更新于：2024-05-01

MMP14

基质金属蛋白酶-14

更新于：2024-05-01

基本信息

别名

基质金属蛋白酶14、matrix metallopeptidase 14、matrix metallopeptidase 14 (membrane-inserted)

+ [14]

简介

Endopeptidase that degrades various components of the extracellular matrix such as collagen. Activates progelatinase A. Essential for pericellular collagenolysis and modeling of skeletal and extraskeletal connective tissues during development (By similarity). May be involved in actin cytoskeleton reorganization by cleaving PTK7 (PubMed:20837484). Acts as a positive regulator of cell growth and migration via activation of MMP15. Involved in the formation of the fibrovascular tissues in association with pro-MMP2 (PubMed:12714657). Cleaves ADGRB1 to release vasculostatin-40 which inhibits angiogenesis (PubMed:22330140).

关联

项与 MMP14 相关的药物

BT-1718

靶点

MMP14 x Tubulin

作用机制

MMP14抑制剂 [+1]

在研机构

Cancer Research UK [+1]

原研机构

Bicycle Therapeutics Plc

在研适应症

肿瘤 [+3]

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

ICT3205

靶点

MMP14

作用机制

MMP14抑制剂

在研机构

University of Bradford

原研机构

University of Bradford

在研适应症

肿瘤 [+1]

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

Pb-BCY20603

靶点

MMP14

作用机制

MMP14抑制剂

在研机构

Orano Med LLC [+1]

原研机构

Bicycle Therapeutics Plc [+1]

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 MMP14 相关的临床试验

NCT03486730 / Completed临床1/2期IIT

A Cancer Research UK Phase I/IIa Clinical Trial of BT1718, (A Bicycle Drug Conjugate) Given Intravenously in Patients With Advanced Solid Tumours.

This clinical trial is looking at a drug called BT1718 in adult patients with advanced solid tumours. The main aim of the study is to find the maximum dose of BT1718 that can be given safely to patients; learn more about the potential side effects of BT1718 and how they can be treated and also what happens to BT1718 inside the body.

开始日期2018-01-24

申办/合作机构

Cancer Research UK

[+1]

NCT00040755 / Completed临床2期IIT

Randomized Phase II Trial of BMS-275291 (NSC 713763, IND 62573) in Hormone Refractory Prostate Cancer

BMS-275291 may stop the growth of prostate cancer by stopping blood flow to the tumor and by blocking the enzymes necessary for tumor cell growth. Randomized phase II trial to study the effectiveness of BMS-275291 in treating patients who have prostate cancer that has not responded to hormone therapy

开始日期2002-05-01

申办/合作机构

National Cancer Institute

NCT00039104 / Completed临床2期IIT

A Phase II, Open-Label, Randomized Trial of Zoledronic Acid (Zometa™) and BMS-275291 (NSC#713763) in Patients With Hormone Refractory Prostate Cancer

Phase II trial to study the effectiveness of combining zoledronate with BMS-275291 in treating patients who have prostate cancer that has not responded to previous hormone therapy. Zoledronate may prevent bone loss and stop the growth of tumor cells in bone. BMS-275291 may stop the growth of tumor cells by blocking the enzymes necessary for cancer cell growth. Combining zoledronate with BMS-275291 may kill more tumor cells.

开始日期2002-04-01

申办/合作机构

National Cancer Institute

100 项与 MMP14 相关的临床结果

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100 项与 MMP14 相关的转化医学

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0 项与 MMP14 相关的专利（医药）

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3,916

项与 MMP14 相关的文献（医药）

2024-02-22·Journal of neuroinflammation

SPOCK2 modulates neuropathic pain by interacting with MT1-MMP to regulate astrocytic MMP-2 activation in rats with chronic constriction injury.

Article

作者: Chenglong Wang ; Yitong Xu ; Miao Xu ; Cong Sun ; Xiaojiao Zhang ; Xueshu Tao ; Tao Song

BACKGROUND:

Neuropathic pain (NP) is a kind of intractable pain. The pathogenesis of NP remains a complicated issue for pain management practitioners. SPARC/osteonectin, CWCV, and Kazal-like domains proteoglycan 2 (SPOCK2) are members of the SPOCK family that play a significant role in the development of the central nervous system. In this study, we investigated the role of SPOCK2 in the development of NP in a rat model of chronic constriction injury (CCI).

