更新于：2024-05-01

VCP

VCP蛋白

更新于：2024-05-01

基本信息

别名

15S Mg(2+)-ATPase p97 subunit、CDC48、IBMPFD

+ [7]

简介

Necessary for the fragmentation of Golgi stacks during mitosis and for their reassembly after mitosis. Involved in the formation of the transitional endoplasmic reticulum (tER). The transfer of membranes from the endoplasmic reticulum to the Golgi apparatus occurs via 50-70 nm transition vesicles which derive from part-rough, part-smooth transitional elements of the endoplasmic reticulum (tER). Vesicle budding from the tER is an ATP-dependent process. The ternary complex containing UFD1, VCP and NPLOC4 binds ubiquitinated proteins and is necessary for the export of misfolded proteins from the ER to the cytoplasm, where they are degraded by the proteasome. The NPLOC4-UFD1-VCP complex regulates spindle disassembly at the end of mitosis and is necessary for the formation of a closed nuclear envelope. Regulates E3 ubiquitin-protein ligase activity of RNF19A. Component of the VCP/p97-AMFR/gp78 complex that participates in the final step of the sterol-mediated ubiquitination and endoplasmic reticulum-associated degradation (ERAD) of HMGCR. Involved in endoplasmic reticulum stress-induced pre-emptive quality control, a mechanism that selectively attenuates the translocation of newly synthesized proteins into the endoplasmic reticulum and reroutes them to the cytosol for proteasomal degradation (PubMed:26565908). Plays a role in the regulation of stress granules (SGs) clearance process upon arsenite-induced response (PubMed:29804830). Also involved in DNA damage response: recruited to double-strand breaks (DSBs) sites in a RNF8- and RNF168-dependent manner and promotes the recruitment of TP53BP1 at DNA damage sites (PubMed:22020440, PubMed:22120668). Recruited to stalled replication forks by SPRTN: may act by mediating extraction of DNA polymerase eta (POLH) to prevent excessive translesion DNA synthesis and limit the incidence of mutations induced by DNA damage (PubMed:23042607, PubMed:23042605). Together with SPRTN metalloprotease, involved in the repair of covalent DNA-protein cross-links (DPCs) during DNA synthesis (PubMed:32152270). Involved in interstrand cross-link repair in response to replication stress by mediating unloading of the ubiquitinated CMG helicase complex (By similarity). Mediates extraction of PARP1 trapped to chromatin: recognizes and binds ubiquitinated PARP1 and promotes its removal (PubMed:35013556). Required for cytoplasmic retrotranslocation of stressed/damaged mitochondrial outer-membrane proteins and their subsequent proteasomal degradation (PubMed:16186510, PubMed:21118995). Essential for the maturation of ubiquitin-containing autophagosomes and the clearance of ubiquitinated protein by autophagy (PubMed:20104022, PubMed:27753622). Acts as a negative regulator of type I interferon production by interacting with RIGI: interaction takes place when RIGI is ubiquitinated via 'Lys-63'-linked ubiquitin on its CARD domains, leading to recruit RNF125 and promote ubiquitination and degradation of RIGI (PubMed:26471729). May play a role in the ubiquitin-dependent sorting of membrane proteins to lysosomes where they undergo degradation (PubMed:21822278). May more particularly play a role in caveolins sorting in cells (PubMed:21822278, PubMed:23335559). By controlling the steady-state expression of the IGF1R receptor, indirectly regulates the insulin-like growth factor receptor signaling pathway (PubMed:26692333).

关联

项与 VCP 相关的药物

KUS-121

靶点

VCP

作用机制

VCP抑制剂

在研机构

Kyoto Drug Discovery & Development Co., Ltd.初创企业 [+1]

原研机构

Kyoto University

在研适应症

视网膜动脉闭塞 [+1]

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

CB-5339

靶点

VCP

作用机制

VCP抑制剂

在研机构

凯信远达医药（中国）有限公司 [+1]

原研机构

Cleave Therapeutics, Inc.

在研适应症

多发性骨髓瘤 [+4]

非在研适应症-

最高研发阶段临床1/2期

首次获批国家/地区-

首次获批日期1800-01-20

UPCDC-30766

靶点

VCP

作用机制

VCP抑制剂

在研机构

Leidos Biomedical Research, Inc.

