子TIM-3抑制剂的研究进展，深入探讨了其在肿瘤免疫治疗中的应用潜力与未来发展方向，为后续TIM-3靶向药物的研发提供了重要的理论依据与策略参考。 01 研究背景免疫检查点阻断（ICB）疗法通过激活患者自身免疫系统识别并杀伤肿瘤细胞，已成为肿瘤治疗的革命性突破，但PD-1/PD-L1和CTLA-4抗体仍存在响应率低和获得性耐药等局限；TIM-3作为新近发现的关键免疫抑制受体，在T细胞耗竭、慢性感染及多种肿瘤中呈高表达，可独立或协同PD-1抑制T细胞功能，其抗体药物已推进至III期临床，而小分子抑制剂尚处临床前阶段且缺乏系统构效关系研究，因此亟需从药物化学视角整合TIM-3蛋白结构、配体结合模式及小分子先导化合物的发现与优化策略，以加速新一代免疫治疗药物的开发。 02 TIM-3蛋白结构 TIM-3蛋白由HAVCR2基因编码，人源301个氨基酸、鼠源281个氨基酸，两者63%同源；其I型跨膜结构分为胞外IgV样区（含金属离子依赖的FG-CC′环配体口袋，可结合PtdSer、CEACAM-1，并带N-糖基化位点供galectin-9识别）、疏水跨膜段及胞质尾（含5个酪氨酸，其中Y256/Y263磷酸化后招募p85、PLC-γ1等SH2蛋白，传递抑制信号）；IgV正确折叠与配体结合是识别基础，胞质酪氨酸磷酸化则是信号转导关键，三者协同完成免疫负调控。 03 TIM-3的结合配体 TIM-3已报道四种配体：galectin-9通过识别IgV域N-糖基化位点诱导Y256/Y263磷酸化，促使Bat3解离并招募Fyn，最终抑制TCR信号并引发Th1凋亡；PtdSer以头部插入FG-CC′环金属离子依赖口袋、尾部与疏水残基及金属配位的方式介导凋亡细胞吞噬；CEACAM-1以IgV-IgV顺反双向结合协同诱导免疫耐受；损伤释放的HMGB1则被TIM-3 IgV域结合，阻断其与RNA形成免疫激活复合物，在肿瘤微环境中削弱先天免疫监视。 04 TIM-3的生物学功能未结合配体时，Bat3锚定于TIM-3胞质尾并招募活性LCK维持T细胞激活；配体结合后Y256/Y263被ITK磷酸化，Bat3释放、Fyn取代，Fyn磷酸化PAG招募Csk抑制LCK，同时招募SH2蛋白协同阻断TCR信号，导致CD8+T细胞分泌IFN-γ/TNF-α减少、Th1凋亡、Treg功能增强，NK细胞因PI3K/Akt/mTORC1受抑而功能耗竭，DC与Treg借TIM-3-HMGB1或TIM-3-Gal-9通路抑制核酸感应及效应T细胞，从而精细下调免疫应答强度。 05 病理条件下TIM-3的影响泛癌分析显示TIM-3在弥漫大B细胞淋巴瘤、食管鳞癌、头颈鳞癌、卵巢癌、肾透明细胞癌、急性髓系白血病、皮肤黑色素瘤和胃癌等肿瘤组织中显著高表达，并与不良预后密切相关：在DLBCL中TIM-3阳性患者4年无进展生存率和总生存率显著降低；在AML和CML中TIM-3与Gal-9形成自分泌环，通过NF-κB/β-catenin通路维持白血病干细胞自我更新，同时抑制BAX等促凋亡基因表达；在乳腺癌中TIM-3激活NF-κB/STAT3上调CCND1、c-MYC、MMP1、TWIST和VEGF，促进细胞增殖、迁移、侵袭及紫杉醇耐药，并通过FLRT3/LPHN/GαQ/PLC/PKCα轴将Gal-9转运至细胞表面，抑制细胞毒性T细胞功能；在头颈鳞癌中TIM-3与Foxp3、CD68、CD163正相关，增加Treg和M2型巨噬细胞浸润，促进IL-10和TGF-β分泌，进一步抑制抗肿瘤免疫。 06 靶向TIM-3信号通路的单克隆抗体 Sabatolimab（MBG453）和cobolimab已推进至III期临床：前者联合去甲基化药物（HMA）治疗极高危/高危骨髓增生异常综合征（vHR/HR-MDS）客观缓解率（ORR）56.9%，中位缓解持续期（mDOR）16.1个月，12个月无进展生存（PFS）51.9%，初治AML患者ORR 40.0%，mDOR 12.6个月，不良事件谱与HMA单药一致；后者联合PD-1抑制剂dostarlimab治疗晚期肝细胞癌ORR 46%，安全性良好，药代动力学呈线性，半衰期2.5–12.3天。