METHODS:

Sprague-Dawley rats were randomly grouped to establish CCI models. We examined the effects of SPOCK2 on pain hpersensitivity and spinal astrocyte activation after CCI-induced NP. Paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) were used to reflects the pain behavioral degree. Molecular mechanisms involved in SPOCK2-mediated NP in vivo were examined by western blot analysis, immunofluorescence, immunohistochemistry, and co-immunoprecipitation. In addition, we examined the SPOCK2-mediated potential protein-protein interaction (PPI) in vitro coimmunoprecipitation (Co-IP) experiments.

RESULTS:

We founded the expression level of SPOCK2 in rat spinal cord was markedly increased after CCI-induced NP, while SPOCK2 downregulation could partially relieve pain caused by CCI. Our research showed that SPOCK2 expressed significantly increase in spinal astrocytes when CCI-induced NP. In addition, SPOCK2 could act as an upstream signaling molecule to regulate the activation of matrix metalloproteinase-2 (MMP-2), thus affecting astrocytic ERK1/2 activation and interleukin (IL)-1β production in the development of NP. Moreover, in vitro coimmunoprecipitation (Co-IP) experiments showed that SPOCK2 could interact with membrane-type 1 matrix metalloproteinase (MT1-MMP/MMP14) to regulate MMP-2 activation by the SPARC extracellular (SPARC_EC) domain.

CONCLUSIONS:

Research shows that SPOCK2 can interact with MT1-MMP to regulate MMP-2 activation, thus affecting astrocytic ERK1/2 activation and IL-1β production to achieve positive promotion of NP.

2024-02-16·iScience

NatD epigenetically activates FOXA2 expression to promote breast cancer progression by facilitating MMP14 expression.

Article

作者: Mengying Xing ; Bing Yao ; Jiaxuan Xu ; Peifen Lu ; Qixiang Li ; Dongliang Wu ; Bing Chen ; Jiwu Wei ; Lei Su ; Quan Zhao

N-α-acetyltransferase D (NatD) mediates N-α-terminal acetylation of histone H4 (Nt-Ac-H4), but its role in breast cancer metastasis remains unknown. Here, we show that depletion of NatD directly represses the expression of FOXA2, and is accompanied by a significant reduction in Nt-Ac-H4 enrichment at the FOXA2 promoter. We show that NatD is commonly upregulated in primary breast cancer tissues, where its expression level correlates with FOXA2 expression, enhanced invasiveness, and poor clinical outcomes. Furthermore, we show that FOXA2 promotes the migration and invasion of breast cancer cells by activating MMP14 expression. MMP14 is also upregulated in breast cancer tissues, where its expression level correlates with FOXA2 expression and poor clinical prognosis. Our study shows that the NatD-FOXA2-MMP14 axis functions as a key signaling pathway to promote the migratory and invasive capabilities of breast cancer cells, suggesting that NatD is a critical epigenetic modulator of cell invasion during breast cancer progression.

2024-02-15·Biochimica et biophysica acta. Molecular basis of disease

Preventing obesity, insulin resistance and type 2 diabetes by targeting MT1-MMP.

Article

作者: Pallavi Asthana ; Hoi Leong Xavier Wong

Obesity is one of the predominant risk factors for type 2 diabetes. Despite all the modern advances in medicine, an effective drug treatment for obesity without overt side effects has not yet been found. The discovery of growth and differentiation factor 15 (GDF15), an appetite-regulating hormone, created hopes for the treatment of obesity. However, an insufficient understanding of the physiological regulation of GDF15 has been a major obstacle to mitigating GDF15-centric treatment of obesity. Our recent studies revealed how a series of proteolytic events predominantly mediated by membrane-type 1 matrix metalloproteinase (MT1-MMP/MMP14), a key cell-surface metalloproteinase involved in extracellular remodeling, contribute to the pathogenesis of metabolic disorders, including obesity and diabetes. The MT1-MMP-mediated cleavage of the GDNF family receptor-α-like (GFRAL), a key neuronal receptor of GDF15, controls the satiety center in the hindbrain, thereby regulating non-homeostatic appetite and bodyweight changes. Furthermore, increased activation of MT1-MMP does not only lead to increased risk of obesity, but also causes age-associated insulin resistance by cleaving Insulin Receptor in major metabolic tissues. Importantly, inhibition of MT1-MMP effectively protects against obesity and diabetes, revealing the therapeutic potential of targeting MT1-MMP for the management of metabolic disorders.