原研机构

Leidos Biomedical Research, Inc.

在研适应症

肿瘤

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

项与 VCP 相关的临床试验

NCT06178055 / Recruiting临床2期

A Phase 2, Double-masked, Randomized, Sham-controlled, Multiple-dose Study of the Efficacy and Safety of Intravitreal KUS121 in the Treatment of Non-Arteritic Central Retinal Artery Occlusion (CRAO)

Central retinal artery occlusion (CRAO) is an ophthalmologic emergency which leads to severe and permanent vision loss. There is no evidence-based therapy for CRAO. The objective of this GION study is to evaluate the efficacy and safety of KUS121 intravitreal (IVT) injection in participants with acute non-arteritic CRAO.

开始日期2024-04-16

申办/合作机构

Kyoto Drug Discovery & Development Co., Ltd.初创企业

NCT04372641 / Withdrawn临床1期IIT

A Phase I Trial of the P97 Inhibitor CB-5339 in Patients With Advanced Solid Tumors and Lymphomas

This phase I trial studies the side effects and best dose of CB-5339 in treating patients with solid tumors that has spread to other places in the body (advanced) or lymphomas. CB-5339 may stop the growth of cancer cells by blocking some of the enzymes needed for cell growth.

开始日期2020-06-18

申办/合作机构

National Cancer Institute

NCT04402541 / Completed临床1期

A Phase 1 Study to Evaluate the Safety and Pharmacokinetic Profiles of CB-5339 in Participants With Relapsed/Refractory Acute Myeloid Leukemia or Relapsed/Refractory Intermediate or High Risk Myelodysplastic Syndrome

This is a multicenter, open-label Phase 1 study of orally administered CB-5339 in participants with R/R AML or participants with R/R intermediate- to high-risk MDS.

开始日期2020-06-08

申办/合作机构

Cleave Therapeutics, Inc.

100 项与 VCP 相关的临床结果

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100 项与 VCP 相关的转化医学

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0 项与 VCP 相关的专利（医药）

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1,827

项与 VCP 相关的文献（医药）

2024-02-22·Molecular cell

Bidirectional substrate shuttling between the 26S proteasome and the Cdc48 ATPase promotes protein degradation.

Article

作者: Hao Li ; Zhejian Ji ; Joao A Paulo ; Steven P Gygi ; Tom A Rapoport

Most eukaryotic proteins are degraded by the 26S proteasome after modification with a polyubiquitin chain. Substrates lacking unstructured segments cannot be degraded directly and require prior unfolding by the Cdc48 ATPase (p97 or VCP in mammals) in complex with its ubiquitin-binding partner Ufd1-Npl4 (UN). Here, we use purified yeast components to reconstitute Cdc48-dependent degradation of well-folded model substrates by the proteasome. We show that a minimal system consists of the 26S proteasome, the Cdc48-UN ATPase complex, the proteasome cofactor Rad23, and the Cdc48 cofactors Ubx5 and Shp1. Rad23 and Ubx5 stimulate polyubiquitin binding to the 26S proteasome and the Cdc48-UN complex, respectively, allowing these machines to compete for substrates before and after their unfolding. Shp1 stimulates protein unfolding by the Cdc48-UN complex rather than substrate recruitment. Experiments in yeast cells confirm that many proteins undergo bidirectional substrate shuttling between the 26S proteasome and Cdc48 ATPase before being degraded.

2024-02-21·Human molecular genetics

Vcp overexpression and leucine supplementation extend lifespan and ameliorate neuromuscular junction phenotypes of a SOD1G93A-ALS mouse model.