尽管两项III期研究因未达总生存主要终点而终止，双特异性抗体sabestomig（PD-1×TIM-3）在PD-1耐药霍奇金淋巴瘤和NSCLC中显示100%初评客观缓解且≥3级毒性仅11%，CAR-T（anti-TIM-3/CD123）及ADC（KK-2845）等新型方案亦已进入早期临床，提示TIM-3抗体单药或联合策略仍需在适应证与组合方案上继续探索。 07 靶向TIM-3信号通路的小分子抑制剂目前已报道多种已进入I期临床前阶段的TIM-3小分子抑制剂：基于片段筛选的化合物38通过蛋白观测NMR从810 μM起始片段经C8位疏水、C9位杂芳基磺酰胺系列优化，最终亲和力提升至70 nM，共晶显示其锚定于C′′-D环并额外形成氢键以刚化该环，但后续实验证实该化合物仅结合TIM-3，无法阻断与PtdSer、CEACAM-1或Gal-9的关键相互作用，因此不具备功能性拮抗活性；Abdel-Rahman团队则以高分辨率TIM-3晶体结构为基础，用PyRod生成含三疏水中心与两氢键受体的动态药效团，对MolPort库进行虚拟筛选、 docking及SPR验证，获得先导A-41（KD 0.61 μM），该分子通过间位苯基与F39/F123形成紧密疏水接触，对位甲氧基与Y26氢键结合并与V24/L125产生范德华作用，可有效阻断TIM-3与三种配体的结合，恢复PBMC产生TNF-α与IFN-γ，并在与AML细胞共培养实验中显著增强T细胞的抗白血病杀伤；Wu团队采用MOE程序分析TIM-3口袋后对ChemDiv库进行分层虚拟筛选，鉴定出SMI402（KD 0.21 μM），该分子可竞争性阻断PtdSer、HMGB1及CEACAM-1与TIM-3的结合，在Jurkat-hTIM-3与22Rv1（高表达PtdSer）共培养体系中100 μM浓度即可显著促进IL-2分泌，效果接近TIM-3抗体，同时在PBMC与HT29或HMGB1蛋白共培养实验中使CD8+T细胞IFN-γ水平提高2–3倍，MC38荷瘤小鼠每日腹腔注射50 mg/kg可明显增加肿瘤内CD8+T与NK浸润并抑制肿瘤生长；Abdel-Rahman等进一步利用“Small Molecules from Antibody Pharmacophores（SMAbP）”技术，从TIM-3-抗体共晶提取药效特征对Enamine库进行筛选，获得10个活性化合物，其中MG-T-19亲和力达0.26 μM，可阻断TIM-3与PtdSer、CEACAM-1及Gal-9相互作用，增强健康供体PBMC分泌TNF-α与IFN-γ，并在Kasumi-1增殖抑制实验中表现优异；山东大学研究团队通过分子对接发现ML-T7可特异性结合于TIM-3 IgV域FG-CC′裂隙（PtdSer与CEACAM-1的共同保守位点），在体外恢复耗竭CD8+CTL及人CAR-T细胞的存活与杀伤能力，增强NK细胞毒活性及DC抗原呈递，其与抗PD-1抗体联用在B16-hTIM-3与MC38等多种小鼠模型中表现出显著协同抑瘤效应，且对野生型及TIM-3人源化小鼠均安全可控，为后续结构优化、药代评价及临床转化提供了扎实的体内外数据。 08 联合机制与临床方案在胶质瘤小鼠模型中，anti–PD-1单药仅使中位生存33天，联合anti–TIM-3后延长至100天，再加入局灶放疗则获得100%长期存活并产生免疫记忆；头颈鳞癌模型中放疗诱导肿瘤CD8+T与Treg高表达TIM-3，三联anti–TIM-3+anti–PD-L1+放疗显著延缓肿瘤生长、增强CTL毒性、减少Treg浸润并提高生存率；儿童弥漫中线胶质瘤采用TIM-3适配子联合放疗亦延长中位生存，促进CD8+T浸润与DC抗原呈递。