更新于：2024-11-01

FN1

更新于：2024-11-01

基本信息

别名

Anastellin、CIG、Cold-insoluble globulin

+ [13]

简介

Fibronectins bind cell surfaces and various compounds including collagen, fibrin, heparin, DNA, and actin (PubMed:3024962, PubMed:3900070, PubMed:3593230, PubMed:7989369). Fibronectins are involved in cell adhesion, cell motility, opsonization, wound healing, and maintenance of cell shape (PubMed:3024962, PubMed:3900070, PubMed:3593230, PubMed:7989369). Involved in osteoblast compaction through the fibronectin fibrillogenesis cell-mediated matrix assembly process, essential for osteoblast mineralization (By similarity). Participates in the regulation of type I collagen deposition by osteoblasts (By similarity). Acts as a ligand for the LILRB4 receptor, inhibiting FCGR1A/CD64-mediated monocyte activation (PubMed:34089617). Binds fibronectin and induces fibril formation. This fibronectin polymer, named superfibronectin, exhibits enhanced adhesive properties. Both anastellin and superfibronectin inhibit tumor growth, angiogenesis and metastasis. Anastellin activates p38 MAPK and inhibits lysophospholipid signaling.

关联

项与 FN1 相关的药物

Ocriplasmin

奥克纤溶酶

靶点

Collagen x FN1 x laminin

作用机制

胶原蛋白抑制剂 [+2]

在研机构

原研机构

在研适应症

非在研适应症

最高研发阶段批准上市

首次获批国家/地区

美国

首次获批日期2012-10-17

Bifikafusp alfa

靶点

EDB-FN x IL-2R

作用机制

EDB-FN抑制剂 [+1]

在研机构

原研机构

在研适应症

非在研适应症

最高研发阶段临床3期

首次获批国家/地区-

首次获批日期1800-01-20

131 I-L19-small immunoprotein(Philogen SpA)

靶点

EDB-FN

作用机制

EDB-FN抑制剂 [+1]

在研机构

原研机构

在研适应症

非在研适应症

最高研发阶段临床2期

首次获批国家/地区-

首次获批日期1800-01-20

项与 FN1 相关的临床试验

NCT06640413 / Not yet recruiting临床1期

A Phase I Study to Evaluate the Safety and Preliminary Signs of Efficacy of [177Lu]Lu-OncoFAP-23 Alone or in Combination with L19-IL2 As a Treatment of Metastatic FAP-positive Solid Tumors

The aim of this study is to assess the safety of [177Lu]Lu-OncoFAP-23 alone or in combination with L19-IL2 for the treatment of advanced/metastatic Fibroblast Activation Protein (FAP)-positive solid tumors and to establish a Recommended Dose (RD).

开始日期2024-12-31

申办/合作机构

Philogen SpA

NCT06284590 / Recruiting临床2期

A Phase 2, Three-arm, Randomized Study of the Efficacy of Intratumorally Administered L19IL2 or L19TNF or L19IL2/L19TNF, All in Combination with Systemic Anti-PD1 Pembrolizumab, in Stage III and IV Unresectable Melanoma Patients with Resistance to or Progressing Upon Anti-PD1 Checkpoint Inhibitors and with Presence of Injectable Metastases

The trial aims to evaluate the efficacy of single agent L19IL2, single agent L19TNF, and combination L19IL2+L19TNF given concurrently with anti-PD1 therapy compared to historical control of anti-PD-1 re-challenge alone for anti-PD1 refractory unresectable stage III-IV melanoma.

开始日期2024-07-12

申办/合作机构

Philogen SpA

[+1]

100 项与 FN1 相关的临床结果

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100 项与 FN1 相关的转化医学

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0 项与 FN1 相关的专利（医药）

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41,469

项与 FN1 相关的文献（医药）

2025-12-01·Journal of Clinical Immunology

Granulomas in Common Variable Immunodeficiency Display Different Histopathological Features Compared to Other Granulomatous Diseases

Article

作者: Dik, Willem A ; van Stigt, Astrid C ; van Hagen, Martin ; von der Thüsen, Jan H ; Mustafa, Dana A M ; van den Bosch, Thierry P P ; Dalm, Virgil A S H ; Vadgama, Disha ; IJspeert, Hanna ; Lila, Karishma A

