Flortaucipir F-18(Flortaucipir F-18) - 药物靶点：TAU_在研适应症：阿尔茨海默病引起的痴呆症，轻度认知障碍，造影剂_专利_临床

概要

基本信息

药物类型

小分子化药、诊断用放射药物

别名

Flortaucipir (18F)、Flortaucipir F 18

+ [9]

靶点

TAU

作用方式

调节剂

作用机制

TAU调节剂(微管相关蛋白tau调节剂)

治疗领域

神经系统疾病其他疾病

在研适应症

阿尔茨海默病引起的痴呆症轻度认知障碍造影剂+ [3]

非在研适应症

创伤性脑损伤慢性创伤性脑病皮质基底节变性+ [3]

原研机构

Siemens Healthineers AG

在研机构

Avid Radiopharmaceuticals, Inc.Eli Lilly Nederland BVPDRadiopharma, Inc.

非在研机构-

权益机构-

最高研发阶段批准上市

首次获批日期

美国 (2020-05-28),

阿尔茨海默症

最高研发阶段(中国)-

特殊审评优先审评 (美国)

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结构/序列

分子式C16H10FN3

InChIKeyGETAAWDSFUCLBS-SJPDSGJFSA-N

CAS号1522051-90-6

关联

69

项与 Flortaucipir F-18 相关的临床试验

NCT06723015

/ Enrolling by invitation临床2期IIT

Study of Tau PET Outcomes in Patients Receiving Anti-amyloid Immunotherapies

This is an imaging study of patients with mild Alzheimer's disease receiving amyloid-targeting therapy and under the care of neurologists at Mayo Clinic in Rochester, MN.

开始日期2025-08-01

申办/合作机构

Mayo Clinic

NCT06297590

/ Recruiting临床1期

A Single- and Multiple-Ascending Dose Study to Evaluate the Safety, Tolerability, Pharmacokinetics, and Pharmacodynamics of LY3954068 in Patients With Early Symptomatic Alzheimer's Disease

The main purpose of this study is to evaluate the safety of LY3954068 in participants with early symptomatic Alzheimer's Disease (AD). The study will also investigate how much LY3954068 gets into the bloodstream and will test the effects of LY3954068 on markers of AD.
The study will be comprised of two parts, A and B. Part B is optional, and participants from Part A may also have the opportunity to join an optional bridging period to a separate potential study where participants would receive LY3954068. Each enrolled participant in Part A will receive a single dose of LY3954068 or placebo (no active drug) given into the spinal fluid. If conducted, each participant in Part B would receive 2 doses of either LY3954068 or placebo administered into the spinal fluid.
The study will last up to approximately 45 weeks for Part A, and, if conducted, 73 weeks for Part B, including the screening period.
If the optional bridging period is conducted, participants in Part A could be enrolled in the separate potential study for up to approximately 96 weeks, including the screening period.

开始日期2024-08-15

申办/合作机构

Eli Lilly & Co.

ChiCTR2500099173

/ RecruitingN/AIIT

Application of 18F-AV-45 and 18F-AV-1451 PET/CT in Alzheimer's Disease: A Cross-Sectional, Diagnostic Clinical Study.

开始日期2024-08-12

申办/合作机构

南昌大学第一附属医院

100 项与 Flortaucipir F-18 相关的临床结果

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100 项与 Flortaucipir F-18 相关的转化医学

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100 项与 Flortaucipir F-18 相关的专利（医药）

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361

项与 Flortaucipir F-18 相关的文献（医药）

2025-03-01·Alzheimer's & Dementia

Relationships between hypometabolism and both β‐amyloid and tau PET in corticobasal syndrome

Article

作者: Ali, Farwa ; Stephens, Yehkyoung C. ; Goodrich, Austin W. ; Schwarz, Chistopher G. ; Graff‐Radford, Jonathan ; Filippi, Massimo ; Ghirelli, Alma ; Whitwell, Jennifer L. ; Machulda, Mary M. ; Lowe, Val J. ; Senjem, Matthew L. ; Agosta, Federica ; Jack, Clifford R. ; Josephs, Keith A.