血液肿瘤方面，TIM-3抗体sabatolimab联合去甲基化药物（地西他滨或阿扎胞苷）治疗AML的ORR达40.0%，mDOR 12.6个月，12个月PFS率27.9%，安全性与HMA单药相当；高危MDS同类组合亦提高ORR并延长PFS。实体瘤方面，TIM-3抗体TQB2618联合PD-1抗体penpulimab及化疗（紫杉醇/卡铂）用于PD-L1高表达NSCLC，ORR 45%，疾病控制率超70%，毒性可控。双免疫阻断方面，anti–TIM-3抗体S095018联合anti–PD-1抗体Sym021治疗既往未接受PD-1/PD-L1抑制剂的晚期胆道癌显示确切抗肿瘤活性；cobolimab联合dostarlimab治疗PD-L1阳性NSCLC的ORR 41.7%，≥3级药物相关不良反应仅5/12例；sabatolimab联合spartalizumab治疗晚期实体瘤的疾病控制率44.2%，显著高于sabatolimab单药的28.7%，≥3级毒性仅11%。此外，TIM-3与LAG-3双阻断在逆转T细胞耗竭、增强细胞毒性方面亦提供额外协同理论依据，提示TIM-3抗体联合放疗、化疗或其他免疫检查点抑制剂具有广泛的临床开发前景。总结与展望作者指出TIM-3作为表达于T、NK、DC等多种免疫细胞的抑制性检查点，通过与配体结合下调免疫信号，在肿瘤、自身免疫和感染性疾病中均表现出高表达与功能耗竭的双重特征，因而成为兼具激活与抑制潜力的治疗靶点；目前抗体药物sabatolimab和cobolimab虽已进入III期临床但两项关键试验因未达总生存终点而终止，提示需重新评估适应证与联合策略，而小分子抑制剂研发尚处早期，仅化合物38、SMI402、A-41、MG-T-19、ML-T7等少数先导被报道，且除A-41与ML-T7外多数缺乏系统构效关系与体内药效数据，距离成药仍有差距；综述系统梳理了TIM-3拓扑结构、配体结合模式、胞质尾磷酸化介导的Bat3-Fyn开关机制以及现有小分子的结合位点、亲和力与功能验证，旨在填补构效关系与成药性研究空白的现状，为药物化学家提供清晰的知识框架与优化方向，以加速新一代TIM-3靶向药物及精准联合方案的开发。文献详细全面信息请跳转原文阅读： https://doi.org/10.1021/acs.jmedchem.5c02693 喜欢我们文章的朋友点个“在看”和“赞”吧，不然微信推送规则改变，有可能每天都会错过我们哦~ 免责声明 “汇聚南药”公众号所转载文章来源于其他公众号平台，主要目的在于分享行业相关知识，传递当前最新资讯。图片、文章版权均属于原作者所有，如有侵权，请在留言栏及时告知，我们会在24小时内删除相关信息。信息来源：药研视角往期推荐本平台不对转载文章的观点负责，文章所包含内容的准确性、可靠性或完整性提供任何明示暗示的保证。

100 项与 Spartalizumab 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D11605	Spartalizumab	-	DB14892

研发状态

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适应症	最高研发状态	国家/地区	公司	日期
黑色素瘤	临床3期	美国	Novartis Pharmaceuticals Corp.	2017-02-17
黑色素瘤	临床3期	日本	Novartis Pharmaceuticals Corp.	2017-02-17
黑色素瘤	临床3期	加拿大	Novartis Pharmaceuticals Corp.	2017-02-17
黑色素瘤	临床3期	德国	Novartis Pharmaceuticals Corp.	2017-02-17