AbstractGranulomatous disease affects up to 20% of patients with Common Variable Immunodeficiency (CVID). Granulomas are comprised of highly activated immune cells, and emerge in response to antigenic triggers. In CVID granulomas however, the underlying pathophysiology is unclear and the specific trigger remains unknown. Granuloma formation in CVID is often compared to sarcoidosis, although clinical context and prognosis differ, suggesting a different pathogenesis. The aim of this study was to investigate if the cellular organization and proteomics of granulomas in CVID is different from other granulomatous diseases. Therefore, tissue slides from formaldehyde fixed paraffin embedded biopsies obtained from patients with CVID, sarcoidosis, tuberculosis and foreign-material induced pseudo-sarcoidosis were stained with hematoxylin and eosin and assessed for histopathological characteristics. Targeted spatial protein analysis was performed, and immune fluorescent multiplex assays were used to analyze the cellular organization. Histological analysis revealed that CVID granulomas were smaller, less circumscribed, with fewer multinucleated giant cells and minimal fibrosis compared to the other granulomatous diseases. Spatial protein analysis showed that granulomas in all diseases expressed CD68, CD11c, CD44, CD127, and PD-L1. However in CVID, reduced expression of the fibrosis-related protein fibronectin, but enrichment of CD163, CD3 and FAPα inside CVID granulomas was observed. Immunofluorescence analysis conformed a different cellular organization in CVID granulomas with increased influx of neutrophils, macrophages, T and B lymphocytes. In conclusion, granulomas in CVID display a different histological and cellular organization with increased influx of myeloid and lymphoid cells, compared to sarcoidosis, tuberculosis and pseudo-sarcoidosis, indicating a distinct pathogenesis underlying granuloma formation.

2025-01-01·Biofabrication

Vascular smooth muscle cells can be circumferentially aligned inside a channel using tunable gelatin microribbons

Article

作者: Sun, Michael ; Mathieu, Pattie ; Fan, Mingyue ; Morss-Clyne, Alisa ; Mastoor, Yusuf ; Han, Li-Hsin ; Karimi, Mahsa ; Ahadi, Fereshteh ; Han, Lin

AbstractThe gold standard to measure arterial health is vasodilation in response to nitric oxide. Vasodilation is generally measured via pressure myography of arteries isolated from animal models. However, animal arteries can be difficult to obtain and may have limited relevance to human physiology. It is, therefore, critical to engineer human cell-based arterial models capable of contraction. Vascular smooth muscle cells (SMCs) must be circumferentially aligned around the vessel lumen to contract the vessel, which is challenging to achieve in a soft blood vessel model. In this study, we used gelatin microribbons to circumferentially align SMCs inside a hydrogel channel. To accomplish this, we created tunable gelatin microribbons of varying stiffnesses and thicknesses and assessed how SMCs aligned along them. We then wrapped soft, thick microribbons around a needle and encapsulated them in a gelatin methacryloyl hydrogel, forming a microribbon-lined channel. Finally, we seeded SMCs inside the channel and showed that they adhered best to fibronectin and circumferentially aligned in response to the microribbons. Together, these data show that tunable gelatin microribbons can be used to circumferentially align SMCs inside a channel. This technique can be used to create a human artery-on-a-chip to assess vasodilation via pressure myography, as well as to align other cell types for 3D in vitro models.

2025-01-01·Experimental Neurology

DDAH1 deficiency exacerbates cerebral vascular endothelial dysfunction by aggravating BBB disruption and oxidative stress in thoracic blast-induced brain injury

Article

作者: Mao, Shun ; Tong, Changci ; Hou, Mingxiao ; Cong, Peifang ; Liu, Yunen ; Shi, Lin

