A Phase Ib/II Open-Label, Dose-Escalation, Safety, Pharmacokinetic, Pharmacodynamic and Efficacy Study of Bemcentinib Plus Pacritinib In Patients With Advanced Lung Adenocarcinoma

This is a Phase Ib/II, open-label, single institution dose-escalation, safety, pharmacokinetics, pharmacodynamic and efficacy study.

开始日期2024-12-27

申办/合作机构

University of Texas Health Science Center At San Antonio

[+1]

NCT05469178

/ Terminated临床1/2期

Phase 1b/2a Safety and Tolerability Study of Bemcentinib With Pembrolizumab/Carboplatin/Pemetrexed in Subjects With Untreated Advanced or Metastatic Non-squamous Non-small Cell Lung Cancer (NSCLC) Without/With a STK11 Mutation

The primary purpose of this study is to determine the safety and tolerability of the combination of bemcentinib with chemo-immunotherapy (CIT) to identify the recommended phase 2 dose (RP2D) when administered as first line (1L) treatment in participants with locally advanced (Stage IIIb/IIIC) or metastatic (Stage IV) non-squamous NSCLC with no actionable mutations and to determine the anti-tumor activity of the combination of bemcentinib with CIT when administered as 1L treatment in participants with locally advanced (Stage IIIb/IIIc) or metastatic (Stage IV) non-squamous NSCLC with serine/threonine kinase 11 (STK11) mutation and no actionable mutations.

开始日期2023-03-06

申办/合作机构

BerGenBio ASA

CTIS2022-500363-12-00

/ Not yet recruiting临床2期IIT

Efficacy and Safety of AXL-Inhibitor bemcentinib for the Treatment of Moderate COVID-19 (AXL-SolidAct) - AXL-SolidAct

开始日期2022-09-27

申办/合作机构-

100 项与 Bemcentinib 相关的临床结果

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100 项与 Bemcentinib 相关的转化医学

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100 项与 Bemcentinib 相关的专利（医药）

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235

项与 Bemcentinib 相关的文献（医药）

2025-03-13·ACS Medicinal Chemistry Letters

A Hybrid Energy-Based and AI-Based Screening Approach for the Discovery of Novel Inhibitors of AXL

Article

作者: Zhao, Jingyi ; Pan, Youlu ; Ying, Xiaojun ; Li, Long ; Lv, Xinting ; Huang, Wenhai ; Wang, Linjun ; Chi, Xinglong ; Pan, Zhichao ; Kang, Youkun

AXL, part of the TAM receptor tyrosine kinase family, plays a significant role in the growth and survival of various tissues and tumors, making it a critical target for cancer therapy. This study introduces a novel high-throughput virtual screening (HTVS) methodology that merges an AI-enhanced graph neural network, PLANET, with a geometric deep learning algorithm, DeepDock. Using this approach, we identified potent AXL inhibitors from our database. Notably, compound 9, with an IC₅₀ of 9.378 nM, showed excellent inhibitory activity, suggesting its potential as a candidate for further research. We also performed molecular dynamics simulations to explore the interactions between compound 9 and AXL, providing insights for future enhancements. This hybrid screening method proves effective in finding promising AXL inhibitors, and advancing the development of new cancer therapies.

2025-03-01·INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY

Bemcentinib enhances sensitivity to estrogen receptor inhibitors in breast cancer cells

Article

作者: Jin, Hyeon-Ok ; Ahn, Se Hee ; Kim, Gyeongmi ; Park, In-Chul ; Park, Chan Sub ; Kim, Hyunggee ; Park, Ki Soo ; Kim, Hyun-Ah ; Kim, Selim ; Seong, Min-Ki ; Jang, Se-Kyeong

Estrogen receptor (ER)-positive breast cancer accounts for a substantial proportion of breast cancer cases and is typically managed using ER inhibitors, such as tamoxifen and fulvestrant. However, the development of resistance to these therapies is a significant clinical challenge, and the improvement of therapeutic strategies is crucial. This study aimed to investigate the potential of bemcentinib, a well-known AXL inhibitor, to enhance the sensitivity of MCF7 breast cancer cells to 4-hydroxytamoxifen (4-OHT) and fulvestrant. Our findings revealed that bemcentinib effectively decreased S6K1 phosphorylation and synergistically induced cell death when used in combination with ER inhibitors. Bemcentinib treatment also unexpectedly activated STAT3, and inhibition of STAT3 enhanced cell death induced by bemcentinib and 4-OHT. Notably, the combination of bemcentinib and 4-OHT effectively induced cell death even in tamoxifen-resistant MCF7 cells (MCF7-TR), highlighting its potential to overcome tamoxifen resistance. Interestingly, AXL knockdown did not enhance the sensitivity to 4-OHT or affect S6K1 signaling in either MCF7 or MCF7-TR cells, suggesting that the sensitizing effect of bemcentinib through S6K1 inhibition may be independent of AXL expression. Our findings suggest that bemcentinib treatment, particularly in combination therapy, could be a promising strategy for improving treatment efficacy and overcoming tamoxifen resistance in ER-positive breast cancer.