项与 MMP14 相关的新闻（医药）

2024-04-02

·今日头条

保肠护关节：高分研究揭示抵御关节炎的肠道因子

04月02日的《热心肠日报》，我们解读了 15 篇文献，关注：关节炎，FMT，IBD，流行病学，乳糜泻，致病菌，肠道免疫细胞，昆虫，LISCure，Affibody，瀚科迈博，加科思，飞鹤。该篇日报由R·AI辅助创作生成，人工审核校对。肠上皮细胞坏死是肠道和关节炎发展之间的关键联系 Annals of the Rheumatic Diseases——[27.4] ① 这项研究确定了肠上皮细胞（IEC）坏死是肠道和关节炎发展之间的关键联系；② 关节炎发作时，IEC经历凋亡和坏死，导致肠道屏障功能受损；③ 在关节炎发作期间，HIF1α被确定为IEC中上调基因之一，在IEC中删除Hif1a增强了IEC坏死，引发肠道炎症并加重了关节炎；④ HIF1α是坏死诱导因子RIPK3的关键转录抑制因子，且在新发病风湿性关节炎患者的肠上皮中也发现了增强的RIPK3表达，表明肠上皮细胞发生坏死；⑤ 通过治疗性稳定HIF1α以及基于小分子的RIPK3抑制剂，在体外和体内拯救了肠道坏死，并抑制了关节炎的发展。【原文信息】 Expression of HIF1α in intestinal epithelium restricts arthritis inflammation by inhibiting RIPK3-induced cell death machinery 2024-03-19 , doi: 10.1136/ard-2023-224491 Nature子刊：粪菌移植治疗溃疡性结肠炎的临床反应与GBP5有关 Nature Communications——[16.6] ① 分析粪菌移植（FMT）在溃疡性结肠炎（UC）患者身上的分子反应，探索FMT如何影响人类结肠黏膜的基因表达；② 相较于安慰剂干预，FMT改变了患者结肠黏膜转录组（受影响的基因数量：3 vs 75），包括对结构、代谢和炎症通路的调节；③ 在疾病缓解的患者中，调节的途径包括紧密连接、钙信号和异物代谢；④ GBP5和IRF4的下调与疾病缓解相关，而GBP5基因缺失的雌性小鼠比野生型同胞更能抵抗结肠炎，表现出更高的结肠IRF4磷酸化水平；⑤ 本研究表明GBP5可能在结肠炎的发展中起到负面作用，而FMT后的结肠粘膜反应能够区分UC患者是否实现缓解。【原文信息】 Profiling the colonic mucosal response to fecal microbiota transplantation identifies a role for GBP5 in colitis in humans and mice 2024-03-26 , doi: 10.1038/s41467-024-46983-5 过去20年IBD的演变与变化 EClinicalMedicine——[15.1] ① 这项跨国多中心研究揭示了过去二十年间炎症性肠病（IBD）表现模式的变化，为改善患者的诊断、管理和预后提供了重要见解；② 共纳入6个国家1430名IBD患者（84.5%溃疡性结肠炎和14.3%克罗恩病），根据首次诊断时间分为3组：超过15年（A组）、5-15年（B组）和近5年（C组）；③ 与C组相比，A组和B组的肠外症状更为普遍、食物敏感率更高；④ 在C组中，左侧结肠炎成为溃疡性结肠炎最常见的亚型，且腹痛和腹胀的发生率增加，而腹泻的频率有所下降；⑤ 在C组中，克罗恩病患者上消化道症状更为普遍，无病发作的患者相对比例增加，表明IBD的管理和治疗可能有所改善。【原文信息】 Inflammatory bowel disease evolution in the past two decades: a chronological multinational study 2024-03-15 , doi: 10.1016/j.eclinm.2024.102542 华北理工：IBD不会独立增加癌症风险 BMC Medicine——[9.3] ① 华北理工大学王友信团队探究了炎症性肠病（IBD）与癌症风险之间的关联，未发现两者之间因果关系的可靠遗传学证据，暴露于IBD可能并不独立地增加癌症风险；② 在东亚或欧洲人群中，IBD、克罗恩病（CD）或溃疡性结肠炎（UC）与癌症之间没有显著的遗传相关性；③ 东亚人群中未观察到IBD与癌症之间的显著因果关系，欧洲人群中CD与卵巢癌之间以及UC与非黑色素瘤皮肤癌之间存在显著关联；④ 多变量孟德尔随机化分析未发现以上任何显著关联；⑤ 使用共定位分析，在东亚或欧洲人群中，没有共享的因果变异体可以证明IBD、CD或UC与癌症之间的关联。