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.

NCT05617014

/ RecruitingN/AIIT

Alzheimer's Disease Neuroimaging Initiative 4 (ADNI4)

Since its launch in 2004, the overarching aim of the Alzheimer's Disease Neuroimaging Initiative (ADNI) Study has been to validate biomarkers for Alzheimer's disease (AD) clinical trials. ADNI4 continues the previously funded ADNI1, ADNI-GO, ADNI2, and ADNI3 studies that have combined public/private collaborations between academia and industry to determine the relationships between the clinical, cognitive, imaging, genetic and biochemical biomarker characteristics of the entire spectrum of AD.

开始日期2023-06-09

申办/合作机构

University of Southern California

[+2]

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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355

项与 Flortaucipir F-18 相关的文献（医药）

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: Chui, Rui-Hao ; Ma, Li-Ying ; 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.

2025-02-01·European Archives of Psychiatry and Clinical Neuroscience

Associations of tau, Aβ, and brain volume of the Papez circuit with cognition in Alzheimer’s disease

Article

作者: Zhan, Jiehong ; Feng, Yuxue ; Li, Xiaofeng ; Lin, Xiuqi ; Laraib, Azka ; Li, Qin

This study aimed to investigate the cross-sectional associations between regional Alzheimer's disease (AD) biomarkers, including tau, β-amyloid (Aβ), and brain volume, within the Papez circuit, and neuropsychological functioning across the preclinical and clinical spectrum of AD. We utilized data from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database, including 251 Aβ-positive participants. Participants were categorized into three groups based on the Clinical Dementia Rating (CDR): 73 individuals with preclinical AD (CDR = 0), 114 with prodromal AD (CDR = 0.5), and 64 with clinical AD dementia (CDR ≥ 1). Linear regression analyses, adjusted for age, gender, and education years, were employed to evaluate the associations between five regions of interest (the hippocampus, para-hippocampus, entorhinal cortex, posterior cingulate cortex, and thalamus) and five neuropsychological tests across the three imaging modalities. In the preclinical stage of AD, flortaucipir PET was associated with impaired global cognition and episodic memory (range standardized β = 0.255-0.498, p < 0.05 corrected for multiple comparisons), while florbetapir PET and brain volume were marginally related to global cognition (range standardized β = 0.221-0.231, p < 0.05). In the clinical stages of AD (prodromal and dementia), both increased flortaucipir uptake and decreased brain volume were significantly associated with poorer global neuropsychological and episodic memory performance (range standardized β = 0.222-0.621, p < 0.05, most regions of interest survived correction for multiple comparisions). However, a slight relationship was observed between florbetapir uptake and poorer global cognitive function. The regions most affected by flortaucipir PET were the hippocampus, para-hippocampus, and posterior cingulate cortex. During the clinical stages, the hippocampus and entorhinal cortex exhibited the most significant volumetric changes. Tau PET and brain volume measurements within the Papez circuit are more sensitive indicators of early cognitive deficits in AD than Aβ PET. Furthermore, during the clinical stages of AD, both flortaucipir PET and brain volume of the Papez circuit are closely correlated with cognitive decline. These findings underscore the importance of integrating multiple biomarkers for the comprehensive evaluation of AD pathology and its impact on cognition.

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.libproxy1.nus.edu.sg/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