2025-02-21·SCIENCE

Neuronal FAM171A2 mediates α-synuclein fibril uptake and drives Parkinson’s disease

Article

作者: Ma, Ling-Zhi ; Zhang, Yi ; Yang, Liu ; Han, Si-Da ; Yang, Zhao-Fei ; Xu, Qian-Hui ; Wu, Bang-Sheng ; Chen, Shu-Fen ; Lu, Bo-Xun ; Le, Wei-Dong ; Liu, Yi-Qi ; Zhang, Ya-Ru ; Zhao, Jue ; Guo, Yu ; Yu, Jin-Tai ; Wu, Kai-Min ; Cui, Mei ; Liu, Cong ; Xiao, Yu-Jie ; Chen, Yi-Lin ; Chen, Shi-Dong ; Li, Jia-Yi ; Wang, Ting-Ting ; Li, Wen-Sheng ; Ye, Keqiang ; Wang, Jian ; Feng, Yi-Wei ; Yuan, Peng ; Shu, You-Sheng

Neuronal accumulation and spread of pathological α-synuclein (α-syn) fibrils are key events in Parkinson's disease (PD) pathophysiology. However, the neuronal mechanisms underlying the uptake of α-syn fibrils remain unclear. In this work, we identified FAM171A2 as a PD risk gene that affects α-syn aggregation. Overexpressing FAM171A2 promotes α-syn fibril endocytosis and exacerbates the spread and neurotoxicity of α-syn pathology. Neuronal-specific knockdown of FAM171A2 expression shows protective effects. Mechanistically, the FAM171A2 extracellular domain 1 interacts with the α-syn C terminus through electrostatic forces, with >1000 times more selective for fibrils. Furthermore, we identified bemcentinib as an effective blocker of FAM171A2–α-syn fibril interaction with an in vitro binding assay, in cellular models, and in mice. Our findings identified FAM171A2 as a potential receptor for the neuronal uptake of α-syn fibrils and, thus, as a therapeutic target against PD.

项与 Bemcentinib 相关的新闻（医药）

2025-04-17

·智药邦

Science｜复旦大学郁金泰团队发现帕金森病全新治疗靶点，并利用AI找到潜在治疗药物

帕金森病（Parkinson’s Disease，PD），是一种影响运动和认知功能的神经退行性疾病，也是世界上第二常见的神经退行性疾病，仅次于阿尔茨海默病（AD），影响着约 1%-2%的65岁及以上老人。随着全球人口老龄化，帕金森病患病率还将大幅增加。病理性α-突触核蛋白（α-Syn）在不同脑区聚集介导了帕金森病的疾病进展。聚集的α-Syn蛋白形成纤维，以朊病毒样（Prion-like）方式发挥作用，在大脑的不同区域传播α-Syn病理，然而，其在神经元之间传递的分子机制，目前仍不清楚。之前的研究显示，α-Syn通过不同受体的内吞作用被内化，然而，其在神经元上的特异性受体仍有待完全鉴定。郁金泰团队曾于2020年10月在Science Advances期刊发表论文，首次发现了FAM171A2基因的单核苷酸多态性（rs708384）与帕金森病等神经退行性疾病的风险增加有关。帕金森病患者的脑脊液（CSF）中FAM171A2蛋白水平增加，并且与脑内α-Syn高聚集的指征相关。2025年2月20日，复旦大学附属华山医院郁金泰教授团队联合复旦大学脑科学转化研究院袁鹏教授及中国科学院上海有机化学研究所刘聪教授（博士后吴凯敏为第一作者），在国际顶尖学术期刊Science上发表了题为：Neuronal FAM171A2 mediates α-synuclein fibril uptake and drives Parkinson’s disease的研究论文。该研究首次发现了帕金森病（PD）的全新治疗靶点——FAM171A2，并利用基于人工智能的蛋白质结构预测和虚拟筛选技术，成功找到了具有潜在治疗作用的小分子化合物。这项研究发现的全新治疗靶点和前在治疗药物有望从疾病早期对帕金森病进行干预，延缓疾病进展，结合现有的对症治疗手段，有望实现帕金森病病因治疗与症状缓解的双重突破。在这项最新研究中，研究团队通过对超过100万样本的大规模全基因组关联分析（GWAS），发现FAM171A2基因的5个突变（例如rs850738、rs708384）与帕金森病风险显著相关。帕金森病患者的脑脊液（CSF）中FAM171A2蛋白水平升高，且与α-Syn病理标志物呈负相关，提示其参与了α-Syn的异常聚集。进一步实验验证显示，过表达FAM171A2会促进α-Syn纤维的被神经元内吞，加剧病理扩散（例如向黑质、纹状体的扩散）和运动功能障碍。而敲低FAM171A2能够减少α-Syn纤维的内吞，保护多巴胺能神经元，从而改善小鼠的运动表现。研究团队在小鼠神经元中特异性敲除FAM171A2，进一步验证了神经元来源的FAM171A2在α-Syn病理传播中是必要的。从机制上来说，FAM171A2蛋白的胞外结构域1通过静电力与α-Syn的C端相互作用，且高度选择性地结合病理性α-Syn（纤维形式），其对纤维形式α-Syn的选择性结合是单体形式α-Syn的超1000倍。也就是说，位于神经元上的FAM171A2蛋白能够高度选择性的结合病理性α-Syn，使其通过内吞作用进入神经元内，诱导神经元内的正常的单体形式的α-Syn发生错误折叠，转变为病理性α-Syn，进而诱导神经元死亡以及在神经元之间传播。接下来，研究团队使用AlphaFold-Multitimer预测了FAM171A2-α-Syn复合物结构，并利用虚拟筛选技术，从7173种化合物中筛选出了一种小分子药物——Bemcentinib，其能够竞争性结合α-Syn的C端，从而阻断FAM171A2与病理性α-Syn结合，抑制FAM171A2介导的神经元对病理性α-Syn的内吞。总的来说，该研究首次阐明了FAM171A2作为病理性α-Syn的神经元受体，揭示了其驱动帕金森病病理传播的分子机制，并成功筛选到了潜在抑制剂，为帕金森病的精准治疗提供了新方向。未来研究可聚焦于靶向FAM171A2的药物开发及多维度验证其临床价值。相关阅读：2024年11月22日，复旦大学附属华山医院郁金泰、毛颖团队与复旦大学类脑智能科学与技术研究院程炜、冯建峰团队合作，在国际顶尖学术期刊Cell在线发表了题为：Atlas of the plasma proteome in health and disease in 53,026 adults的研究论文。这项研究全面绘制了人类健康与疾病蛋白质组图谱，并结合人工智能大数据分析方法，构建了疾病诊断预测模型以及发现了26个药物治疗新靶点，为精准医学的实施提供了重要科学依据。该研究于2025年1月9日，登上了Cell期刊封面，该封面描绘了一个由蛋白质构成的人类，正在借助人工智能（由芯片和二进制代码代表）的帮助来检查自己的健康状况（通过心电图监测界面来体现）。参考资料：1.https://www.science.org/doi/10.1126/sciadv.abb30632.https://www.science.org/doi/10.1126/science.adp36453.https://www.cell.com/cell/fulltext/S0092-8674(24)01268-6--------- End ---------感兴趣的读者，可以添加小邦微信加入读者实名讨论微信群。添加时请主动注明姓名-企业-职位/岗位或姓名-学校-职务/研究方向。