As terrorist incidents and underground explosion events have become more frequent around the world, brain injury caused by thoracic blast exposure has been more highlighted due to its injured organ, subsequent social and economic burden. It has been reported dimethylarginine dimethylaminohydrolase 1 (DDAH1) plays important roles in regulating vascular endothelial injury repair and angiogenesis, but its role in thoracic blast-induced brain injury remains to be explained. This study seeks to investigate the mechanism of DDAH1 on thoracic blast-induced brain injury. 40 C57BL/6 wild type mice and 40 DDAH1 knockout mice were randomly and equally divided into control group and blast group, respectively. The integrity of blood-brain barrier (BBB) was detected by Evans blue test. The serum inflammatory factors, nitric oxide (NO) contents, and asymmetric dimethylarginine (ADMA) levels were determined through ELISA. HE staining and reactive oxygen species (ROS) detection were performed for histopathological changes. Western blot was used to detect the proteins related to oxidative stress, tight junction, focal adhesion, vascular endothelial injury, and the DDAH1/ADMA/eNOS signaling pathway. DDAH1 deficiency aggravated thoracic blast-induced BBB leakage, inflammatory response, and the increased levels of inflammatory-related factors. Additionally, DDAH1 deficiency also increased ROS generation, MDA and IRE-α expression. Regarding cerebral vascular endothelial dysfunction, DDAH1 deficiency increased the expression of MCAM, FN1, LIMK1, VEGF, MMP9, Vimentin and N-cadherin, while lowering the expression of FMR1, Occludin, claudin-3, claudin-5, Lyn, LIMA1, Glrb, Sez6, Dystrophin, and phosphorylation of VASP. Also, DDAH1 deficiency exacerbated explosion-induced increase of ADMA and decrease of eNOS activity and NO contents. Thus, we conclude that DDAH1 could prevent cerebral vascular endothelial dysfunction and related injury by inhibiting ADMA signaling and increasing eNOS activity in thoracic blast induced brain injury.

102

项与 FN1 相关的新闻（医药）

2024-10-29

·PRNewswire

Biond Biologics Announces Clinical Trial Collaboration and Supply Agreement with Merck KGaA, Darmstadt, Germany to Evaluate BND-35 in Combination with Cetuximab in a Phase 1 Clinical Study in Patients with Solid Tumors

MISGAV, Israel, Oct. 29, 2024 /PRNewswire/ -- Biond Biologics Ltd. ("Biond" or the "Company"), is a private clinical-stage biopharmaceutical company focusing on novel immunotherapies for cancer and innovative platforms for the intracellular delivery of biologics. Biond is pleased to announce a clinical trial collaboration and supply agreement with Merck KGaA, Darmstadt, Germany, to evaluate its immunotherapy agent BND-35 in combination with Merck KGaA, Darmstadt, Germany's anti-EGFR monoclonal antibody cetuximab (Erbitux®) in a Phase 1 clinical trial (BND-35-001, NCT06274437) for the treatment of patients with unresectable or metastatic solid tumors. Under the terms of this agreement, Merck KGaA, Darmstadt, Germany will supply Biond Biologics with cetuximab to support Biond's Phase 1 clinical trial, aimed at evaluating the safety and efficacy of BND-35 in combination with cetuximab. Enrollment to the BND-35 dose-escalation monotherapy arm has already begun and several patients have already been dosed. BND-35 is a novel anti-ILT3 (LILRB4) antibody that inhibits the interaction between ILT3 and various extracellular matrix ligands, including fibronectin, a major component of many tumor microenvironments (TME). ILT3 is expressed on myeloid suppressive cells and contributes to a pro-tumorigenic TME. Additionally, ILT3 reduces the effectiveness of targeted antibody therapies that leverage antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP), immunological mechanisms known to eliminate tumor cells. BND-35 reprograms the suppressive TME to a more pro-inflammatory one and reverses the inhibitory effects of ILT3 on ADCC and ADCP mechanisms. "We are thrilled to partner with Merck KGaA, Darmstadt, Germany to secure the supply of cetuximab for our clinical trial and thank Merck KGaA, Darmstadt, Germany for their interest in BND-35" said Tal Sines, VP of Business Development at Biond Biologics. "Our preclinical data show that BND-35 can synergize with therapies such as cetuximab, that promote ADCC and ADCP activities. It could provide a potential new treatment option for patients with solid tumors. About BND-35 BND-35, an innovative anti-ILT3/LILRB4 antibody designed to remodel the tumor microenvironment. BND-35 is currently under evaluation as a monotherapy in a Phase 1 clinical trial, which is exploring the safety, tolerability, and potential anti-tumor activity of BND-35 (NCT06274437). BND-35 is being assessed as monotherapy in the BND-35-001 trial, and in combination with established anti-EGFR (cetuximab) and PD-L1 therapies across various indications. About Biond Biologics Biond Biologics stands at the cutting edge of innovative therapies that target novel oncology pathways and enable the intracellular delivery of biologics. The company is dedicated to leverage advanced science and pioneering technologies into transformative drugs for diseases with significant unmet medical needs. Biond Biologics actively seeks synergistic collaborations with leading biopharmaceutical entities to bring novel medicines to patients worldwide. The company's robust pipeline also includes BND-22 (SAR444881), a groundbreaking first-in-class ILT2-blocking antibody in partnership with Sanofi, and BND-67, targeting CD28 shedding, a newly discovered immune evasion mechanism. Additionally, Biond is advancing INspire, a revolutionary platform for the intracellular delivery of protein therapeutics, including antibodies, proteins, or enzymes into cells. Media Contact: Tal Sines VP of Business Development Biond Biologics Ltd. +972-4 884 4337 [email protected] SOURCE Biond Biologics Ltd. WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