AbstractINTRODUCTIONAlzheimer's disease (AD) pathology causes corticobasal syndrome (CBS) in 21%–50% of patients. Studies have assessed hypometabolism in CBS according to β‐amyloid (A) positron emission tomography (PET), but the understanding of the association of both AD‐tau (T) and A with hypometabolism is incomplete.METHODSThirty‐three CBS patients and 45 controls underwent fluorodeoxyglucose (FDG), flortaucipir, and Pittsburgh compound‐B PET and were classified as A± and T±. FDG‐PET uptake was extracted for 12 regions‐of‐interest in dominant (most affected) and non‐dominant hemispheres and compared across A/T groups.RESULTSA+T+ patients had greater hypometabolism in temporo‐parieto‐occipital cortices than A+T‐ and A‐T‐ groups, with no differences observed between the A+T‐ and A‐T‐ groups. FDG asymmetry was more accentuated in A+T+ patients. Medial temporal and basal ganglia metabolism were similar across AT groups.DISCUSSIONAmyloid and tau positivity contribute synergistically to hypometabolism and asymmetry in temporo‐parieto‐occipital cortices in CBS, with AD‐like patterns of hypometabolism observed only in A+T+ patients.Highlights

Amyloid (A) and tau PET (T) status can be used to stratify CBS patients.

A+T+ CBS patients show more hypometabolism in temporo‐parieto‐occipital cortices.

Medial temporal metabolism (typical AD pattern) is similar across AT groups.

Parieto‐occipital cortices should be assessed when investigating AT pathology in CBS.

Amyloid and tau positivity contribute synergistically to hypometabolism and asymmetry in CBS.

2025-03-01·European Journal of Medicinal Chemistry

Progress in the study of anti-Alzheimer's disease activity of pyrimidine-containing bioactive molecules

Review

作者: Ma, Li-Ying ; Chui, Rui-Hao ; Zhang, Qi ; Zhang, Qian ; Li, Bing-Qian ; Zhang, Di ; Liu, Yu-Lin ; Zhang, Lin-Lin

Pyrimidines are aromatic, heterocyclic organic compounds characterized by a six-membered ring that contains four carbon atoms and two nitrogen atoms. They have been reported to exhibit a variety of biological activities such as antifungal, antiviral, and anti-Parkinsonian effects. Recently, there has been an increased focus on their potential anti-Alzheimer's properties. Several pyrimidine-based drugs and their analogs are currently undergoing various phases of clinical trials, indicating pyrimidine as a promising chemical structure for drug development. Notably, modifications to the pyrimidine structure significantly influence their activity against Alzheimer's disease. For instance, the introduction of heteroatoms into the pyrimidine ring or alternations in the length of the linkage region have been shown to enhance therapeutic efficacy. This review provides a comprehensive overview of pyrimidine derivatives as potential therapeutics for Alzheimer's disease, with a focus on structure-activity relationship (SAR) studies, design strategies, and binding mechanisms. These insights could pave the way for the development of more effective anti-Alzheimer's medications.

2025-03-01·Nuclear Medicine and Biology

Transmembrane protein 106B amyloid is a potential off-target molecule of tau PET tracers in the choroid plexus

Article

作者: Iwata, Ren ; Kudo, Kaede ; Harada, Ryuichi ; Yokoyama, Yuka ; Furumoto, Shozo ; Okamura, Nobuyuki ; Kudo, Yukitsuka

PURPOSETau positron emission tomography (PET) has become an essential tool for the clinical diagnosis of neurodegenerative diseases and the study of tau pathology in the brain. However, some tau tracers exhibit off-target binding in the basal ganglia, choroid plexus, and meninges. Recently, transmembrane protein 106B (TMEM106B) was identified to form novel amyloid filaments in the brain during aging. In this study, we explored the possibility that TMEM106B aggregates might be responsible for off-target binding of tau PET tracers in the choroid plexus.METHODSThe binding properties of ¹⁸F-labeled tau and amyloid tracers against choroid plexus tissues from postmortem human brains were evaluated through in vitro autoradiography and in vitro binding assays and compared with histochemical staining.RESULTSAutoradiography showed strong binding of [¹⁸F]PM-PBB3 followed by [¹⁸F]flortaucipir in the choroid plexus. Immunostaining of the same sections revealed a high level of transmembrane protein 106B aggregates, which are thioflavin-S-labeled Biondi ring structures, in the choroid plexus epithelium and co-localization with PM-PBB3-stained structures. In contrast, co-localization of flortaucipir with TMEM106B immunoreactivity was not confirmed because flortaucipir had a low fluorescence intensity. In vitro binding assays for [¹⁸F]PM-PBB3 and [¹⁸F]flortaucipir demonstrated high affinities for collagenase A-treated choroid plexus homogenate containing transmembrane protein 106B aggregates.CONCLUSIONThis study demonstrated high affinity of [¹⁸F]PM-PBB3 for TMEM106B aggregates in the choroid plexus. In vivo off-target binding of [¹⁸F]PM-PBB3 to the choroid plexus might result from binding to TMEM106B aggregates.