申请上市临床研究

2025-03-06

·PRNewswire

TEPMETKO Continues to Strengthens its Position as a Leading METex14 Skipping NSCLC Therapy | DelveInsight

With increasing biomarker-driven cancer treatments, TEPMETKO benefits from growing adoption in precision oncology. Competition from other MET inhibitors like TABRECTA (capmatinib) exists, but TEPMETKO's once-daily dosing and efficacy profile offer differentiation. LAS VEGAS, March 6, 2025 /PRNewswire/ -- DelveInsight's " TEPMETKO Market Size, Forecast, and Market Insight Report" highlights the details around TEPMETKO, a kinase inhibitor indicated for the treatment of adult patients with metastatic NSCLC harboring MET exon 14 skipping alterations. The report provides product descriptions, patent details, and competitor products (marketed and emerging therapies) of TEPMETKO. The report also highlights the historical and forecasted sales from 2020 to 2034 segmented into 7MM [the United States, the EU4 (Germany, France, Italy, and Spain), the United Kingdom, and Japan]. EMD Serono's TEPMETKO (tepotinib) Overview TEPMETKO is a kinase inhibitor prescribed for adult patients with metastatic non-small cell lung cancer (NSCLC) carrying MET exon 14 skipping alterations. The active component is Tepotinib (as hydrochloride monohydrate), administered orally. Patients should be cautioned about the heightened risk of severe or fatal interstitial lung disease/pneumonitis, liver toxicity, and potential embryo-fetal toxicity, necessitating effective contraception during and shortly after treatment. Tepotinib specifically targets MET, including variants with exon 14 skipping mutations. It blocks HGF-dependent and independent MET phosphorylation, disrupting MET-driven signaling pathways. Additionally, at clinically relevant concentrations, Tepotinib inhibits melatonin 2 and imidazoline 1 receptors. In vitro studies show that it suppresses tumor cell proliferation, anchorage-independent growth, and migration of MET-dependent cancer cells. In mouse models with MET-driven tumors, including those with MET exon 14 skipping alterations, Tepotinib reduced tumor growth, sustained MET phosphorylation inhibition, and, in one case, decreased metastasis formation. The recommended dose of TEPMETKO is 450 mg taken orally once daily until disease progression or intolerable toxicity occurs. Patients should take it at the same time each day, swallowing tablets whole without chewing, crushing, or splitting them. If a dose is missed and less than eight hours remain until the next scheduled dose, patients should skip it. In cases of vomiting after taking TEPMETKO, the next dose should be taken at the usual time. Learn more about TEPMETKO projected market size for NSCLC @ TEPMETKO Market Potential Non-small cell lung cancer (NSCLC) is the most common type of lung cancer, accounting for 81% of all diagnosed cases. Early detection greatly improves outcomes, but diagnosing NSCLC and other lung cancers is challenging because their symptoms are often mistaken for common illnesses or the long-term effects of smoking. Consequently, 80% of NSCLC cases are already at advanced stages by the time they are identified, making treatment more difficult. Around 80% of EGFR mutations in NSCLC involve either exon 19 deletions or the exon 21 L858R substitution, both of which are classified as sensitizing mutations. Until the last decade, chemotherapy was the primary treatment for advanced and metastatic lung cancer. However, this changed in 2015 with the approval of the first immune checkpoint inhibitor (ICI), KEYTRUDA (pembrolizumab), as a second-line therapy for advanced cases. This was followed by TECENTRIQ (atezolizumab) in 2016. Both therapies were later approved for first-line treatment, broadening their use to a larger patient population. In 2020, the combination of OPDIVO (nivolumab) and ipilimumab also received approval as a first-line treatment for metastatic NSCLC. According to DelveInsight, the NSCLC market size across the 7MM is projected to grow from USD 30 billion in 2024, with a substantial CAGR through 2034. This growth is largely driven by the introduction of emerging therapies during the forecast period (2025–2034). Discover more about the NSCLC market in detail @ Non-small Cell Lung Cancer Market Report Emerging Competitors of TEPMETKO The NSCLC pipeline is very robust with the promising therapies such as Telisotuzumab vedotin (AbbVie), Patritumab deruxtecan (Daiichi Sankyo/AstraZeneca), Datopotamab deruxtecan (Daiichi Sankyo/AstraZeneca), Eftilagimod alpha (Immutep), BNT311/GEN1046 (acasunlimab) (Genmab), V940 (mRNA-4157) + Pembrolizumab (Moderna Therapeutics/Merck), Plinabulin + Docetaxel (BeyondSpring), Olomorasib (LY3537982) (Eli Lilly and Company), Zipalertinib (Cullinan Oncology/Taiho Pharma), Ceralasertib (AZD6738) (AstraZeneca), TEDOPI (EP-2101; IDM 2101; OSE-2101) (OSE Immuno-therapeutics), Sigvotatug vedotin (PF08046047) (Pfizer), ANKTIVA (N-803) (ImmunityBio), Aumolertinib/Almonertinib/HS-10206 (Jiangsu Hansoh Pharmaceutical), Niraparib (GSK), Savolitinib (AstraZeneca/Hutchison MediPharma), TRODELVY (Gilead Sciences), Pyrotinib (Jiangsu HengRui Medicine), Ociperlimab (BGB-A1217) (BieGene), Volrustomig (AstraZeneca), Gotistobart (BNT316/ONC-392) (OncoC4/BioNTech), Ivonescimab (AK112/SMT112) (Akeso Biopharma/Summit Therapeutics), ZYNYZ (retifanlimab/INCMGA00012) (Incyte/Macrogenics), Divarasib (GDC-6036) (Roche/Genentech), Tiragolumab (RG6058) (Roche), Sacituzumab Tirumotecan (Merck and Kelun-Biotech), JEMPERLI (dostarlimab/TSR-042) (GSK and AnaptysBio), Zongertinib (BI-1810631) (Boehringer Ingelheim), BAY 2927088 (Bayer), Serplulimab (HLX10) (Shanghai Henlius Biotech), Rilvegostomig (AZD2936) (AstraZeneca), MK-1084 (Merck, Taiho Pharmaceutical, and Astex), Domvanalimab (Arcus Biosciences and Gilead Sciences), OPDUALAG (nivolumab and relatlimab) (Bristol-Myers Squibb), Belrestotug + JEMPERLI (iTeos Therapeutics and GSK), Firmonertinib (ArriVent BioPharma), Sunvozertinib (DZD9008) (Dizal Pharmaceutical), Cobolimab (GSK), Livmoniplimab (AbbVie), Fianlimab (REGN3767) (Regeneron Pharmaceuticals), BNT327/PM8002 (Biotheus/BioNTech), HS-20117 (Hansoh BioMedical), IO102-IO103 + Pembrolizumab (IO Biotech), Naptumomab estafenatox (NeoTX Therapeutics/Active Biotech), FF-10832 (FUJIFILM Corporation), BNT116 (BioNTechSE/Regeneron Pharmaceuticals), CAN-2409 (Candel Therapeutics), Mecbotamab Vedotin (BA3011/CAB-AXL-ADC) (BioAtla), Bemcentinib (BGB 324/BGB-3234/R-428) (BerGenBio/Rigel Pharmaceuticals), DOVBLERON (taletrectinib/AB-106/IBI-344) (Nuvation Bio/Innovent Biologics/Daiichi Sankyo/Nippon Kayaku), Lifileucel (Iovance Biotherapeutics), IBI363 (Innovent Biologics), Sotevtamab (AB-16B5) (Alethia Biotherapeutics), Avutometinib (VS6766) (Verastem Oncology), Vebreltinib (APL-101) (Apollomics), LP-300 (Lantern Pharma), JNJ-90301900 (Johnson & Johnson Innovative Medicine), AMG 193 (Amgen), Luveltamab tazevibulin (Sutro Biopharma), PRT3789 (Prelude Therapeutics), Disitamab vedotin (Seagen), PADCEV (enfortumab vedotin) (Astellas Pharma), RP1 (Replimune), TIVDAK (tisotumab vedotin) (Seagen), Zanidatamab (Jazz Pharmaceuticals), Utidelone injectable (UTD1) (Beijing Biostar Pharmaceuticals), REGN5093-M114 (Regeneron Pharmaceuticals), SLC-391 (SignalChem Lifesciences), fulzerasib (GenFleet), Davutamig (REGN5093) (Regeneron Pharmaceuticals), TAS3351 (Taiho Oncology), H002 (RedCloud Bio), JIN-A02 (J INTS BIO), FWD1509 (Forward Pharma), Sabestomig (AZD7789) (AstraZeneca), Sasanlimab (Pfizer), Selvigaltin (GB1211) (Galecto Biotech), Vepafestinib Helsinn (Healthcare/Taiho Pharmaceutical), EP0031 (A400/ KL590586) (Ellipses Pharma/Kelun-Biotech), Pamvatamig (MCLA-129) (Merus), Zidesamtinib (NVL-520) (Nuvalent), NVL-655 (Nuvalent), RMC-4630 (Revolution Medicines), REQORSA (quaratusugene ozeplasmid) (Genprex), PDC*lung01 (PDC*line Pharma), Evalstotug (BA3071) (BioAtla and BeiGene), PT-112 (Promontory Therapeutics), MRT-2359 (Monte Rosa Therapeutics), GAIA-102 (GAIA BioMedicine), Rigosertib (Traws Pharma), HMBD-001 (Hummingbird Bioscience), PLB1004 (Avistone Biotechnology), ANS03 (Avistone Biotechnology), MYTX-011 (Mythic Therapeutics), A166 (Sichuan Kelun-Biotech Bio-pharmaceutical), Atamparib (BN-2397) (Ribon Therapeutics), DELTACEL (KB-GDT-01) (Kiromic BioPharma), Carotuximab (ENV-105) (Kairos Pharma), YL202 (MediLink Therapeutics), and others. To know more about the number of competing drugs in development, visit @ TEPMETKO Market Positioning Compared to Other Drugs Key Milestones of TEPMETKO In February 2024, the FDA granted traditional approval to TEPMETKO for adult patients with metastatic NSCLC harboring MET exon 14 skipping alterations. In February 2022, the EC approved TEPMETKO as monotherapy for the treatment of adult patients with advanced NSCLC harboring alterations leading to METex14 skipping who require systemic therapy following prior treatment with immunotherapy and/or platinum-based chemotherapy. In February 2021, Merck announced that the US FDA has approved TEPMETKO following priority review for the treatment of adult patients with metastatic NSCLC harboring MET exon 14 skipping alterations. This indication was approved under accelerated approval based on ORR and DOR. In October 2020, TEPMETKO received ODD for treating NSCLC with MET genomic tumor aberrations In March 2020, EMD Serono (the biopharmaceutical business of Merck KGaA), announced that the MHLW approved TEPMETKO for the treatment of patients with unresectable, advanced, or recurrent NSCLC with METex14 skipping alterations. In September 2019, the US FDA granted BTD for tepotinib