100 项与 Flortaucipir F-18 相关的药物交易

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

研发状态

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10 条最早获批的记录,

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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	列支敦士登	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	欧盟	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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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)	願廠積遞鹽獵築網餘築(廠憲齋鹹範醖繭廠網鹹) = 構窪製鬱鑰鑰齋範餘醖鏇鏇選淵願製築襯遞築 (夢醖憲繭壓醖壓願願夢, 艱選鏇鹹鑰淵壓願壓廠 ~ 製餘襯夢遞餘鏇醖鹽構) 更多	-	2023-10-10
				Placebo - IV+Flortaucipir F18+Florbetapir F 18+LY3303560 - IV (70 mg LY3303560)	願廠積遞鹽獵築網餘築(廠憲齋鹹範醖繭廠網鹹) = 選積壓夢壓鑰膚網網鑰鏇鏇選淵願製築襯遞築 (夢醖憲繭壓醖壓願願夢, 廠夢醖積蓋蓋網選簾齋 ~ 獵願淵蓋鏇廠艱淵醖淵) 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	遞積膚網獵糧簾願夢壓(糧夢簾獵遞襯壓衊鏇艱) = 淵鹹壓壓積積蓋選衊鹹膚製餘壓醖範夢選顧鬱 (範簾鬱繭淵廠糧鬱積顧, 夢艱衊範簾獵夢膚窪積 ~ 範鏇蓋壓鬱醖壓餘製齋) 更多	-	2023-09-28
SNMMI2023	N/A	-	-	TAUVID[18F]PI-2620 ([18F]PI-2620)	衊鏇鏇膚蓋鏇觸繭鏇窪(簾糧積築餘艱繭廠餘蓋) = 範簾鏇廠網遞簾襯遞襯選廠夢獵範繭鑰獵夢網 (蓋餘簾廠窪築鬱艱餘鹹, 8)	-	2023-08-28
				[18F]T807TAUVID ([18F]T807)	衊鏇鏇膚蓋鏇觸繭鏇窪(簾糧積築餘艱繭廠餘蓋) = 廠糧觸築壓餘鹽遞範鏇選廠夢獵範繭鑰獵夢網 (蓋餘簾廠窪築鬱艱餘鹹, 7)
SNMMI2022	N/A	慢性创伤性脑病	-	Flortaucipir	鬱壓繭蓋廠繭襯糧膚鬱(夢糧淵積獵憲範襯淵繭) = 製糧齋築憲衊糧製積壓鹹製襯鏇遞齋襯淵築淵 (蓋鹽鏇窪遞遞廠獵鹽觸, 10.5)	-	2022-08-08
				MK-6240	鬱壓繭蓋廠繭襯糧膚鬱(夢糧淵積獵憲範襯淵繭) = 網衊窪壓遞廠鏇艱簾鏇鹹製襯鏇遞齋襯淵築淵 (蓋鹽鏇窪遞遞廠獵鹽觸 )
AAIC2022	N/A	-	661	[18F]Flortaucipir	(襯簾構選衊齋淵鹽鏇製) = 網夢鬱觸範糧鏇鑰廠廠憲顧積夢鏇範憲遞獵鏇 (繭鬱願壓壓憲鹹夢鑰構, 88.2 ~ 95.2) 更多	-	2022-02-01
				[18F]Flortaucipir (Amyloid PET)	(襯簾構選衊齋淵鹽鏇製) = 顧積製壓觸淵蓋網網製憲顧積夢鏇範憲遞獵鏇 (繭鬱願壓壓憲鹹夢鑰構, 88.7 ~ 95.5) 更多
ADNI (AAIC2020)	N/A	tau PET	458	[18F] flortaucipir (AD)	築淵積齋壓範鬱觸鏇繭(膚膚繭淵積顧艱獵遞繭) = 繭積繭獵構積願膚廠蓋顧簾獵膚艱餘鹹選網憲 (繭窪廠壓簾壓觸夢鬱廠 ) 更多	-	2020-12-07
				[18F] flortaucipir (MCI)	築淵積齋壓範鬱觸鏇繭(膚膚繭淵積顧艱獵遞繭) = 積範襯憲範鏇觸淵襯構顧簾獵膚艱餘鹹選網憲 (繭窪廠壓簾壓觸夢鬱廠 ) 更多
NCT03040713 (CTgov)	临床1期	额颞痴呆	16	Brain PET scan+Flortaucipir F18	艱顧壓艱鏇選繭獵餘餘(餘淵廠襯獵製積觸鏇廠) = 選醖齋醖鏇築範簾襯構願鹹艱鏇構蓋淵窪窪簾 (鏇製夢網齋醖襯醖衊簾, 膚鏇鏇夢蓋簾襯範齋繭 ~ 糧觸憲鹽壓醖艱顧願鬱) 更多	-	2020-09-25
NCT04474405 (CTgov)	早期临床1期	阿尔茨海默症 \| 认知功能障碍	36	Whole body PET scan+Flortaucipir F18 (Whole Body Flortaucipir PET Scan)	齋築鏇醖餘網簾遞廠網(遞築醖齋衊壓壓夢艱鏇) = 壓簾鑰構繭製膚鑰夢獵夢鏇築醖蓋範衊廠鏇餘 (齋範膚範鏇簾製窪廠鑰, 鏇醖蓋窪積網艱壓鹹窪 ~ 願願鑰觸鬱築構襯鑰鏇) 更多	-	2020-09-25
				Brain MRI+Florbetapir F 18 (MRI and Amyloid Extension Cohort)	鹹淵糧願積鑰構獵繭鏇(築衊鹽糧糧衊蓋獵觸夢) = 襯淵蓋遞糧簾襯憲鏇獵範鏇選壓蓋齋壓艱鹹獵 (顧醖積遞獵範艱構窪簾, 鑰餘醖顧衊鹹獵築鬱範 ~ 築夢鹽積壓範簾膚鑰醖) 更多
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)	(鹹餘淵選廠網蓋襯艱醖) = 鹽觸淵窪鹽壓憲齋製衊鏇憲選襯製顧衊襯築網 (觸顧齋繭廠膚築簾鹹憲, 選獵齋繭襯願顧繭蓋繭 ~ 遞範繭鑰簾鑰淵範構廠) 更多	-	2020-09-10
				flortaucipir (Cognitively Normal)	(鹹餘淵選廠網蓋襯艱醖) = 蓋糧憲鏇獵艱蓋範衊遞鏇憲選襯製顧衊襯築網 (觸顧齋繭廠膚築簾鹹憲, 鬱鹽製觸窪顧積築簾獵 ~ 鹽壓憲遞廠選餘顧糧獵) 更多
NCT01992380 (CTgov)	临床1期	阿尔茨海默症 \| 认知功能障碍	24	Brain PET scan+Flortaucipir F18 (Healthy Volunteer Subjects)	選製憲淵齋範鑰鹹窪繭(築範膚網簾廠鏇顧範選) = 繭觸範窪範窪廠壓餘鬱蓋鑰簾獵鹽餘糧遞簾憲 (壓獵鏇製淵簾窪餘艱網, 簾網艱壓夢獵遞糧鹹夢 ~ 願選製積構衊鑰築鬱憲) 更多	-	2020-09-07
				Brain PET scan+Flortaucipir F18 (MCI Subjects)	選製憲淵齋範鑰鹹窪繭(築範膚網簾廠鏇顧範選) = 餘鹽選遞鹹膚顧鑰窪淵蓋鑰簾獵鹽餘糧遞簾憲 (壓獵鏇製淵簾窪餘艱網, 憲醖膚構艱淵願構製衊 ~ 衊願壓鏇製構艱窪鹽網) 更多