临床1期免疫疗法引进/卖出

2024-10-25

·精准药物

【Adv. Sci.】转移性黑色素瘤新的靶点和治疗策略

【导读】葡萄膜黑色素瘤（UM）是主要的眼部原发性恶性肿瘤，常进展为肝转移，且治疗手段有限。 10月18日，中山大学研究团队在期刊《Advanced Science》上发表了研究论文，题为“Neuropeptide Precursor VGF Promotes Liver Metastatic Colonization of Gαq Mutant Uveal Melanoma by Facilitating Tumor Microenvironment via Paracrine Loops”，本研究中，研究人员阐明了神经生长因子诱导基因（VGF），一种分泌型神经肽前体，在Gαq突变UM中的作用。研究人员采用多组学方法，包括转录组和分泌组分析，揭示了VGF在UM进展中的复杂作用。VGF在Gαq突变型UM细胞中表达上调，且与UM患者不良预后相关。靶向VGF可显著抑制UM在体内外的生长。进一步的证据表明，Gαq通过MAPK/CREB通路调控VGF。联合抑制Gαq和MEK可显著降低UM移植瘤的肿瘤负荷。值得注意的是，VGF通过自分泌和旁分泌环路触发UM的肝脏转移定植，并激活肝星状细胞（HSCs）的纤维化，创造有利的微环境。此外，VGF直接结合TGFBR2，调控TGF-β-SMAD信号通路，从而调控内皮-间充质转化（EMT）相关基因，促进肿瘤转移。综上所述，这些发现证实了VGF是Gαq突变UM进展和转移的关键驱动因素，并为UM患者提供了一个有前景的治疗靶点和策略。 https://onlinelibrary-wiley-com.libproxy1.nus.edu.sg/doi/10.1002/advs.202407967 背景信息 01 葡萄膜黑色素瘤（UM）是成人最常见的原发性眼内恶性肿瘤，主要发生于脉络膜（90%）、睫状体（6%）和虹膜（4%）。UM患者起病隐匿，早期症状易被忽视，确诊时多已处于晚期。不仅如此，近50%的UM患者会发展为转移性疾病，通常在1年内死亡。肝脏是最常见的转移部位，肝转移患者的1年和2年总生存率分别为13%和8%。虽然对原发肿瘤的治疗有效，但UM转移瘤对化疗和靶向治疗的应答较差，通常对免疫检查点抑制剂无应答。目前，还没有有效的治疗方法来预防肿瘤的转移。因此，迫切需要探索潜在的机制，并开发新的有效的治疗方法，以预防和治疗致死性UM转移。超过85%的UM由GNAQ或α 11 （GNA11）突变引起，其中95%为Q209P/L单位点突变，是UM发病和进展的关键致癌因素。突变型Gαq蛋白有望成为发现抗UM新型化合物的治疗靶点。遗憾的是，直接抑制Gαq的药物，如YM-254890和FR900359，无法区分野生型和突变型Gαq，且难以从天然来源分离和合成，使其具有毒性，不适合临床应用。此外，目前G蛋白通路下游效应分子的抑制剂（如MEK和PKC）在UM治疗中显示出有限的临床获益。因此，迫切需要探索驱动Gαq突变UM进展和转移的新靶点和机制，以改进UM治疗。 