24

项与 Flortaucipir F-18 相关的新闻（医药）

2025-03-06

·PRNewswire

Inaugural ADDF Scientific Summit Convenes Pioneering Scientists Leading and Shaping Alzheimer's Research

Daniel M. Skovronsky, MD, PhD, of Eli Lilly & Company, Receives Prestigious 2025 Melvin R. Goodes Prize, Nobel Prize of Alzheimer's Research Goodes Prize Winners Declare Future of Alzheimer's Treatment Will Rest on Combination Therapies and Precision Medicine NEW YORK and PALM BEACH, Fla., March 6, 2025 /PRNewswire/ -- The Alzheimer's Drug Discovery Foundation (ADDF) marked its Inaugural ADDF Scientific Summit in a momentous celebration of Alzheimer's science which brought together the most innovative and respected researchers in the field. The event, held on March 5th, featured the presentation of the esteemed Melvin R. Goodes Prize to Dr. Daniel M. Skovronsky, Chief Scientific Officer, Lilly, and President, Lilly Research Labs, and an address from Dr. Sanjay Gupta, CNN Chief Medical Correspondent, bestselling author, and practicing neurosurgeon. The Summit convened eight of the ten previous winners of the esteemed Goodes Prize for a symposium moderated by Dr. Niranjan Bose, Managing Director for Health & Life Sciences at Gates Ventures, spotlighting the cutting-edge advancements driving Alzheimer's therapeutics, biomarkers, and prevention, as well as the promising future of the field. These world-renowned scientists have each contributed novel ideas based around the biology of aging that are helping to revolutionize research. They, along with the ADDF, are leading and shaping the Alzheimer's field, propelling us toward combination therapies and precision medicine, the same strategy that has proven successful in cancer treatment. "It has been truly incredible to witness the pace of breakthroughs in Alzheimer's research over the past few years," said Dr. Howard Fillit, Co-Founder and Chief Science Officer of the ADDF. "Our trailblazing Goodes Prize recipients are catalyzing innovations that will enable us to tailor treatment approaches based on patients' individual biomarker profiles and combine drugs that target the specific causes of their disease. We are driving the next generation of care, which will use novel drugs targeting the underlying disease biology in tandem with current treatments to change the course of Alzheimer's." The Goodes Prize, recognized as the Nobel Prize of Alzheimer's research, is presented annually to a pioneering scientist to mark exceptional contributions to the Alzheimer's field. Skovronsky was recognized for his visionary work to develop critical diagnostic tests for Alzheimer's and for his leadership in developing and commercializing Kisunla, one of the first disease-modifying therapies for Alzheimer's patients. The game-changing diagnostics developed with Skovronsky's help include the Amyvid PET scan, the first FDA-approved diagnostic test for Alzheimer's which was developed with seed funding from the ADDF; the Tauvid PET scan, the first and only FDA-approved diagnostic for Tau in the brain; and a blood biomarker test for p-tau217 for the early diagnosis of Alzheimer's disease. "It is a profound honor to accept the 2025 Melvin R. Goodes Prize," said Skovronsky. "This recognition is a testament to the hard work and dedication of more than 35 years of Alzheimer's disease research to fight against this terrible disease. This award celebrates the power of collaboration and the unwavering commitment of the Alzheimer's Drug Discovery Foundation. Together, we can and will make history and change the world for patients everywhere." Skovronsky's work has been critical to the approvals of the first class of amyloid-targeting drugs for Alzheimer's, which offer patients options to delay disease progression for the first time and have set the foundation for the future of Alzheimer's therapies. As the next wave of therapeutics aimed at novel targets continues to advance, they can be combined with these anti-amyloids to increase efficacy and stop the disease in its tracks. "Six months ago, the ADDF celebrated the tenth anniversary of the Goodes Prize in Stockholm's City Hall, which is synonymous with the Nobel Prize. Now at our Inaugural ADDF Scientific Summit, we are once again highlighting the innovators driving progress in Alzheimer's on a global stage," said Ronald Lauder, Co-Founder and Co-Chairman of the ADDF. "Listening to our Goodes Prize scientists, it's amazing to hear how much progress has been made since my brother and I founded the ADDF in 1998 and to see the ADDF's fingerprints on the advancements we now take for granted – new drugs, new tests, and new prevention methods." Preceding the symposium, featured speaker Dr. Sanjay Gupta presented an address, highlighting the many reasons for hope as Alzheimer's science continues to make huge strides toward the next generation of treatments and prevention strategies. Gupta has earned multiple Emmy and Peabody awards for his health reporting and recently explored his own family history with Alzheimer's disease through filming a documentary, Dr. Sanjay Gupta Reports: The Last Alzheimer's Patient, which aired this past summer on CNN. "It was an honor to be a part of the ADDF's inaugural event celebrating its work for Alzheimer's patients," said Gupta. "We used to think about heart disease the way we thought about brain disease just a few years ago, as hopeless. But now that has changed. We can prevent heart disease, and thanks to exciting strides in how we treat and diagnose Alzheimer's, we will soon be able to prevent neurodegenerative diseases too. I am excited and I am optimistic about the future of Alzheimer's." About The Alzheimer's Drug Discovery Foundation (ADDF) Founded in 1998 by Leonard A. and Ronald S. Lauder, the Alzheimer's Drug Discovery Foundation is dedicated to rapidly accelerating the discovery of drugs to prevent, treat and cure Alzheimer's disease. The ADDF is the only public charity solely focused on funding the development of drugs for Alzheimer's, employing a venture philanthropy model to support research in academia and the biotech industry. The ADDF's leadership and contributions to the field have played a pivotal role in bringing the first Alzheimer's PET scan (Amyvid®) and blood test (PrecivityAD®) to market, as well as fueling the current robust and diverse drug pipeline. Through the generosity of its donors, the ADDF has awarded more than $370 million to fund 765 Alzheimer's drug discovery programs, biomarker programs and clinical trials in 21 countries. To learn more, please visit: . Media Contact: Emily Berkowitz, Senior Director of Communications, ADDF [email protected] 617-894-3540 SOURCE Alzheimer's Drug Discovery Foundation WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