Article

作者: Tzyy-Nan Huang ; Yu-Tzu Shih ; Tzu-Li Yen ; Yi-Ping Hsueh

Many genes with distinct molecular functions have been linked to genetically heterogeneous amyotrophic lateral sclerosis (ALS), including SuperOxide Dismutase 1 (SOD1) and Valosin-Containing Protein (VCP). SOD1 converts superoxide to oxygen and hydrogen peroxide. VCP acts as a chaperon to regulate protein degradation and synthesis and various other cellular responses. Although the functions of these two genes differ, in the current report we show that overexpression of wild-type VCP in mice enhances lifespan and maintains the size of neuromuscular junctions (NMJs) of both male and female SOD1G93A mice, a well-known ALS mouse model. Although VCP exerts multiple functions, its regulation of ER formation and consequent protein synthesis has been shown to play the most important role in controlling dendritic spine formation and social and memory behaviors. Given that SOD1 mutation results in protein accumulation and aggregation, it may direct VCP to the protein degradation pathway, thereby impairing protein synthesis. Since we previously showed that the protein synthesis defects caused by Vcp deficiency can be improved by leucine supplementation, to confirm the role of the VCP-protein synthesis pathway in SOD1-linked ALS, we applied leucine supplementation to SOD1G93A mice and, similar to Vcp overexpression, we found that it extends SOD1G93A mouse lifespan. In addition, the phenotypes of reduced muscle strength and fewer NMJs of SOD1G93A mice are also improved by leucine supplementation. These results support the existence of crosstalk between SOD1 and VCP and suggest a critical role for protein synthesis in ASL. Our study also implies a potential therapeutic treatment for ALS.

2024-02-13·Comparative biochemistry and physiology. Part B, Biochemistry & molecular biology

Dramatic genome-wide reprogramming of mRNA in hypometabolic muscle.

Article

作者: Nicholas J Hudson ; Rebecca L Cramp ; Craig E Franklin

In response to seasonal droughts, the green striped burrowing frog Cyclorana alboguttata enters a reversible hypometabolic state called aestivation where heart rate and oxygen consumption can be reduced despite warm (>25C°) ambient temperatures. With a view to understanding molecular mechanisms we profiled aestivating versus control gastrocnemius muscle using mRNA sequencing. This indicated an extensive metabolic reprogramming, with nearly a quarter of the entire transcriptome (3996 of 16,960 mRNA) exhibiting a nominal >2-fold change. Consistent with a physiological adaptation to spare carbohydrate reserves, carbohydrate catabolism was systemically downregulated. A 630-fold downregulation of ENO3 encoding the enolase enzyme was most striking. The 590 frog orthologs of mRNA encoding the mitoproteome were, viewed as a population, significantly downregulated during aestivation, although not to the same extent as mRNA encoding carbohydrate catabolism. Prominent examples include members of the TCA cycle (IDH2), electron transport chain (NDUFA6), the ATP synthase complex (ATP5F1B) and ADP/ATP intracellular transport (SLC25A4). Moreover, mRNA derived from the mt genome itself (e.g. mt-ND1) were also downregulated. Most prominent among the upregulated mRNA are those encoding aspects of regulated proteolysis including the proteosome (e.g. PSME4L), peptidases (USP25), atrogins (FBXO32) and ubiquitination (VCP). Finally, we note the ∼5-fold upregulation of the mRNA EIFG3 that encodes part of the EIF4F complex. This possesses global control of protein synthesis. Given protein synthesis is repressed in aestivating frogs this indicates the skeletal musculature is poised for accelerated translation of mRNA upon emergence, supporting a strategy to rapidly restore function when the summer rains come.