in patients with metastatic NSCLC harboring METex14 skipping alterations who progressed following platinum-based cancer therapy Discover how TEPMETKO is shaping the NSCLC treatment landscape @ TEPMETKO NSCLC TEPMETKO Market Dynamics TEPMETKO competes in a growing but highly specialized market where MET-targeted therapies are gaining traction due to their efficacy in addressing MET-altered tumors. The market for MET inhibitors is expanding as precision oncology advances and molecular diagnostics become more widely available, enabling better identification of patients who would benefit from targeted treatments like TEPMETKO. A key factor shaping TEPMETKO's market dynamics is competition. It directly competes with Novartis' TABRECTA (capmatinib), another MET inhibitor approved for the same indication. While TEPMETKO offers the advantage of once-daily dosing compared to TABRECTA's twice-daily regimen, both drugs have similar efficacy profiles, making physician and patient preference an important differentiator. Additionally, broader competition from next-generation MET inhibitors and combination therapies in clinical trials could impact TEPMETKO's long-term market position. Regulatory approvals and market access play a crucial role in TEPMETKO's adoption. The drug has been approved in multiple regions, including the U.S., Europe, and Japan, but reimbursement and pricing strategies vary by market. Payer policies, along with the cost-benefit analysis of MET inhibitors compared to other targeted therapies, influence prescription trends. Furthermore, real-world evidence and post-marketing studies will be critical in demonstrating TEPMETKO's sustained effectiveness and safety, which could support expanded indications and increased market penetration. Looking ahead, the MET inhibitor market is expected to grow with advances in biomarker-driven therapy, further refining patient selection. TEPMETKO's success will depend on continued clinical development, potential label expansions, and strategic partnerships to strengthen its competitive edge. As new entrants emerge, Merck KGaA's ability to differentiate TEPMETKO through combination strategies or enhanced formulations may determine its long-term sustainability in this evolving landscape. Dive deeper to get more insight into TEPMETKO's strengths & weaknesses relative to competitors @ TEPMETKO Market Drug Report Table of Contents Related Reports Non-small Cell Lung Cancer Market Non-small Cell Lung Cancer Market Insights, Epidemiology, and Market Forecast – 2034 report deliver an in-depth understanding of the disease, historical and forecasted epidemiology, as well as the market trends, market drivers, market barriers, and key NSCLC companies including Daiichi Sankyo, AstraZeneca, Gilead Sciences, BieGene, AbbVie, Roche, Merck, Novartis, Pfizer, Takeda Pharmaceuticals, Eli Lilly, BerGenBio, GlaxoSmithKline, Duality biologics, among others. Non-small Cell Lung Cancer Pipeline Non-small Cell Lung Cancer Pipeline Insight – 2025 report provides comprehensive insights about the pipeline landscape, pipeline drug profiles, including clinical and non-clinical stage products, and the key non-small cell lung cancer companies, including BridgeBio Pharma, Daiichi Sankyo, EMD Serono, Merck, BridgeBio Pharma, Abbvie, Pfizer, Eli Lilly and Company BioNTech SE, Shenzhen TargetRx, Taiho Pharmaceutical, Chong Kun Dang, Bristol Myers Squibb, Innovent Biologics, Xuanzhu Biopharmaceutical, Bayer, GeneScience Pharmaceuticals, InventisBio, Apollomics, Imugene, Ono Pharmaceutical, Pierre Fabre, Jiangsu Hengrui Medicine Co., Bristol-Myers Squibb, Surface Oncology, Inhibrx, Sinocelltech, Mirati Therapeutics, REVOLUTION Medicines, Yong Shun Technology Development, Iovance Biotherapeutics, Galecto Biotech, among others. C-MET Metastatic Non-small Cell Lung Cancer Market C-MET Metastatic Non-small Cell Lung Cancer Market Insights, Epidemiology, and Market Forecast – 2034 report deliver an in-depth understanding of the disease, historical and forecasted epidemiology, as well as the market trends, market drivers, market barriers, and key C-MET mNSCLC companies, including Novartis, Merck, EMD Serono, AbbVie, Regeneron Pharmaceuticals, Mythic Therapeutics, Apollomics, Johnson & Johnson Innovation, Haihe Biopharma, among others. C-MET Non-small Cell Lung Cancer Pipeline C-MET Non-small Cell Lung Cancer Pipeline Insight – 2025 report provides comprehensive insights about the pipeline landscape, pipeline drug profiles, including clinical and non-clinical stage products, and the key C-MET non-small cell lung cancer companies, including AbbVie, Janssen Research & Development, Beijing Pearl Biotechnology Limited Liability Company, Novartis, among others. 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上市批准免疫疗法优先审批