VGF触发肝星状细胞纤维化和活化促进UM肝转移 02 多项研究表明，HSC是肝纤维化中重要的纤维化细胞类型之一，并可能通过重塑肝转移前微环境促进肝转移。鉴于之前的研究发现VGF调节TGF-β信号通路，而TGF-β信号通路与纤维化密切相关，研究人员下一步研究VGF是否通过活化HSC促进UM细胞在肝脏的定植。 qRT-PCR和免疫印迹分析显示，从Gαq突变的UM细胞（MP41和92.1）获得的CM（同样富含vgf）比从MUM2B细胞获得的CM显著增加LX-2细胞的纤维化相关标志物α-平滑肌作用（α-SMA）和FN的表达。研究人员观察到LX-2细胞被MP41细胞和过表达vgf的MUM2B细胞获得的CM刺激激活。此外，过表达VGF或rVGF处理LX-2细胞后，α-SMA和FN的蛋白水平也增加。α-SMA免疫荧光染色进一步证实了在富含VGF的CM或rVGF处理下LX-2细胞的活化。提示VGF可激活HSC，为UM肝转移提供有利的微环境。图1：VGF触发肝星状细胞纤维化和活化，促进葡萄膜黑色素瘤肝转移 LX-2细胞全细胞裂解物的免疫印迹分析显示，过表达VGF或rVGF处理也轻微增加了TGFBR2的表达和SMAD3的磷酸化。考虑到VGF是一种分泌蛋白，可以刺激hsc的活化，研究人员想知道UM细胞分泌的VGF是否与HSC中的TGFBR2结合。进一步，研究人员在LX-2细胞中强制表达TGFBR2，然后将LX-2细胞（OE-HA-TGFBR2）暴露于过表达Flag-VGF的MUM2B细胞制备的CM。免疫荧光染色显示UM细胞分泌的VGF也与LX-2细胞表达的TGFBR2相互作用，提示VGF也可能通过旁分泌环通过TGF-β-SMAD信号通路激活HSC。既往研究发现癌细胞诱导HSC活化，活化的HSC在肿瘤转移过程中进一步反馈促进肿瘤生长和转移。然后，研究人员探索活化的HSC是否会触发UM细胞的生长。在迁移共培养体系中，将UM细胞暴露于LX-2细胞（失活的命名为qLX-2或活化的命名为αLX-2，经TGF-β预处理24 h）的培养环境中，如图1H所示。MP41、92.1细胞与qLX-2、αLX-2细胞共培养后侵袭能力增强，与αLX-2细胞共培养后侵袭能力更强。相比之下，这种治疗对MUM2B没有诱导这样的促进作用。综上所述，本研究结果表明，VGF可能通过TGF-β-SMAD信号通路，通过自分泌和旁分泌环路触发HSC的活化，活化的HSC进一步反馈增强Gαq突变型UM细胞的侵袭能力，从而促进UM的肝转移定植。本研究加深了我们对UM复杂转移过程的理解，并可能为转移性UM提供新的靶点和治疗策略。【参考资料】 https://onlinelibrary-wiley-com.libproxy1.nus.edu.sg/doi/10.1002/advs.202407967 声明：发表/转载本文仅仅是出于传播信息的需要，并不意味着代表本公众号观点或证实其内容的真实性。据此内容作出的任何判断，后果自负。若有侵权，告知必删！长按关注本公众号粉丝群/投稿/授权/广告等请联系公众号助手觉得本文好看，请点这里↓