项与 VCP 相关的新闻（医药）

2024-01-13

·Science Daily

A novel pathway regulating lipid biosynthesis by fatty acids

Sterol regulatory element-binding proteins (SREBPs) play a crucial role in lipid biosynthesis. In a recent study, researchers identified a novel cleavage enzyme of SREBP-1c, a key player in fatty acid biosynthesis. Moreover, the team unveiled, for the first time, that the biosynthesis process of fatty acid in the liver is activated by saturated fatty acids and inhibited by polyunsaturated fatty acids, providing new insights into the intricate workings of this cleavage system. Researchers have been studying the transcription factor SREBP, a critical regulator of lipid biosynthesis. Precursor SREBP proteins, located in the endoplasmic reticulum (ER) of the cell, are transported through the golgi apparatus to the nucleus. Here, they promote the transcription of genes associated with lipid biosynthesis, playing a pivotal role in regulating cholesterol. SREBP-1c, a specific member of the SREBP family, is known to activate fatty acid synthesis. Interestingly, this process is inhibited by polyunsaturated fatty acids. The exact mechanism behind this regulation, however, remains to be elucidated. The research team elucidated a novel cleavage mechanism of SREBP-1c, a protein involved in fatty acid synthesis, and confirmed its regulation by fatty acids. The cleavage of SREBP-1c occurs in the endoplasmic reticulum, with the rhomboid protease RHBDL4, located in the ER membrane, identified as a new cleavage enzyme for SREBP-1c. This cleavage process is activated by saturated fatty acids and deactivated by polyunsaturated fatty acids, suggesting that RHBDL4's activity is modulated by the type of fatty acid. Additionally, the team discovered a unique mechanism where the VCP complex extracts the cleaved SREBP-1c protein from the endoplasmic reticulum. In the livers of mice deficient in the RHBDL4 gene and fed a high-fat and high-cholesterol diet, the activation of SREBP-1c cleavage was suppressed. This inhibited the expression of a group of target genes involved in fatty acid synthesis, polyunsaturated fatty acid synthesis and uptake, and lipoprotein secretion, which improved fatty liver pathophysiology, as observed in wild-type mice. The RHBDL4-SREBP-1c pathway, uncovered in this study, represents a lipid homeostasis mechanism regulated by fatty acids. This groundbreaking discovery is anticipated to pave the way for developing new therapeutic strategies for metabolic disorders and lifestyle-related diseases stemming from abnormal lipid metabolism. This work was supported by Grants-in-Aid for Scientific Research on Innovative Areas program (Inflammation Cellular Sociology) JP17H06395 (to H.S.), Scientific Research (A) 15H02541 and 18H04051 (to H.S.), and Scientific Research (C) 16K01811 and 19K11737 (to S.-I.H.) from the Ministry of Science, Education, Culture, and Technology of Japan; AMED-CREST Grant Number 16gm0910003h0002 (to H.S.) from the Japan Agency for Medical Research and Development, AMED; and Ono Medical Research Foundation (to S.-I.H.).