2025-03-05

·药学进展

学科前沿 | 复旦大学郁金泰教授团队联合袁鹏教授团队、中科院上海有机化学研究所刘聪教授团队在帕金森病发病机制研究方面取得进展

“ 点击蓝字关注我们复旦大学郁金泰教授团队联合袁鹏教授团队、中科院上海有机化学研究所生物与化学交叉研究中心刘聪教授团队在帕金森病发病机制研究方面取得进展 PPS 在国家自然科学基金项目（批准号：82271471、82401676、92249305）等资助下，复旦大学附属华山医院郁金泰教授团队联合复旦大学脑科学转化研究院袁鹏教授团队、中科院上海有机化学研究所生物与化学交叉研究中心刘聪教授团队在帕金森病发病机制研究方面取得进展。研究成果以“神经元FAM171A2介导α-突触核蛋白纤维摄取并促进帕金森病发生（Neuronal FAM171A2 mediates α-synuclein fibril uptake and drives Parkinson's disease）”为题，于2025年2月20日在线发表于《科学》（Science）杂志，论文链接：https://www.science.org/doi/10.1126/science.adp3645。帕金森病（Parkinson's disease, PD）是第二常见的神经退行性疾病，我国65岁以上老年人群中帕金森病患病率为1.7%，到2030年，我国帕金森病患者数预计将达500万，几乎占到全球患者数的一半。既往研究发现α-突触核蛋白在病理条件下会发生错误折叠并聚集形成病理性α-突触核蛋白，破坏神经元功能并导致其死亡，是PD的关键致病蛋白。这些致病蛋白还会像“种子”一样播散，入侵邻近神经元，募集神经元内α-突触核蛋白单体发生错误折叠，形成更多的致病“种子”。这些致病“种子”可以在神经元间传播，当传播到中脑黑质区域时，可导致多巴胺能神经元死亡，从而出现动作迟缓、静止性震颤、肌强直等PD运动症状。但目前病理性α-突触核蛋白在神经元间传播机制尚不清楚，临床仍然缺乏有效干预手段。研究团队首先通过大规模人群的全基因组关联分析，发现FAM171A2是PD风险基因；并基于PD患者临床样本分析发现，患者大脑中FAM171A2蛋白含量增高，且FAM171A2含量越高的患者，其脑内病理性α-突触核蛋白含量也越高。进一步研究发现在神经元细胞膜上，FAM171A2可选择性的结合病理性α-突触核蛋白，并携带其进入到神经元中，诱导神经元内单体形式的α-突触核蛋白发生错误折叠，造成神经元死亡和其在神经元间的传播。团队随后研究证实敲除小鼠神经元上FAM171A2，可以有效控制小鼠帕金森样症状的进展。基于前述发现，研究团队利用人工智能的蛋白结构预测和虚拟筛选技术，从7000余种药物中成功筛选出候选小分子bemcentinib，并在体外实验和动物实验证实该小分子可有效抑制FAM171A2蛋白和病理性α-突触核蛋白结合，并抑制多巴胺能神经元对病理性α-突触核蛋白的摄取。该研究发现了神经元上病理性α-突触核蛋白潜在膜受体FAM171A2蛋白，揭示了FAM171A2蛋白是促进病理性α-突触核蛋白传播的关键，筛选出FAM171A2有效阻断剂bemcentinib是治疗PD的候选小分子。该研究结果为PD的治疗提供了潜在新靶点和新思路。文章来源：国家自然科学基金委员会美编排版：陈鑫茹文章审核：周碧远陈鑫茹罗琪【免责声明】以上内容来源于互联网，不代表本平台立场或观点；如有侵犯作者著作权，请及时与我们联系（Tel：025-83271227，或直接在微信平台留言），我们将及时更正或删除。《药学进展》杂志由国家教育部主管、中国药科大学和中国药学会共同主办，中国科技核心期刊（中国科技论文统计源期刊）。刊物以反映药学科研领域的新方法、新成果、新进展、新趋势为宗旨，以综述、评述、行业发展报告为特色，以药学学科进展、技术进展、新药研发各环节技术信息为重点，是一本专注于医药科技前沿与产业动态的专业媒体。《药学进展》注重内容策划、加强组稿约稿、深度挖掘、分析药学信息资源、在药学学科进展、科研思路方法、靶点机制探讨、新药研发报告、临床用药分析、国际医药前沿等方面初具特色；特别是医药信息内容以科学前沿与国家战略需求相合，更加突出前瞻性、权威性、时效性、新颖性、系统性、实战性。根据最新统计数据，刊物篇均下载率连续三年蝉联我国医药期刊榜首，复合影响因子1.216，具有较高的影响力。《药学进展》编委会由国家重大专项化学药总师陈凯先院士担任主编，编委由新药研发技术链政府监管部门、高校科研院所、制药企业、临床医院、CRO、金融资本及知识产权相关机构近两百位极具影响力的专家组成。联系《药学进展》↓↓↓ 编辑部官网：pps.cpu.edu.cn；邮箱：yxjz@163.com；电话：025-83271227。欢迎投稿、订阅！往期推荐聚焦“兴药为民·2023生物医药创新融合发展大会”“兴药为民·2023生物医药创新融合发展大会”盛大启幕！院士专家齐聚杭城，绘就生物医药前沿赛道新蓝图“兴药强刊”青年学者论坛暨《药学进展》第二届青年编委会议成功召开“兴药为民·2023生物医药创新融合发展大会”路演专场圆满收官！校企合作新旅程已启航我知道你在看哟