黑色素瘤	临床3期	意大利	Novartis Pharmaceuticals Corp.	2017-02-17
黑色素瘤	临床3期	荷兰	Novartis Pharmaceuticals Corp.	2017-02-17
黑色素瘤	临床3期	西班牙	Novartis Pharmaceuticals Corp.	2017-02-17
黑色素瘤	临床3期	瑞士	Novartis Pharmaceuticals Corp.	2017-02-17
不可切除的黑色素瘤	临床3期	美国	Novartis Pharmaceuticals Corp.	2017-02-17
不可切除的黑色素瘤	临床3期	日本	Novartis Pharmaceuticals Corp.	2017-02-17

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临床结果

适应症

分期

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT04581343 (PanCAN-SR1, CTgov)	临床1期	转移性胰腺癌 \| 转移性胰腺导管腺癌	10	Canakinumab	廠鹹鏇簾膚齋鬱觸淵鹽 = 簾鑰製鏇獵鹹構壓廠衊鹹積淵襯憲衊鬱餘繭範 (餘製艱鹽艱鏇蓋鏇蓋範, 範鹽觸襯膚夢膚顧餘鬱 ~ 糧鹹鑰簾願顧鹽衊廠積) 更多	-	2025-04-08
NCT03668431 (NEWS) 人工标引	临床2期	BRAF V600E突变结直肠癌 BRAF V600E	37	Dabrafenib + Trametinib + Spartalizumab	膚齋壓獵壓築齋築簾蓋(鏇鑰膚鏇蓋窪網範網壓) = 襯醖顧壓鹹鹽製願憲餘繭鹽範選積觸艱憲鬱願 (壓構顧憲鬱衊製糧餘構 ) 更多	积极	2025-03-01
NCT04310397 (CTgov)	临床2期	BRAF V600K 阳性黑色素瘤 \| 皮肤黑色素瘤	4	Dabrafenib+trametinib+Spartalizumab	齋繭淵鏇鑰襯鹽觸簾艱(構鑰製觸糧窪廠壓膚憲) = 鹽衊繭窪餘網願築鹹艱繭獵鏇鑰網夢鏇壓構範 (選鏇鏇製顧窪遞夢廠糧, 鏇壓選蓋窪願鏇衊膚壓 ~ 憲構獵獵醖齋鏇繭鏇構) 更多	-	2024-10-30
NCT03064854 (not available, Pubmed \| BMC Cancer) 人工标引	临床1期	转移性非小细胞肺癌一线	-	Spartalizumab 300 mg Q3W + Gemcitabine/Cisplatin	繭簾壓衊築襯築鏇壓艱(襯鏇範構窪鏇築製憲遞) = 憲衊鏇衊鹹艱選艱築築餘鹹壓淵蓋艱糧鑰遞積 (餘積衊壓淵廠憲壓願獵 ) 更多	积极	2024-10-24
				Spartalizumab 300 mg Q3W + Pemetrexed/Cisplatin	繭簾壓衊築襯築鏇壓艱(襯鏇範構窪鏇築製憲遞) = 構簾窪構選鏇艱憲齋鹽餘鹹壓淵蓋艱糧鑰遞積 (餘積衊壓淵廠憲壓願獵 ) 更多
NCT04544111 (ESMO2024) 人工标引	临床2期	难治性甲状腺癌	19	TrametinibPDR001	醖廠膚醖選衊積鹹糧餘(範願廠遞憲鑰遞廠蓋餘) = 壓壓鬱簾憲鹹膚淵齋願餘夢壓繭簾觸範糧顧鑰 (選願齋蓋壓遞觸鏇範觸 ) 更多	积极	2024-09-16
				dabrafenib+PDR001 (BRAFV600E- tumors after progression on BRAF-directed therapy)	醖廠膚醖選衊積鹹糧餘(範願廠遞憲鑰遞廠蓋餘) = 淵網膚鹹淵廠網鏇襯醖餘夢壓繭簾觸範糧顧鑰 (選願齋蓋壓遞觸鏇範觸 ) 更多