2023-12-27

·生物谷

Molecular Cell | 蒋辉实验室揭示线粒体自噬的感知和抑制因子PPTC7及其对线粒体数量的调控作用

线粒体自噬(mitophagy)是重要的线粒体质量及数量调控机制, 与发育、癌症、衰老和神经退行性病变等生理病理状况高度相关。现已知两类哺乳动物mitophagy通路：由PINK1-Parkin介导的泛素依赖途径，以及由BNIP3, NIX和FUNDC1等介导的受体依赖途径。然而，人们对mitophagy调控机制及其生理病理意义仍有待探索。突出的表现是，缺失已知mitophagy通路的小鼠(如Pink1-/-、Parkin-/-、Bnip3-/-等)表型微弱，与普遍认知的mitophagy重要性有明显差距。2023年12月26日，北京生命科学研究所/清华大学生物医学交叉研究院蒋辉实验室在Molecular Cell在线发表了题为"A mitophagy sensor PPTC7 controls BNIP3 and NIX degradation to regulate mitochondrial mass"的论文。该论文发现了一个感知并抑制mitophagy的因子PPTC7，阐明了PPTC7调控mitophagy的分子机制并揭示其对线粒体数量和代谢稳态的调控作用。作为监控mitophagy水平的关键因子，PPTC7感知mitophagy受体BNIP3和NIX的蛋白水平，进而起始BNIP3/NIX-PPTC7-SCFFBXL4完整复合物的组装，促进SCFFBXL4泛素化和降解BNIP3和NIX，从而抑制mitophagy。该通路对维持细胞线粒体数量、代谢平衡、和个体存活至关重要。01FBXL4介导的mitophagy调控与退行性疾病MTDPS13蒋辉实验室长期从事线粒体蛋白稳态调控机制研究，之前报道了一个线粒体外膜复合物UBXD8-VCP介导BNIP3降解，从而抑制mitophagy(链接：EMBO Reports | 蒋辉实验室揭示UBXD8调控凋亡和线粒体自噬的分子机制)。为进一步发掘mitophagy调控机制，研究生曹钰通过靶向线粒体的遗传筛选发现多个mitophagy抑制因子，其中包括FBXL4和PPTC7(链接：EMBO Journal | 蒋辉实验室揭示线粒体自噬调控及线粒体疾病新机制)。已知FBXL4突变导致致死性退行性疾病线粒体DNA耗竭综合征13(MTDPS13)1,2，但其机理未明。作者发现FBXL4定位于线粒体外膜，与Skp1和Cullin1组成SCFFBXL4 E3泛素连接酶。SCFFBXL4通过泛素化降解BNIP3和NIX来抑制mitophagy。而病人来源的FBXL4突变抑制SCFFBXL4组装，导致BNIP3和NIX蛋白积累和mitophagy过度激活。FBXL4突变患者表现出mtDNA耗竭、线粒体数量减少、酸中毒、神经和肌肉退行性病变等严重症状。与FBXL4突变病人类似，Fbxl4-/-小鼠表现出BNIP3和NIX蛋白积累、mitophagy失控、线粒体数量减少、代谢紊乱和围产期死亡等严重表型。更重要的是，在Fbxl4-/-小鼠中敲除Bnip3或Nix可以挽救线粒体数量、恢复代谢平衡并挽救小鼠寿命。这些结果表明过度mitophagy导致的线粒体数量减少是MTDPS13的致病原因并为治疗提供了思路。02PPTC7调控FBXL4介导的BNIP3和NIX降解鉴于BNIP3和NIX强大且危险的线粒体清除能力，细胞必须牢牢控制其水平，但细胞监控并调节BNIP3和NIX降解的分子机制仍不清楚。研究生孙雨秋研究另一个筛选发现的mitophagy抑制因子PPTC7。前人研究表明PPTC7是定位于线粒体基质的磷酸酶。但令人诧异的是，与敲除FBXL4类似，敲除PPTC7同样导致BNIP3和NIX的积累和过度mitophagy；Pptc7-/-小鼠表现出mitophagy失控、线粒体数量减少和围产期死亡的表型，且该表型可以被Nix敲除所挽救(图1)。此外，PPTC7过表达可促进内源BNIP3和NIX被FBXL4降解，而FBXL4过表达则没有效果，提示PPTC7作为上游限速因子调控FBXL4介导的BNIP3和NIX降解。但是，线粒体基质蛋白PPTC7如何调控线粒体外膜上的蛋白降解？图1PPTC7缺失过度激活BNIP3和NIX依赖的mitophagy，造成线粒体数量减少和小鼠死亡。A,Pptc7 -KO升高小鼠肝脏中mitophagy受体BNIP3和NIX的蛋白水平(红框)并导致其他线粒体蛋白减少(蓝框)。B,小鼠生存曲线。03PPTC7前体通过与BNIP3/NIX直接互作，滞留在线粒体外膜通常情况下，线粒体基质蛋白的前体形式(precursor)在N端定位序列(targeting sequence)的引导下进入线粒体，并在线粒体基质切除定位序列，完成成熟过程。作者发现在野生型细胞里，PPTC7以成熟形式(mature form,切除了定位序列)存在于线粒体基质，而在FBXL4-KO细胞里，PPTC7同时具有定位于线粒体基质的成熟形式和定位于线粒体外膜的前体形式。