【原文信息】 Association between inflammatory bowel disease and cancer risk: evidence triangulation from genetic correlation, Mendelian randomization, and colocalization analyses across East Asian and European populations 2024-03-25 , doi: 10.1186/s12916-024-03352-9 麦醇溶蛋白肽寡聚化或可增加肠道通透性 Angewandte Chemie International Edition——[16.6] ① 本研究揭示了33-mer去酰胺化麦醇溶蛋白肽（DGP）在乳糜泻中的新作用机制；② 33-mer DGP是一种代谢修饰的小麦麸质抗原，可自发地组装成直径为24纳米的寡聚体；③ 33-mer DGP寡聚体主要呈现两种次级结构：主要的多脯氨酸II螺旋和次要的β-折叠结构；④ 33-mer DGP刺激下会导致肠上皮细胞模型Caco-2的通透性显著增加，伴随着紧密连接蛋白zonula occludens-1（ZO-1）的重新分布；⑤ 本研究为33-mer DGP对乳糜泻的影响进行了深入探究，并提示麦醇溶蛋白肽寡聚化与乳糜泻的相关性。【原文信息】 The Celiac-Disease Superantigen Oligomerizes and Increases Permeability in an Enterocyte Cell Model 2024-03-18 , doi: 10.1002/anie.202317552 山一大团队：沙门氏菌操纵巨噬细胞，突破肠-血管屏障 EMBO Journal——[11.4] ① 肠道病原体沙门氏菌在侵袭肠道上皮细胞后迅速进入血液循环，山东第一医科大学的李冰清和陈启鑫团队发表文章，揭示了沙门氏菌在早期感染时通过操控CX3CR1+巨噬细胞迁移来穿透肠-血管屏障，进入血液循环；② 沙门氏菌依赖于宿主细胞的肌动蛋白和病原体效应蛋白SteC来诱导巨噬细胞的迁移/侵袭特性；③ SteC招募宿主肌球蛋白轻链蛋白Myl12a并磷酸化其Ser19和Thr20残基，Myl12a的磷酸化导致肌动蛋白重排，增强了巨噬细胞的迁移和侵袭能力；④ SteC能够利用多种NTPs，而不仅仅是ATP，对Myl12a进行磷酸化；⑤ 解析了SteC的晶体结构，揭示了其非典型的二聚体介导的催化机制，并证实了SteC介导的细胞骨架操控对沙门氏菌穿透肠血管屏障和扩散至靶器官至关重要。【原文信息】 Salmonella manipulates macrophage migration via SteC-mediated myosin light chain activation to penetrate the gut-vascular barrier 2024-03-25 , doi: 10.1038/s44318-024-00076-7 CD4+CD8αα+肠道上皮内淋巴细胞发育的途径和机制（综述） Trends in Immunology——[16.8] ① CD4+CD8αα+T细胞是由成熟的CD4+ T细胞通过转录因子重编程分化而来，在小肠上皮中具有独特的发育途径；② 微生物代谢产物、细胞因子、MHC-II及其他细胞表面分子的共同作用促进了CD4+ T细胞向CD4+CD8αα+ T细胞的表型和功能转变；③ CD4+CD8αα+ T细胞兼具CD4+辅助T细胞和CD8+细胞毒性T细胞的标志物和分子，并具有广泛的免疫调节功能，从肠上皮细胞的细胞溶解到肠黏膜的免疫抑制，其功能可能取决于不同的环境条件，有待进一步研究。