2025-02-20

·PRNewswire

The Alzheimer's Drug Discovery Foundation Announces Daniel M. Skovronsky, MD, PhD, of Eli Lilly & Company, as Recipient of Prestigious 2025 Melvin R. Goodes Prize

Skovronsky will be recognized for his extraordinary work with the Amyvid PET scan, the first FDA-approved diagnostic test for Alzheimer's.The Goodes Prize – referred to the Nobel Prize of Alzheimer's research – honors scientists making extraordinary and lasting contributions to the Alzheimer's field. NEW YORK, Feb. 20, 2025 /PRNewswire/ -- The Alzheimer's Drug Discovery Foundation (ADDF) will present its 2025 Melvin R. Goodes Prize to Daniel M. Skovronsky, MD, PhD, Chief Scientific Officer, Lilly, and President, Lilly Research Labs, at the Inaugural ADDF Scientific Summit on Wednesday, March 5th. Skovronsky will be recognized for his groundbreaking work to develop critical diagnostic tests for Alzheimer's in addition to his leadership in developing and commercializing Kisunla, one of the first disease-modifying therapies for Alzheimer's patients. Continue Reading Daniel M. Skovronsky, MD, PhD, of Eli Lilly & Company, announced as the 2025 Melvin R. Goodes Prize The game-changing diagnostics developed with Skovronsky's help include the Amyvid PET scan, the first FDA-approved diagnostic test for Alzheimer's; the Tauvid PET scan, the first and only FDA-approved diagnostic for Tau in the brain; and a blood biomarker test for p-tau217 for the early diagnosis of Alzheimer's disease. The Goodes Prize, referred to as the Nobel Prize of Alzheimer's research, is presented annually to a leading scientist to mark exceptional contributions to the Alzheimer's field. This international award was established by the late Melvin R. Goodes to advance critical science aimed at fighting Alzheimer's disease and related dementias. "Dan is the epitome of a Goodes Prize awardee, a leading scientist who has advanced innovative and bold ideas to transform how we diagnose and develop new treatments for Alzheimer's," said Howard Fillit, MD, Co-Founder and Chief Science Officer at the ADDF. "The Goodes Prize emphasizes our ongoing commitment to accelerating drug development for Alzheimer's and honors the legacy of Mel Goodes, a trailblazer in the pharmaceutical industry. We are thrilled to recognize Dan's outstanding work and partnership with the ADDF, which spans more than 20 years. His efforts to develop the Amyvid PET scan made recent Alzheimer's drug approvals possible, including Lilly's Kisunla, and will benefit patients now and for years to come." The Amyvid PET scan, which received early seed funding from the ADDF, is a brain imaging test that helps detect Alzheimer's disease by combining a positron emission tomography (PET) scan and an injection of Amyvid, a radioactive tracer. Amyvid was instrumental in the approval of the first disease-modifying Alzheimer's drugs – Aduhelm in 2021, Leqembi in 2023, and Kisunla in 2024 – providing the biomarker data needed for regulatory approval. "Over the past decade, we have witnessed remarkable advances in Alzheimer's research," said Dr. Daniel Skovronsky, Chief Scientific Officer, Lilly, and President, Lilly Research Labs. "It is my belief that through early detection and early intervention we can someday make Alzheimer's a preventable disease. I am deeply honored to receive the prestigious Goodes Prize award and look forward to joining fellow recipients who are leading the way in developing new treatments for Alzheimer's. The early support from the ADDF for my work, which aimed to revolutionize how we diagnose patients to ensure the right ones were included in our studies, was