进一步分析表明，FBXL4-KO细胞中积累的BNIP3和NIX导致PPTC7前体出现在线粒体外膜;在野生型细胞中直接过表达BNIP3或NIX也可诱导PPTC7前体出现在线粒体外膜定位。通过体外重组蛋白实验，作者发现BNIP3和NIX与PPTC7直接互作，并使用交联质谱分析了NIX-PPTC7的互作区域。在截去NIX与PPTC7的直接互作区域后，NIX无法诱导PPTC7前体的外膜定位，表明BNIP3和NIX通过与PPTC7的直接互作，将PPTC7前体定位于线粒体外膜。04弱化的PPTC7定位序列帮助PPTC7在线粒体外膜滞留有意思的是，作者发现与经典线粒体基质定位序列相比，PPTC7的定位序列长度短且引导能力差，推测该特征削弱了PPTC7前体进入线粒体基质的能力，有利于PPTC7前体被外膜BNIP3/NIX滞留。因此，研究者将PPTC7的定位序列替换成经典序列，发现它使PPTC7全部进入线粒体基质，无法被滞留在外膜，失去调节BNIP3和NIX降解的能力。05外膜PPTC7起始组装BNIP3/NIX-PPTC7-SCFFBXL4复合物那么外膜PPTC7如何促进SCFFBXL4介导的BNIP3和NIX降解呢？作者发现除与BNIP3/NIX直接互作之外，PPTC7还与SCFFBXL4复合物中的Cullin1直接互作。作者表达纯化了NIX，PPTC7，FBXL4,Cullin1-Rbx1和Skp1的重组蛋白，发现只有在所有蛋白都存在的情况下，这些蛋白才能组装成完整的NIX-PPTC7-SCFFBXL4复合物，缺少NIX，PPTC7，FBXL4任何一个组分都导致复合物散架。以上结果提供了一个mitophagy的负反馈调控模型:积累在线粒体外膜的mitophagy受体BNIP3和NIX与PPTC7前体直接互作，将其滞留在外膜，起始BNIP3/NIX-PPTC7-SCFFBXL4复合物的组装，从而泛素化和降解BNIP3和NIX，防止mitophagy过度激活(图2)。06禁食情况下，肝脏诱导PPTC7来抑制mitophagy和维持代谢稳态一个重要的问题是在负反馈调控mitophagy之外，PPTC7是否还会响应生理信号？鉴于PPTC7过表达能促进BNIP3和NIX降解，作者重点研究了生理信号对PPTC7表达的调节，发现禁食不改变骨骼肌PPTC7的表达，但在肝脏强烈诱导PPTC7。与之相对应，禁食强烈诱导骨骼肌mitophagy，但不改变肝脏mitophagy水平，作者推测肝脏mitophagy受到PPTC7上调的压制。因此，作者在小鼠肝脏敲除PPTC7，发现禁食导致缺失PPTC7的肝脏丢失大量线粒体。禁食情况下，肝脏负有重要使命-通过糖异生(gluconeogenesis)维持血糖水平。而糖异生需要线粒体提供两个重要支持：ATP和丙酮酸羧化酶(pyruvate carboxylase)。作者发现，敲除肝脏PPTC7导致禁食状态下肝脏ATP缺乏，糖异生受阻，造成严重的低血糖。因此，禁食情况下，肝脏特异上调PPTC7以压制mitophagy，从而维持线粒体数量和代谢稳态(图2)。图2 PPTC7调控mitophagy的工作模型。1. mitophagy的负反馈稳态调控。正常情况下，PPTC7表达后进入线粒体基质行使正常功能。当mitophagy受体BNIP3和NIX积累时，BNIP3/NIX将PPTC7前体滞留于外膜，起始BNIP3/NIX-PPTC7-SCFFBXL4复合物组装，从而降解BNIP3和NIX，防止mitophagy过度激活和线粒体丢失。2. 在禁食情况下，肝脏上调PPTC7以压制mitophagy，从而维持肝脏能量供应和糖异生通路活力，维持血糖水平。综上，该工作报道了一个感知和抑制mitophagy的PPTC7-SCFFBXL4通路。PPTC7作为关键调控因子，能够整合稳态维持和生理信号来调控mitophagy水平，以此维持线粒体数量和细胞代谢稳态。该通路的发现显著增进了我们对mitophagy与线粒体数量控制(mitochondrial mass control)的理解。禁食情况下，肝脏和骨骼肌对mitophagy的差异化调节及其功能研究也丰富了我们对生理情况下组织特异性mitophagy调控的认知。清华大学生物医学交叉研究院博士生孙雨秋为论文第一作者，蒋辉博士为通讯作者。该论文其他作者包括蒋辉课题组的曹钰和万华云，董梦秋实验室的阿达莱提买买提明和董梦秋博士，代谢组学中心的马燕博士和曹杨，蛋白质组中心的陈涉博士和李琳，遗传筛选中心的李祺博士和吴重阳，刘清华实验室的王濛。该研究由科技部、北京市政府和清华大学共同资助，在北京生命科学研究所完成。论文链接：https://www.cell.com/molecular-cell/fulltext/S1097-2765(23)01014-6本文仅用于学术分享，转载请注明出处。若有侵权，请联系微信：bioonSir 删除或修改！