【原文信息】 Pathways and mechanisms of CD4+CD8αα+ intraepithelial T cell development 2024-03-20 , doi: 10.1016/j.it.2024.02.006 中性粒细胞促进结直肠癌中血管生成 Journal of Clinical Investigation——[15.9] ① 这项研究揭示了中性粒细胞（PMN）在结直肠癌（CRC）中的组织特异性重编程，导致其促进肿瘤的血管生成；② 通过对血液和组织中性粒细胞的转录组分析，发现定位于外周血液、炎症性结肠和肿瘤的PMN三者的转录程序有明显差别；③ 肿瘤相关中性粒细胞（TANs）独特地富集血管生成和血管发育途径，且体外培养、结肠炎诱导的小鼠CRC和患者来源的异种移植模型等功能研究证明TANs在促进肿瘤血管化中具有关键作用；④ Spp1和Mmp14在TANs中高度诱导，对内皮细胞趋化和分支有关键调控作用；⑤ TCGA数据集和临床标本证实了SPP1和MMP14在高级别CRC患者中的富集，但在UC患者中并不富集；⑥ 使用药理学抑制TANs迁移或MMP14活性有效减少肿瘤血管密度，导致结直肠癌消退。【原文信息】 Tissue-specific reprogramming leads to angiogenic neutrophil specialization and tumor vascularization in colorectal cancer 2024-02-08 , doi: 10.1172/JCI174545 Cell子刊：衰老细胞与巨噬细胞合作促进果蝇肠道转化 Developmental Cell——[11.8] ① 本研究探索体内如何整合多种诱导衰老信号来驱动仅少数细胞的衰老机制；② 在果蝇肠道转化模型中，AKT、JNK和DNA损伤信号同时激活导致部分细胞表现出多种衰老特征；③ 通过遗传手段或使用衰老细胞清除剂消除衰老细胞，可减少组织过度生长并提高存活率；④ 衰老细胞通过招募果蝇巨噬细胞到转化组织中，导致JNK信号的非自主激活，从而促进肿瘤发生；⑤ 本研究揭示了在果蝇肠道转化模型中，衰老细胞通过与巨噬细胞的相互作用，通过多激酶信号网络促进肠道转化的新机制。【原文信息】 Senescent cells and macrophages cooperate through a multi-kinase signaling network to promote intestinal transformation in Drosophila 2024-01-31 , doi: 10.1016/j.devcel.2024.01.009 土壤细菌定植昆虫肠道激活免疫系统的奇妙之旅 PNAS——[11.1] ① 昆虫缺乏获得性免疫，也曾被认为没有免疫记忆，但最近的研究报道了“免疫印记”现象，即低剂量的病原体或非病原微生物刺激免疫并预防病菌感染，但其潜在机制尚不清楚；② PNAS发表的研究性论文揭示了摄入特定的土壤细菌Burkholderia能够穿透豆虫Riptortus pedestris的前肠道上皮细胞，迁移到体液中，从而激活系统性免疫，包括体液和细胞免疫反应；③ 这种激活的免疫反应不仅不会对宿主的健康产生负面影响，反而能够保护昆虫免受后续的病原细菌感染；④ 研究还发现，一旦中断了Burkholderia菌株与肠道上皮细胞的接触，宿主的免疫力会回落到感染前的水平，使昆虫更容易受到微生物感染，说明持续获取环境细菌对于维持有效免疫至关重要。【原文信息】 Ingested soil bacteria breach gut epithelia and prime systemic immunity in an insect 2024-03-04 , doi: 10.1073/pnas.2315540121 LISCure活菌药LB-P8治疗PSC获FDA快速通道资格认定 ① 3月29日，LISCure Biosciences公司宣布，旗下治疗原发性硬化性胆管炎（PSC）活菌药LB-P8获得FDA快速通道资格认定；② LB-P8是目前在治疗PSC上唯一报告进入临床开发阶段的活菌药产品；③ LB-P8已在2022年获得治疗PSC的孤儿药资格认定，目前正处于2期临床研究阶段；④ LISCure Biosciences公司计划在美国和欧洲多个医疗机构开展该临床研究，并预计在2025年初获得初步结果。