申请上市

100 项与 Bemcentinib 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D11438	Bemcentinib	-	DB12411

研发状态

10 条进展最快的记录,

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适应症	最高研发状态	国家/地区	公司	日期
转移性非鳞状非小细胞肺癌	临床2期	美国	BerGenBio ASA	2023-03-06
转移性非鳞状非小细胞肺癌	临床2期	法国	BerGenBio ASA	2023-03-06
转移性非鳞状非小细胞肺癌	临床2期	希腊	BerGenBio ASA	2023-03-06
转移性非鳞状非小细胞肺癌	临床2期	匈牙利	BerGenBio ASA	2023-03-06
转移性非鳞状非小细胞肺癌	临床2期	意大利	BerGenBio ASA	2023-03-06
转移性非鳞状非小细胞肺癌	临床2期	波兰	BerGenBio ASA	2023-03-06
转移性非鳞状非小细胞肺癌	临床2期	西班牙	BerGenBio ASA	2023-03-06
新型冠状病毒感染	临床2期	印度	BerGenBio ASA	2020-10-20
新型冠状病毒感染	临床2期	南非	BerGenBio ASA	2020-10-20
转移性胰腺癌	临床2期	美国	BerGenBio ASA	2019-01-03

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临床结果

适应症

分期

评价

查看全部结果

研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT03184571 (BGBC008, AACR2025)	临床2期	难治性肺癌 granzyme B \| cDC1 \| phospho-STAT3	29	Bemcentinib + Pembrolizumab	範窪築鏇糧簾蓋築願範(壓選膚餘蓋醖遞積鏇簾) = 觸齋選鹽構顧顧鬱繭觸鹹積選膚鬱夢鹹糧觸夢 (製觸製獵製鑰襯簾製窪 )	积极	2025-04-30
				Bemcentinib (AXL-PD1-STAT3 axis)	範窪築鏇糧簾蓋築願範(壓選膚餘蓋醖遞積鏇簾) = 糧願醖製築膚願範襯選鹹積選膚鬱夢鹹糧觸夢 (製觸製獵製鑰襯簾製窪 )
NCT02424617 (CTgov)	临床1/2期	非小细胞肺癌	40	Bemcentinib (Phase 1- Run in Arm (Bemcentinib Monotherapy))	齋繭積鏇觸鬱鏇鬱壓遞 = 壓壓淵構壓繭獵壓鏇鑰鹹壓觸範憲鏇艱鑰糧壓 (鑰蓋築齋積遞襯餘餘憲, 築簾選憲鹹膚艱衊鏇鑰 ~ 餘齋鹽廠憲觸鹹膚蓋網) 更多	-	2025-02-26
				Erlotinib+Bemcentinib (Phase 1- Arm A (Bemcentinib + Erlotinib))	齋繭積鏇觸鬱鏇鬱壓遞 = 艱艱壓鏇獵鑰醖糧艱繭鹹壓觸範憲鏇艱鑰糧壓 (鑰蓋築齋積遞襯餘餘憲, 積壓廠夢壓構襯糧願繭 ~ 築鏇觸選鏇鏇糧網範網) 更多
NCT06469138 (8479217, CTgov)	临床1期	急性髓性白血病 \| 新型冠状病毒感染 \| 恶性间皮瘤 ... 更多	6	Bemcentinib	願窪膚鏇範積遞壓遞願(構築壓醖網製壓網齋鹹) = 顧鏇齋鬱鏇鏇鹹齋壓衊願衊鏇蓋廠遞簾齋鬱憲 (齋構獵窪窪顧齋鬱夢鬱, 26.8) 更多	-	2025-01-29