crucial to advancing the field, and I will always be grateful for that support." The Goodes Prize, which celebrated its 10th anniversary last year in Stockholm with a program featuring Queen Silvia of Sweden and U.S. Ambassador to Sweden Erik Ramanathan, honors scientists who are leading new approaches to developing Alzheimer's therapeutics and diagnostics. "To have pioneering scientists like Dan who have received this award out there in the field, pushing research forward, is truly a gift," said Nancy Goodes, ADDF Board Member. "The breakthroughs being made in the name of the Goodes Prize are the most meaningful legacy for my husband." The 11th annual Goodes Prize will be presented at 6:00 p.m. ET on Wednesday, March 5, 2025 during the inaugural ADDF Scientific Summit. This celebration of Alzheimer's science will be hosted by Dr. Howard Fillit and features a keynote address from Dr. Sanjay Gupta, MD, CNN Chief Medical Correspondent, bestselling author and practicing neurosurgeon. The summit will highlight nine world-renowned scientists and recipients of the Melvin R. Goodes Prize discussing therapeutics, biomarkers, prevention, and what is coming next in the field. Skovronsky will be the latest to join the ranks of these accomplished scientists who have helped bring the biology of aging to the forefront of Alzheimer's research. "The Goodes Prize represents our mission to treat, prevent, and ultimately cure Alzheimer's disease," commented Mark Roithmayr, ADDF Chief Executive Officer. "We support one of the largest and most diverse clinical development portfolios for Alzheimer's disease, and pioneering research, like Dan's, is critical to our goal of driving meaningful innovation and change in drug development." The Melvin R. Goodes Prize for Excellence in Drug Development was established in 2015 in honor of Melvin R. Goodes, former CEO of Warner-Lambert Company, who channeled his unique knowledge of the drug industry into Alzheimer's advocacy after being diagnosed with the disease. The award recognizes individual researchers whose work has significantly advanced our understanding of Alzheimer's, paving the way for potential breakthroughs in treatment and prevention. Previous Goodes Prize recipients have demonstrated tremendous innovation and perseverance in the quest for effective treatment options for Alzheimer's. Internationally lauded as the highest recognition in Alzheimer's research, the Goodes Prize has helped move the field forward by facilitating thought provoking discussions among leading scientists from academia, industry, and philanthropy in pursuit of a future free of Alzheimer's. About The Alzheimer's Drug Discovery Foundation (ADDF) Founded in 1998 by Leonard A. and Ronald S. Lauder, the Alzheimer's Drug Discovery Foundation is dedicated to rapidly accelerating the discovery of drugs to prevent, treat and cure Alzheimer's disease. The ADDF is the only public charity solely focused on funding the development of drugs for Alzheimer's, employing a venture philanthropy model to support research in academia and the biotech industry. The ADDF's leadership and contributions to the field have played a pivotal role in bringing the first Alzheimer's PET scan (Amyvid®) and blood test (PrecivityAD®) to market, as well as fueling the current robust and diverse drug pipeline. Through the generosity of its donors, the ADDF has awarded more than $370 million to fund 765 Alzheimer's drug discovery programs, biomarker programs and clinical trials in 21 countries. To learn more, please visit: . SOURCE Alzheimer's Drug Discovery Foundation WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