【原文信息】 LISCure Biosciences receives U.S. FDA Fast Track designation for LB-P8 for the treatment of primary sclerosing cholangitis (PSC) 2024-03-29 , CISION Affibody PET显像剂ABY-025 2期临床首例胃食管癌患者入组 ① 3月26日，Affibody AB公司宣布，旗下PET/CT显像剂ABY-025，其2期临床试验的首例胃食管癌患者完成入组；② 胃食管癌早期诊断和治疗仍然是医学界面临的难题之一，患者HER2基因表达水平是衡量患者能否从靶向治疗中获益的重要标志；③ 使用ABY-025进行PET/CT成像，可以在注射后3-4小时确认肿瘤HER2基因表达水平的高低，从而预测靶向药物治疗效果；④ 研究还将比较PET/CT成像与组织活检获得的HER2表达水平数据，从而评估这一靶向检测手段能否带来新的治疗契机。【原文信息】 FIRST GASTROESOPHAGEAL CANCER PATIENTS ENROLLED IN PHASE 2 BASKET TRIAL USING AFFIBODY’S PET IMAGING AGENT ABY-025 2024-03-28 , Affibody 瀚科迈博创新药HuA21 1b/2期临床完成首例患者入组 ① 3月29日，瀚科迈博自主研发的1类创新药HuA21注射液，其1b/2期临床试验完成首例受试者入组；② 该研究旨在评估HuA21注射液联合曲妥珠单抗化疗，治疗HER2阳性胃癌患者的安全性、耐受性和有效性；③ 该研究由复旦大学附属中山医院刘天舒教授和安徽医科大学第一附属医院孙倍成教授共同牵头；④ HuA21在1期临床试验中展现了优异的抗肿瘤活性，有望成为改变现阶段治疗方案的新药，瀚科迈博具有完全自主知识产权。【原文信息】瀚科迈博创新药HuA21注射液 Ib/II 期临床研究完成首例受试者入组 2024-03-29 , 安科生物加科思JAB-30355片临床试验申请获CDE受理 ① 3月28日，北京加科思新药研发有限公司宣布其1类新药JAB-30355片的临床试验申请获国家药品审评中心（CDE）受理；② JAB-30355片是一款针对P53 Y220C的激活剂，用于治疗局部晚期或转移性实体瘤；③ 研究表明，JAB-30355片在多种肿瘤模型中实现了肿瘤消退，包括胃癌、乳腺癌和肺癌等；④ 该药物在美国已获批新药研究申请（IND），将开展针对晚期实体瘤的1/2a期临床试验；⑤ 此外，加科思布局了KRAS G12C抑制剂、SHP2抑制剂、BET抑制剂、GUE抑制剂等多款在研项目。【原文信息】加科思「P53 Y220C激活剂」在华申报临床 2024-03-29 , 药智新闻飞鹤取得加拿大首张婴幼儿配方奶粉生产执照 ① 近日，飞鹤旗下加拿大皇家妙克公司获得加拿大食品检验局（CFIA）批准生产婴幼儿配方奶粉许可；② 该公司计划今年夏天将产品推向加拿大当地零售分销渠道；③ 飞鹤在加拿大的奶粉生产工厂是当地第一家婴幼儿配方奶粉生产企业，且在投产后也是加拿大当地生产、销售的第一个奶粉品牌；④ 2016年年底，飞鹤与加拿大金斯顿市签约，拟在该市投资建厂，该厂于2017年6月份开建，2019年调试完成。【原文信息】飞鹤取得加拿大首张婴幼儿配方奶粉生产执照 2024-03-29 , FoodTalks 感谢本期日报的审核者：章台柳，九卿臣，RZN，注册营养师陈彬林，圆圈儿，好雨，Richard，Alex Zhang 点击阅读过去10天的日报： 0401 | 3月，最值得关注的35篇肠道健康要闻！ 0331 | 聚焦特殊人群：老年人和孕妈妈的饮食新知 0330 | Akk菌或是免疫性肾病帮凶？Science子刊揭示机制 0329 | 33页综述纵论：超加工食品健康转型的新策略 0328 | Science子刊：锁定肠道中让病毒逃脱免疫的"避风港" 0327 | 10文聚焦菌群-肠-脑轴研究新进展 0326 | 100分综述详解：IBD细胞因子疗法最前沿 0325 | 大肠癌患病为何年轻化？遗传与生活方式的双重影响 0324 | 大型临床试验：补钙补D如何影响老年女性长期健康？ 0323 | Lancet+JAMA领衔，聚焦炎症性肠病诊断与治疗