临床1期蛋白降解靶向嵌合体引进/卖出

2023-08-02

·美通社

【创新大赛】武汉华中赛（外科/微创/植介入)即将开赛附路演项目

第六届（2023）中国医疗器械创新创业大赛武汉 2023年8月2日 /美通社/ -- 中国医疗器械创新创业大赛（"科创中国"系列活动）在中国科协和科技部相关单位的指导下已连续成功举办了五届。五届分别征集到来自海内外医疗器械创新项目283个、607个、665个、831个及733个，大赛及配套活动合计有近3000家企业以及创新服务与投资机构参与，现场约4万人次观摩并有多位部委领导、院士及百余位来自监管和产业的权威专家现场指导，前五届决赛共评出一二三等奖项目共369个，赛后半年跟踪统计获奖项目融资额共计近67亿元，部分项目后续还获得部委、省市区的课题资助及其他各种赛事奖项。大赛有力地助推了医疗器械的成果转化。大赛主KV 为了更好的助推中国医疗器械外科微创及高值耗材类创新成果转化及创新技术交流，以赛促转化、以赛促招商，由国家医疗器械产业技术创新联盟携手九州通医药集团将于 8月7-8日于湖北武汉九州通天鹅酒店共同举办第六届（2023）中国医疗器械创新创业大赛华中赛（外科/微创/植介入）。此次赛事是由国家医疗器械产业技术创新联盟、武汉市汉阳区人民政府、医疗器械创新网主办，由九州通医药集团股份有限公司、汉阳区大健康产业办、汉阳区人民政府龙阳街道办事处承办，由汉阳区人民政府琴断口街道办事处、医疗器械产业联盟代工服务平台、浙江国创医疗器械有限公司协办。日程安排华中赛事日程备注：日程安排可能根据实际行程有轻微调整，请以大赛现场最终日程为准。入围项目公示项目编号项目名称单位 /团队名称 897202301 点阵脉冲铥激光百健嘉屹（宁波）光电科技有限公司 755202301 基于杠杆重建平衡理论设计研发的仿生髋关节假体北京大学人民医院 534202301 神经外科多功能等离子体手术系统的研发北京市神经外科研究所 / 成都京成科技有限公司 805202301 X 射线牙片机束光器复旦大学附属口腔医院 047202301 光声科技 - 新型精准影像诊断技术的开拓者广东光声科技有限公司 008202301 " 窥 " 见天地 - 基于全景 VR 技术的腹腔镜系统哈尔滨医科大学附属第二医院 036202301 基于医用水凝胶技术平台的消化道黏膜下可注射隆起凝胶瀚凝（常州）医疗科技有限公司 893202301 高活性可吸收仿生纳米钙磷人工骨杭州彗搏科技有限公司 516202301 机器人辅助髌骨骨折微创器械研发和临床应用航天中心医院 830202301 跌倒风险智能评估系统河南卫尔康医疗科技有限公司 791202301 肩关节连续被动运动康复器械产品的研发华中科技大学同济医学院附属同济医院 019202301 高端医用核心部件 X- 射线球管研发及产业化霍夫曼（苏州）电子科技有限公司 819202301 可视化医用牵引器江苏独角兽电子科技有限公司 837202301 一次性使用支气管镜江苏独角兽电子科技有限公司 478202301 介入式心腔内超声成像江苏霆升科技有限公司 542202301 一次性使用 1205 型电动肛肠套扎器及其关键组件的研发江苏孜航精密五金有限公司 838202301 股骨头坏死轴向骨搬移术关键器械江西省人民医院 792202301 肠道无创介入治疗系统江西圣丹康医学科技有限公司 1011202301 便携式全自动口腔印模清洗消毒系统空军军医大学第三附属医院 624202301 脑出血的内镜内微创微创技术及相关器械研制开发南方医科大学南方医院 808202301 兼具筋膜缝合的套管穿刺器诺信医学科技（山东）有限公司 535202301 心房分流器植入系统启晨（上海）医疗器械有限公司 820202301 电磁驱动髓内延长机器人清华大学机械系 741202301 腹腔镜肠阻拦网陕西省安康市中心医院 631202301 