2025-02-11

·奇点网

《自然·医学》：逃脱早发性阿尔茨海默病的幸运儿！科学家报告携带遗传基因但70岁仍未发病病例，tau病理受限或是关键丨临床大发现

*仅供医学专业人士阅读参考阿尔茨海默病（AD）是最主要的神经退行性疾病之一，随着社会老龄化的加剧，已经成为人类健康的重大威胁。遗憾的是，我们目前应对AD的手段有限，尚不足以有效治愈。击溃AD的关窍到底在哪？今日发表在《自然·医学》杂志上的一份病例报告为我们指出了关键——tau蛋白。研究对象是一名携带致病基因突变早老素2（PSEN2） p.Asn141Ile突变、具有显性遗传性AD家族史的男性个体。携带该突变的患者，包括研究对象的兄弟姐妹，都在50岁前发病，但这位研究对象直到71岁还保持着完全正常的认知能力，且并未携带已知的具有AD保护能力的基因。影像学和生物标志物分析结果显示，这位男性的Aβ病理与其他PSEN2 p.Asn141Ile突变携带者的特征一致，但他的tau病理沉积受限于枕叶区域、并未扩散。研究者猜测，这就是他能够维持认知能力的原因。论文题图这位研究对象是DIAN研究的参与者，这是一项致力于研究显性遗传性AD的大型研究项目。研究对象在61岁时参与DIAN研究，并在随后的多年随访中评估了认知能力、日常生活能力、脑成像和生物标志物等指标的变化。研究对象携带PSEN2 p.Asn141Ile突变，他的母亲和13个兄弟姐妹中的11个也是携带者。携带者普遍在50岁左右发病，最晚的一个人发病时也已经58岁。但奇怪的是，研究对象直到71岁（2021年），都没有表现出任何认知和AD临床症状。研究对象的认知测试一直表现正常在随访过程中，研究对象表现出的唯一异常就是2017年开始偶尔出现的右手震颤，不过他的帕金森病评定量表结果一直在正常范围内。分析研究对象的基因，他除了PSEN2 p.Asn141Ile突变外，APOE基因型为APOE3纯合子，也不携带APOE3-Christchurch或RELN-COLBOS等已知的保护性突变。影像学检查给了我们更多的线索。 PiB PET检测发现研究对象的脑部有明显的Aβ沉积，与PSEN2 p.Asn141Ile突变携带者的典型表现是一致的；AV1451 PET检测的是tau蛋白沉积，有趣的是，研究对象脑内的tau蛋白沉积主要表现在枕叶区域，这与AD患者脑内多个认知区域存在tau沉积的典型表现不同。 FDG PET检测脑内葡萄糖代谢的结果也显示，研究对象脑内代谢减低的情况是局部的、尤其是tau蛋白沉积的枕叶区域，与AD患者的典型表现不同。此外，研究对象的脑脊液（CSF）生物标志物结果也发现，Aβ42：40等Aβ标志物水平与其他携带者相当；磷酸化tau蛋白（p-tau）水平则介于携带者和非携带者之间。据此，研究者猜测，tau蛋白病理的受限可能是研究对象认知得以保存的关键。研究对象Aβ病理与其他携带者一致，tau病理受限于枕叶区域基因上没有什么特别之处，那是什么让研究对象能抵御AD？研究者发现，研究对象有一段有趣的经历。他曾经负责舰船柴油机修理，需要在高温环境下持续工作几小时，这期间他会用冷水冲身防止过热。研究者猜测这与他的耐受性有关。相较其他携带者，研究对象的蛋白质组学和代谢组学特征表现出了一定的不同。在丰度较高的近300种蛋白质中，富集了与蛋白质折叠相关的通路并包括多个热休克蛋白家族成员。综合蛋白质组学和代谢组学，研究者发现，与蛋白质合成、抗衰老和抗氧化相关的三个通路有显著的不同。虽然这只是一个个例，不过分析结果还是很有参考意义的，论文提出限制tau病理扩散作为AD早期干预和治疗的新思路，热休克蛋白等细胞保护机制也非常值得继续讨论。 2024年对AD来说是重要的一年，我们获得了能够真正改变AD进程的药物，在AD的检测、预防和病理学探索上也有颇多进益。我们在《医学趋势 30讲》中详细总结了近两年来AD的重磅进展，相信能给你带来全新的理解，感兴趣的读者可以试听相关章节↓ 参考资料： [1]Llibre-Guerra, J.J., Fernandez, M.V., Joseph-Mathurin, N. et al. Longitudinal analysis of a dominantly inherited Alzheimer disease mutation carrier protected from dementia. Nat Med (2025). https://doi.org/10.1038/s41591-025-03494-0 本文作者丨代丝雨

临床结果临床研究临床终止

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KEGG	Wiki	ATC	Drug Bank
-	Flortaucipir F-18	V04C	DB14914

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适应症	国家/地区	公司	日期
阿尔茨海默病引起的痴呆症	英国	Eli Lilly Nederland BV	2024-11-23
轻度认知障碍	英国	Eli Lilly Nederland BV	2024-11-23
造影剂	欧盟	Eli Lilly Nederland BV	2024-08-22
造影剂	挪威	Eli Lilly Nederland BV	2024-08-22
造影剂	冰岛	Eli Lilly Nederland BV	2024-08-22
造影剂	列支敦士登	Eli Lilly Nederland BV	2024-08-22
阿尔茨海默症	美国	Avid Radiopharmaceuticals, Inc.	2020-05-28