临床研究

2024-02-07

·BioSpace

Bicycle Therapeutics to Participate in the Oppenheimer 34th Annual Healthcare Life Sciences Conference

CAMBRIDGE, England & BOSTON--(BUSINESS WIRE)-- Bicycle Therapeutics Limited (NASDAQ:BCYC), a biotechnology company pioneering a new and differentiated class of therapeutics based on its proprietary bicyclic peptide (Bicycle®) technology, today announced that management will participate in a fireside chat at the Oppenheimer 34th Annual Healthcare Life Sciences Conference on February 14, 2024, at 10 a.m. ET. A live webcast of the fireside chat will be accessible from the Investor section of the company’s website, . A replay of the webcast will be archived and available following the event. About Bicycle Therapeutics Bicycle Therapeutics is a clinical-stage biopharmaceutical company developing a novel class of medicines, referred to as Bicycle® molecules, for diseases that are underserved by existing therapeutics. Bicycle molecules are fully synthetic short peptides constrained with small molecule scaffolds to form two loops that stabilize their structural geometry. This constraint facilitates target binding with high affinity and selectivity, making Bicycle molecules attractive candidates for drug development. The company is evaluating BT8009, a Bicycle Toxin Conjugate (BTC®) targeting Nectin-4, a well-validated tumor antigen; BT5528, a BTC targeting EphA2; and BT7480, a Bicycle TICA® targeting Nectin-4 and agonizing CD137, in company-sponsored Phase 1/2 trials. In addition, BT1718, a BTC that targets MT1-MMP, is being investigated in a Phase 1/2a clinical trial sponsored by the Cancer Research UK Centre for Drug Development. Bicycle Therapeutics is headquartered in Cambridge, UK, with many key functions and members of its leadership team located in Cambridge, Mass. For more information, visit bicycletherapeutics.com.

临床研究

2023-11-30

·BioSpace

Bicycle Therapeutics to Host R&D Day on December 14

CAMBRIDGE, England & BOSTON--(BUSINESS WIRE)-- Bicycle Therapeutics Limited (NASDAQ:BCYC), a biotechnology company pioneering a new and differentiated class of therapeutics based on its proprietary bicyclic peptide (Bicycle®) technology, today announced that the company will host its first Research and Development (R&D) Day on Thursday, December 14. The event will take place in New York City from 8 a.m. to 12 p.m. Eastern Time and will be simultaneously webcast. Bicycle Therapeutics executives will provide investors and analysts with an overview of the company’s R&D strategy and pipeline opportunities, with an emphasis on clinical updates for BT8009, BT5528 and BT7480. The company will also highlight the broad capabilities of its novel Bicycle® platform technology. Analysts and investors who are interested in attending in person should contact bicycle@argotpartners.com. A live webcast of the R&D Day will be accessible from the Investor section of the company’s website, . A replay of the webcast will be archived and available following the event. About Bicycle Therapeutics Bicycle Therapeutics is a clinical-stage biopharmaceutical company developing a novel class of medicines, referred to as Bicycles, for diseases that are underserved by existing therapeutics. Bicycles are fully synthetic short peptides constrained with small molecule scaffolds to form two loops that stabilize their structural geometry. This constraint facilitates target binding with high affinity and selectivity, making Bicycles attractive candidates for drug development. The company is evaluating BT8009, a Bicycle Toxin Conjugate (BTC™) targeting Nectin-4, a well-validated tumor antigen; BT5528, a BTC targeting EphA2; and BT7480, a Bicycle TICA™ targeting Nectin-4 and agonizing CD137, in company-sponsored Phase 1/2 trials. In addition, BT1718, a BTC that targets MT1-MMP, is being investigated in a Phase 1/2a clinical trial sponsored by the Cancer Research UK Centre for Drug Development. Bicycle Therapeutics is headquartered in Cambridge, UK, with many key functions and members of its leadership team located in Cambridge, Mass. For more information, visit bicycletherapeutics.com.

临床研究