NCT04323436 (CTgov)	临床2期	非小细胞肺癌	31	Spartalizumab+Capmatinib (Run-in Part: Capmatinib 400 mg BID + Spartalizumab 400 mg Q4W)	簾廠膚選遞醖夢鑰夢壓 = 鹽繭簾選鬱窪淵窪構範憲獵憲蓋憲鹽製簾齋鏇 (憲壓鹽繭鹹襯衊糧醖餘, 鏇積繭簾憲憲淵築鑰餘 ~ 網窪顧膚範網餘構網壓) 更多	-	2024-02-06
				Spartalizumab+Capmatinib (Run-in Part: Capmatinib 400mg BID + Spartalizumab 400mg Q4W (Prior Discontinuing Spartalizumab))	構憲鹹獵鬱製襯衊築願(夢糧壓構繭膚鏇願窪鑰) = 構觸獵選構窪觸蓋餘範築構遞築範廠顧襯繭網 (範齋鬱鹹選築窪齋壓膚, 鑰襯鹹鏇壓齋衊遞簾壓 ~ 膚壓壓餘糧廠蓋積餘衊) 更多
NCT03785496 (KCSG HN18-17 \| K-MASTER project 12, Pubmed) 人工标引	临床2期	食管鳞状细胞癌	44	Spartalizumab 300 mg	構選願築願醖製鑰築膚(衊淵觸簾範淵糧衊製廠) = 艱鬱夢願鏇膚鏇製觸繭獵艱蓋繭觸網憲鹹獵糧 (醖繭艱鑰獵獵簾鏇窪製, 8.5 ~ 32.4) 更多	积极	2024-01-01
NCT02795429 (Pubmed) 人工标引	临床1/2期	肝细胞癌二线	62	Capmatinib 40Spartalizumabartalizumab 300 mg q3w	餘顧製選夢製壓衊網衊(製鑰繭襯築觸願鑰膚遞) = 襯壓鬱膚選齋築鏇膚鬱艱憲餘艱壓繭製鹹鹽鹽 (糧壓觸餘顧鹽觸獵齋鏇 )	不佳	2024-01-01
				Spartalizumab alone	餘顧製選夢製壓衊網衊(製鑰繭襯築觸願鑰膚遞) = 艱鹹廠觸製範鑰鹽襯醖艱憲餘艱壓繭製鹹鹽鹽 (糧壓觸餘顧鹽觸獵齋鏇 )
NCT04736485 (GASPAR, ESMO 12023 \| ESMO 22023) 人工标引	临床2期	胃癌一线	67	spartalizumab + fluorouracil+leucovorin+oxaliplatin+ docetaxel	網選淵夢餘繭廠鑰餘醖(鹽窪繭構鏇廠繭範鬱鹹) = 構築築壓窪壓築鏇選壓齋鹹齋鏇鑰積餘繭鹹鹽 (夢蓋範獵築製範窪遞鬱 ) 更多	积极	2023-10-23
				spartalizumab + fluorouracil+leucovorin+oxaliplatin+ docetaxel (operative)	獵築範觸簾壓艱壓鑰蓋(糧壓遞鹹壓蓋蓋醖艱襯) = 築廠鑰餘觸鹹鑰構遞顧獵憲繭壓獵選範廠廠鑰 (鹽廠遞獵顧餘淵願遞遞 ) 更多
NCT02967692 (COMBI-i, CTgov)	临床3期	黑色素瘤 \| 不可切除的黑色素瘤	568	Dabrafenib+Trametinib+PDR001 (Part 1- Safety run-in: PDR001 400 mg Q4W + Dabrafenib 150 mg BID + Trametinib 2 mg QD)	夢遞壓醖襯蓋願鬱夢衊 = 膚糧齋鏇繭遞壓選憲觸壓糧範鹽艱選製衊憲夢 (襯觸艱齋顧襯糧選顧製, 築襯鏇製選醖網壓餘簾 ~ 鑰壓鑰鏇遞遞淵鏇獵製) 更多	-	2023-07-24
				Dabrafenib+Trametinib+PDR001 (Part 2- Biomarker Cohort: PDR001 400 mg Q4W + Dabrafenib 150 mg BID + Trametinib 2 mg QD)	蓋簾糧蓋選觸願襯範鏇(獵簾顧簾壓鏇廠襯鏇積) = 鹽築蓋願蓋繭簾築餘鑰鏇顧廠選鏇獵鑰糧艱製 (蓋顧襯鹹範鏇願網膚鹹, 13.05) 更多