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适应症	最高研发状态	国家/地区	公司	日期
神经退行性疾病	临床3期	美国	Avid Radiopharmaceuticals, Inc.	2016-09-01
认知障碍	临床1期	美国	Avid Radiopharmaceuticals, Inc.	2016-08-01
阿尔茨海默症	药物发现	澳大利亚	Avid Radiopharmaceuticals, Inc.	2015-09-01
创伤性脑损伤	药物发现	美国	Avid Radiopharmaceuticals, Inc.	2014-12-01
抑郁症	药物发现	美国	Avid Radiopharmaceuticals, Inc.	2014-12-01
皮质基底节变性	药物发现	美国	Avid Radiopharmaceuticals, Inc.	2014-08-12
进行性核上性麻痹	药物发现	美国	Avid Radiopharmaceuticals, Inc.	2014-08-12
慢性创伤性脑病	药物发现	美国	Avid Radiopharmaceuticals, Inc.	2014-06-01
轻度认知障碍	药物发现	美国	Avid Radiopharmaceuticals, Inc.	2013-12-01
认知功能障碍	药物发现	美国	Avid Radiopharmaceuticals, Inc.	2013-11-13

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临床结果

适应症

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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


NCT03019536 (Phase I Clinical Trial, CTgov)	临床1期	阿尔茨海默症 \| 认知功能障碍	22	Placebo - IV+Flortaucipir F18+Florbetapir F 18 (Placebo IV)	淵鹽艱遞觸齋繭積壓鬱(膚膚範糧簾糧糧構鹽鏇) = 齋壓製壓鑰顧壓衊觸壓憲築餘選淵淵鹽淵顧鹽 (襯鏇製鑰積淵獵艱淵蓋, 網願蓋顧積襯鹽鏇繭衊 ~ 糧壓選遞觸夢膚顧糧廠) 更多	-	2023-10-10
				Placebo - IV+Flortaucipir F18+Florbetapir F 18+LY3303560 - IV (70 mg LY3303560)	淵鹽艱遞觸齋繭積壓鬱(膚膚範糧簾糧糧構鹽鏇) = 鹹築築顧糧獵膚遞築積憲築餘選淵淵鹽淵顧鹽 (襯鏇製鑰積淵獵艱淵蓋, 廠廠築選築鏇醖範積廠 ~ 鹹網鬱鑰憲淵鬱鬱蓋齋) 更多
NCT04080544 (CTgov)	临床2期	阿尔茨海默症 \| 认知功能障碍	125	Positron Emission Tomography+[18F]AV-1451	製構窪鹽顧鹹艱壓網遞(製遞鑰糧襯醖範觸願選) = 遞襯餘構構衊窪醖繭壓壓蓋鹽築網壓鑰鹹鹽糧 (餘襯構構範範憲顧鹽憲, 廠襯廠積構範襯憲鑰積 ~ 築鬱膚衊繭襯窪鹹膚獵) 更多	-	2023-09-28
SNMMI2023	N/A	-	-	TAUVID[18F]PI-2620 ([18F]PI-2620)	淵夢壓網醖網願淵糧簾(構襯網醖鬱願膚製獵鬱) = 餘鹽蓋壓衊範廠淵蓋蓋壓艱艱鹹網蓋範繭鏇顧 (簾鏇構鏇襯糧簾淵觸壓, 8)	-	2023-08-28
				[18F]T807TAUVID ([18F]T807)	淵夢壓網醖網願淵糧簾(構襯網醖鬱願膚製獵鬱) = 繭範壓鬱選淵願鹽糧鹽壓艱艱鹹網蓋範繭鏇顧 (簾鏇構鏇襯糧簾淵觸壓, 7)
SNMMI2022	N/A	慢性创伤性脑病	-	Flortaucipir	選選膚膚獵觸餘艱夢衊(淵選艱顧鹽製廠壓遞膚) = 鑰積鹽鏇願衊簾餘膚鬱築鏇夢夢製鹽鑰遞衊構 (餘鬱窪鏇網齋獵壓窪顧, 10.5)	-	2022-08-08