一次性使用可通气式胃镜牙垫陕西省人民医院 728202301 云链智康 —— 打造微创术中影像记录与分析新模式陕西云链智康科技团队 030202301 多孔手术机器人系统国产化关键器械研发与胸外科临床应用研究上海市胸科医院 027202301 基于深度感知的声带麻痹（ VCP ）微创治疗的光动力多点穿刺注射装置研发上海市胸科医院 393202301 基于高密度多肽阵列芯片的无痛血检装备深圳市华云智能健康有限公司 547202301 第二代低温等离子手术消融系统深圳市荔辉医疗科技有限公司 139202301 用于腰椎的微动结构以及辅助装置首都医科大学宣武医院 422202301 一种重症医学科用内窥镜天津医科大学总医院 517202301 半导体激光治疗仪武汉尚振医疗科技有限公司 815202301 不停跳心肌切除器（魏氏刀）武汉微新坦医疗科技有限公司 587202301 腹腔镜下肝脏支撑器襄阳市中心医院 831202301 变径皮质骨螺纹螺钉在骨质疏松人群腰椎内镜下融合术中生物力学及产品研发新疆医科大学第一附属医院 397202301 功能性聚醚醚酮种植体设计及应用云起高科生物科技（深圳）有限公司 099202380 国内首创解决慢性失眠共病抑郁、焦虑等难治性脑疾病项目正量源健康产业（武汉）有限公司 554202301 AI 数字化高分辨率小型 CT 中日友好医院 — 清华大学 — 锐视智慧医工交叉团队 616202301 面向肝部的机器人辅助穿刺定位导航系统珠海横乐医学科技有限公司观众通道 http://gdw-innomd.mikecrm.com/Jxp76OA 欢迎各企业、科研院所、投融资机构、创新服务机构等相关单位和有识之士一同探索精彩赛事。九州通健康城九州通医药集团股份有限公司九州通为科技驱动型的全链医药产业综合服务商，搭建起行业稀缺的"千亿级"医药供应链服务平台，主营业务包括数字化医药分销与供应链服务、总代品牌推广业务、医药工业自产及OEM业务、新零售与万店加盟业务（C端）、医疗健康（C端）与技术增值服务、数字物流技术与供应链解决方案六大方面。九州通是国内最大的民营医药商业企业，位列中国医药商业企业第四位，是行业内首家获评5A级物流企业及唯一获评国家十大智能化仓储物流示范基地的企业；公司位列2022年"中国企业500强"第207位和"中国民营企业500强"第68位。 2022年，九州通营业收入再创新高，达1404.24亿元，同比增长14.72%。公司全渠道B端客户增至51.9万家，其中城市及县级公立医院客户1.28万家，连锁及单体药店客户19.6万家（合计覆盖零售药店数量约37万家），基层及民营医疗机构客户22.3万家（其中民营医院客户1.29万余家），下游医药分销商1万余家，其他客户近1.2万家。面向未来，九州通坚持以"争做中国最专业的大健康服务平台"为企业愿景，秉承"以客户为中心、以业绩为导向、以文化为驱动、以质量为生命"的核心价值观，深度发展合伙模式，持续推动公司新战略转型升级，与广大合作伙伴共同开创医药健康发展新局面。九州通健康城项目介绍九州通健康城项目是九州通集团投资25亿元打造的大健康产业集群。项目占地约4.6万平方米，总建面约30万方，由九州通总部大厦、甲级写字楼、商务楼、九州通天鹅酒店、会议会展中心等多种物业类型组成。 6号楼九州通写字楼介绍及招商情况健康城6号楼为总建筑面积约5.4万平方米甲级写字楼，高约140米，地上共36层，是九州通倾力打造的集智能、健康、生态于一体的高品质商务空间，也是承载国家级医药创业孵化器、健康产业集群的物理空间。 6号楼写字楼为集团和上下游企业的高效融合与协同发展创造了良好的契机，依托九州通集团总部，实现大健康关联企业的聚合发展，合力构建医药大健康产业生态圈。该楼宇依托市、区两级政府规划的龙阳湖健康谷为产业核心，重点引进医药电商、健康管理、医疗器械、智慧医疗等企业入驻。目前企业入驻率约70%。