NCT04890509 (CTgov)	临床2期	新型冠状病毒感染	115	SOC	築淵廠衊憲選憲觸觸廠(糧鑰壓艱壓齋廠淵製衊) = 齋鹹糧窪獵遞餘齋鹹憲鹹憲獵廠顧積艱範遞選 (淵糧鏇齋遞糧糧遞廠憲, 艱壓獵鏇願餘簾膚鏇構 ~ 醖醖繭積繭鹹觸鬱築淵) 更多	-	2024-10-16
NCT02488408 (BGBC003, ASH2023)	临床1/2期	急性髓性白血病	32	Bemcentinib + Low-dose Cytarabine	憲淵製構鏇鏇遞餘網衊(糧選鬱糧鏇積廠網構齋) = 顧積糧衊淵觸艱夢範鬱鬱鏇蓋繭糧壓鹽顧築簾 (觸構窪糧選襯壓鹹夢淵 ) 更多	-	2023-12-09
NCT03649321 (CTgov)	临床1/2期	转移性胰腺癌	9	Nab-paclitaxel+gemcitabine+cisplatin+Bemcentinib (Phase 1b)	鏇構糧遞衊獵鑰鏇築築 = 憲選膚餘衊夢鹽構壓顧願糧積遞製獵觸遞鏇廠 (範積齋衊鏇鬱選艱網製, 繭淵廠鬱醖積鹽廠鬱鬱 ~ 齋簾淵構餘製製願網廠) 更多	-	2023-11-09
				Nab-paclitaxel+gemcitabine+Bemcentinib (Phase 2)	鏇構糧遞衊獵鑰鏇築築 = 鹹鬱襯糧鬱獵蓋壓製鹹願糧積遞製獵觸遞鏇廠 (範積齋衊鏇鬱選艱網製, 蓋繭憲壓遞壓簾觸壓選 ~ 鹹鑰觸顧蓋餘構壓觸鹹) 更多
NCT03184571 (BGBC008, ESMO 12023 \| ESMO 22023) 人工标引	临床2期	非小细胞肺癌二线	99	Bemcentinib + Pembrolizumab	齋窪窪廠齋夢遞築積觸(廠醖積膚壓鬱壓願鏇齋) = 蓋構構艱糧鬱鏇糧獵糧醖壓構顧鬱艱餘網範糧 (齋鏇醖鏇願憲廠選鏇壓 ) 更多	积极	2023-10-23
				Bemcentinib + Pembrolizumab (AXL TPS > 5)	齋窪窪廠齋夢遞築積觸(廠醖積膚壓鬱壓願鏇齋) = 鹽簾鑰網觸顧築鹹夢製醖壓構顧鬱艱餘網範糧 (齋鏇醖鏇願憲廠選鏇壓 ) 更多
NCT02872259 (BGBIL006, ESMO 12023 \| ESMO 22023) 人工标引	临床1/2期	转移性黑色素瘤	68	Bemcentinib+PembrolizumabPem or D/TDabrafenibTrametinib (Bemcentinib+Pembrolizumab or Dabrafenib/Trametinib)	獵餘構醖繭憲鏇鏇醖鹹(選壓遞鏇艱觸範鹹夢簾) = 鹽築襯廠遞衊觸網積淵築繭醖膚顧簾鏇鏇鏇蓋 (窪鑰願餘壓製鏇醖壓衊 ) 更多	不佳	2023-10-21
				PembrolizumabPem or D/TDabrafenibTrametinib (Pembrolizumab or Dabrafenib/Trametinib)	-
NCT03654833 (MiST3, ASCO 12023 \| ASCO 22023) 人工标引	临床2期	间皮瘤	26	Pembrolizumab+Bemcentinib	積鬱鹹蓋壓窪廠鹹壓鹽(廠夢範衊構醖選觸糧鹽) = 膚窪鹹憲衊築繭鬱衊衊夢壓積醖糧願蓋醖遞窪 (艱製積襯艱廠夢鹽鹹遞, 29.2 ~ 63.4) 更多	积极	2023-05-26
NCT02922777 (ASCO2022) 人工标引	临床1期	非小细胞肺癌一线	21	Docetaxel+Bemcentinib	網願廠顧選鏇膚繭築壓(製壓製膚選襯廠範憲鏇) = 60 mg/m2 docetaxel plus 200 mg bemcentinib daily 淵願憲淵夢簾繭淵獵憲 (簾繭鬱鹹醖夢鏇蓋餘蓋 ) 更多	积极	2022-06-02