				MK-6240	選選膚膚獵觸餘艱夢衊(淵選艱顧鹽製廠壓遞膚) = 鏇鏇顧窪壓淵艱廠窪醖築鏇夢夢製鹽鑰遞衊構 (餘鬱窪鏇網齋獵壓窪顧 )
AAIC2022	N/A	-	661	[18F]Flortaucipir	(壓網艱醖願醖獵鹹觸網) = 鹹鹹鏇糧餘艱鏇網憲鏇壓顧窪淵觸夢積築繭襯 (鹽顧範壓鹽糧獵鹽糧觸, 88.2 ~ 95.2) 更多	-	2022-02-01
				[18F]Flortaucipir (Amyloid PET)	(壓網艱醖願醖獵鹹觸網) = 遞蓋鑰鏇構鑰鏇網構壓壓顧窪淵觸夢積築繭襯 (鹽顧範壓鹽糧獵鹽糧觸, 88.7 ~ 95.5) 更多
ADNI (AAIC2020)	N/A	tau PET	458	[18F] flortaucipir (AD)	壓糧窪衊範鏇衊壓襯獵(顧構餘鹹鹽廠製製襯淵) = 製範鏇膚簾窪襯鹽構膚膚壓蓋範製鏇齋鹹膚淵 (壓顧艱壓鬱積鹹醖餘夢 ) 更多	-	2020-12-07
				[18F] flortaucipir (MCI)	壓糧窪衊範鏇衊壓襯獵(顧構餘鹹鹽廠製製襯淵) = 遞夢願窪築衊願醖觸鹽膚壓蓋範製鏇齋鹹膚淵 (壓顧艱壓鬱積鹹醖餘夢 ) 更多
NCT04474405 (CTgov)	早期临床1期	阿尔茨海默症 \| 认知功能障碍 \| 轻度认知障碍	36	Whole body PET scan+Flortaucipir F18 (Whole Body Flortaucipir PET Scan)	廠構膚艱襯艱簾蓋願觸(範選鹹淵範窪艱選鹹製) = 餘膚範艱壓鏇衊艱選鏇醖餘淵鹽網觸夢構鬱選 (製餘膚醖蓋糧積膚製憲, 積選簾構簾壓簾鹽壓淵 ~ 壓積艱窪構積網遞夢醖) 更多	-	2020-09-25
				Brain MRI+Florbetapir F 18 (MRI and Amyloid Extension Cohort)	鹽鹹齋蓋顧選簾衊壓範(製鏇觸構襯範觸簾艱構) = 膚壓襯襯鹹齋遞膚構構願壓範鹹淵窪繭鏇夢製 (膚網獵觸願餘顧窪壓製, 製網壓製鑰鑰選範廠構 ~ 顧蓋製鹽鹹艱願獵獵壓) 更多
NCT03040713 (CTgov)	临床1期	额颞痴呆	16	Brain PET scan+Flortaucipir F18	壓選壓選繭遞鑰製襯襯(積膚窪製糧構壓鬱製壓) = 餘壓憲齋鏇鬱構窪網鏇願齋範壓繭壓選積構鹹 (觸憲構餘壓蓋鑰鏇簾顧, 憲艱製膚鏇遞鹹壓積繭 ~ 壓蓋選淵構齋獵願齋鏇) 更多	-	2020-09-25
NCT02278367 (CTgov)	临床2期	阿尔茨海默症 \| 抑郁症 \| 创伤性脑损伤	179	flortaucipir (Cognitively Impaired)	(獵襯艱憲選壓獵鹹鬱憲) = 鏇範範襯鹽網憲範壓窪衊齋願選鏇壓遞醖夢窪 (鹹築齋齋窪願夢鹽淵壓, 製襯艱窪淵鏇廠選窪艱 ~ 淵壓襯糧窪構艱廠獵鏇) 更多	-	2020-09-10
				flortaucipir (Cognitively Normal)	(獵襯艱憲選壓獵鹹鬱憲) = 艱構齋鑰遞艱觸觸艱壓衊齋願選鏇壓遞醖夢窪 (鹹築齋齋窪願夢鹽淵壓, 簾鏇製繭鑰願簾鏇衊獵 ~ 獵築製醖淵鬱淵憲網衊) 更多
NCT02051764 (CTgov)	临床2期	阿尔茨海默症	44	flortaucipir (Cognitively Impaired)	鏇製淵夢襯簾鏇網鏇憲(選蓋網簾築淵糧築鏇夢) = 網憲範餘構遞築廠遞醖糧願鹽壓蓋構獵膚網範 (鬱網製鏇餘憲觸顧觸顧, 構襯艱餘衊鹽願網憲淵 ~ 顧鬱鏇窪遞製製鑰襯簾) 更多	-	2020-09-07
				flortaucipir (Healthy Volunteers)	鏇製淵夢襯簾鏇網鏇憲(選蓋網簾築淵糧築鏇夢) = 築顧範積齋簾糧願衊觸糧願鹽壓蓋構獵膚網範 (鬱網製鏇餘憲觸顧觸顧, 繭願選膚範積顧艱選壓 ~ 願艱觸齋積構製選淵餘) 更多