抗体药物偶联物

2024-10-11

·药精通Bio

双杀IBD和HIV，通吃自免+感染！

OTC2024类器官前沿应用与3D细胞培养论坛圆满落幕，点击图片可查看会后报告，咨询OTC2025类器官论坛请联系：王晨 180 1628 8769 引言：要说起这几年来自免领域，什么适应症的交易最火，那非IBD（炎症性肠病）莫属！针对IBD，我们之前的文章中写过TNF-α、JAK、TL1A等靶点（感兴趣的朋友可点相关蓝字观看）！今天这篇我们要写一个自免领域一个非常牛掰的靶点：α4β7！它的牛掰之处在于，横跨自免和抗感染两大领域！绝对有爆款潜质！针对此靶点开发的维多珠单抗已经成为IBD领域的一颗明珠，同时近几年也有公司另辟蹊径，针对此靶点开发了治疗HIV的产品，且已进入临床二期，不过最重要的事情先说在前面：这个靶点目前还不卷！图注：现有自免靶点、靶向药物和作用机制(MOA)。 01 α4β7 靶点介绍整合素α4β7是一种异二聚体的I型跨膜糖蛋白，由α4和β7亚基组成，也是由这两个亚基而得名。 α4β7作为在淋巴细胞表面表达的归巢受体，在T细胞、B细胞、NK细胞及其他免疫细胞上表达。通过与粘膜地址蛋白细胞粘附分子-1（MAdCAM-1）的相互作用，介导淋巴细胞运输到肠道相关淋巴组织（GALT）。 MAdCAM-1作为α4β7的主要天然配体，表达在肠粘膜高内皮小静脉（HEV）的管腔表面。除MAdCAM-1外，动物细胞中大多数细胞外基质蛋白（包括胶原蛋白、纤连蛋白和层粘连蛋白）的主要受体也是整合素。整合素以较低的亲和力和他们结合，除发挥粘附作用外，也具有将细胞外信号向细胞内传递的作用。 02 α4β7在IBD和HIV发病中的病理作用淋巴细胞归巢是指在正常生理条件下，淋巴细胞选择性地迁移到某些淋巴器官。这种迁移由粘附分子（包括整合素α4β7、整合素LFA-1和L-选择素）之间的级联相互作用介导。在病理条件下，淋巴细胞不受控地迁移到炎症部位，产生自身免疫疾病等病症。在这种情况下，淋巴细胞首先附着在内皮细胞上，然后沿着内皮细胞滚动。最终，粘附稳定下来，并实现向HEV的迁移。这种病理过程主要由整合素α4β7和MAdCAM-1的相互作用介导。 2.1 IBD 慢性炎症性肠病（IBD），包括克罗恩病和溃疡性结肠炎，是由自身免疫反应引起的肠道疾病。克罗恩病主要累及回肠和结肠, 且整个小肠和大肠的任意位置都有可能发生病变，患者的典型症状是肛周病变、瘘管和组织学肉芽肿。溃疡性结肠炎则主要累及直肠和部分结肠。此外, 溃疡性结肠炎患者的典型特征为血性腹泻, 并伴随着腹痛、体重减轻、呕吐等症状。 IBD的免疫学病理特征是肠系膜血管中淋巴细胞粘附和迁移受阻，导致淋巴细胞不受控制地聚集在肠道。如上文所述，α4β7与高内皮小静脉（HEV）的AdCAM-1间的相互作用在此过程中起着关键作用。因此，靶向α4β7和MAdCAM-1成为了开发IBD药物的策略之一。 2.2 HIV 肠道相关淋巴组织(GALT)是HIV-1复制的主要部位。在感染的急性期，GALT 中的CD4+ T细胞是HIV-1的主要靶标。高表达α4β7的CD4+ T细胞更容易受到HIV-1的生产性感染。HIV-1包膜蛋白gp120可与α4β7结合，导致CD4+T细胞LFA-1快速激活，从而促进HIV-1的高效细胞间传播。艾伯维开发的ABBV-382可以通过干扰α4β7与其配体MAdCAM-1和gp120之间的相互作用来阻断CD4+ T细胞刺激和HIV-1感染。另外，ABBV-382还可以与HIV-1 形成免疫复合物，增强抗原的免疫原性，从而潜在地诱导HIV-1特异性免疫反应。目前，ABBV-382与抗PD-1单抗Budigalimab联合使用，正在进行一项二期研究（NCT06032546）。 03 已上市的大单品——维多珠单抗维多珠单抗是武田开发的，靶向α4β7的，异二聚体单抗药物。2014年5月20日被FDA批准上市，随后在全球不同领域获得批准，获批的适应症为中度至重度活动性溃疡性结肠炎和活动性克罗恩病。作为肠道选择性的α4β7整合素拮抗剂，维多珠单抗通过选择性阻断α4β7整合素与其天然配体 MAdCAM-1间的相互作用，抑制T淋巴细胞进入肠道固有层和肠道相关淋巴组织（GALT），减轻肠道炎症，而不损害全身免疫反应。维多珠单抗是武田的主要资产之一，为公司的整体收入带来了巨大的利润。2022年，Entyvio（商品名）的总销售额为$5364M，2018年-2022年的五年销售情况见下图。 04 有哪些玩家？因为这个靶点的“通吃”特点，其前景那是非常无法估量的，虽然目前只有一个药物获批，但胖猫认为，将来这个靶点肯定能在药物江湖中掀起“腥风血雨”！除武田外，其实布局该靶点的管线并不多。这样一个已经被验证有效性且横跨两个大的治疗领域的靶点，为啥就没有人卷呢？值得立项的团队深思！目前处于后期的管线如下表所示：除此外，我们还人肉整理了自免适应症领域的上市药物，请大家自行参考。其中，标黄的一栏为维多珠单抗。 END 免责声明：本文仅作知识交流与分享及科普目的，不涉及商业宣传，不作为相关医疗指导或用药建议。文章如有侵权请联系删除。 OTC2024类器官前沿应用与3D细胞培养论坛圆满落幕，点击图片可查看会后报告，咨询OTC2025类器官论坛请联系：王晨 180 1628 8769

临床结果临床2期临床1期临床终止引进/卖出