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更新于：2025-11-03

Florquinitau F18

更新于：2025-11-03

概要

概要

基本信息

药物类型

小分子化药、诊断用放射药物

别名

F18-MK6240、FLUORINE-18-MK6240、MK-6240

+ [7]

靶点

TAU

作用方式

调节剂、增强剂

作用机制

TAU调节剂(微管相关蛋白tau调节剂)、PET imaging(正电子发射断层成像术增强剂)

治疗领域

神经系统疾病其他疾病

在研适应症

阿尔茨海默症轻度认知障碍认知功能障碍+ [1]

非在研适应症-

原研机构

Merck Sharp & Dohme Corp.

在研机构

北京先通国际医药科技股份有限公司

University of CaliforniaEnigma Biomedical Group, Inc.

非在研机构

Merck Sharp & Dohme Corp.

Invicro LLC

权益机构

Ionis Pharmaceuticals, Inc.

Lantheus Holdings, Inc.

Nihon Medi-Physics Co., Ltd.

+ [12]

最高研发阶段申请上市

首次获批日期-

最高研发阶段(中国)临床3期

特殊审评快速通道 (美国)

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结构/序列

分子式C16H11FN4

InChIKeyKAXAUWZJVWGFDO-SJPDSGJFSA-N

CAS号1841444-25-4

关联

项与 Florquinitau F18 相关的临床试验

NCT06600880

/ Not yet recruiting临床1期IIT

Neuronavigation-guided Focused Ultrasound-induced Blood-brain Barrier Opening in Alzheimer's Disease Patients and Its Effects on Brain Amyloid and Tau

The primary purpose of this phase 1b study is to further assess the safety and reversibility of focused ultrasound induced blood-brain barrier opening (FUS-BBBO) in participants with Alzheimer´s Disease (AD) using a single-element transducer with neuronavigation guidance. Preliminary results from our phase 1a study demonstrate that our neuronavigation-guided FUS system was capable of safely and transiently open the BBB in participants with AD. The information collected in this new study may be used to design future clinical trials to ultimately provide a viable alternative for treatment of AD in a safe and noninvasive manner.
Our secondary objective includes the assessment of the therapeutic efficacy of FUS-BBBO in reducing amyloid beta and neurofibrillary tangles, the main hallmark pathologies of AD, using PET tracers. Based on our preclinical studies in AD transgenic mouse models, FUS-BBBO alone was able to reduce both the amyloid beta and tau protein load, resulting in improvements in behavioral tasks assessing memory. Therefore, in this new study, the effect of FUS-BBBO on the amyloid beta and tau protein load in patients with AD will be assessed through the use of PET tracers.

开始日期2026-08-01

申办/合作机构-

NCT06999434

/ Recruiting临床1期IIT

Exploring the Utility of [18F]3F4AP for Demyelination Imaging

The overall objective is to obtain an assessment of the pharmacokinetics of [18F]3F4AP in healthy volunteers and subjects with demyelinating diseases such as mild cognitive impairment (MCI), Alzheimer's Disease (AD), Multiple Sclerosis (MS), Spinal Cord Injury (SCI) and Spinal radiculopathy (SR).

开始日期2025-05-05

申办/合作机构

Yale University

[+2]

NCT07115238

/ Recruiting临床3期

A Phase 3, Multicenter Study to Evaluate the Efficacy and Safety of PET Visual Assessment Using XTR006 Injection for Detection of Brain Neurofibrillary Tangles (NFTs) in Elderly Subjects

The goal of this clinical trial is to evaluate the efficacy and safety of XTR006 injection PET visual reading in detecting brain neurofibrillary tangles (NFTs) in elderly subjects with Mild Cognitive Impairment (MCI), Alzheimer's Disease (AD), and cognitively normal individuals. The main question it aims to answer is:
• What is the sensitivity and specificity of XTR006 PET visual reading results compared to the truth standard across MCI, AD, and cognitively normal subjects?
Participants will:
* Receive XTR006 injection
* Undergo PET/CT scanning

开始日期2024-11-20

申办/合作机构

北京先通国际医药科技股份有限公司

100 项与 Florquinitau F18 相关的临床结果

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100 项与 Florquinitau F18 相关的转化医学

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100 项与 Florquinitau F18 相关的专利（医药）

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项与 Florquinitau F18 相关的文献（医药）

2025-09-02·JAMA Network Open

Abnormal Amyloid-β Duration, Tau, and Neurodegeneration in Cranial Images.

Article

作者: Chin, Nathaniel A ; Stephenson, Henry Gilreath ; Christian, Bradley T ; Asthana, Sanjay ; Van Hulle, Carol ; Du, Lianlian ; Langhough, Rebecca ; Johnson, Sterling C ; Okonkwo, Ozioma C ; Jonaitis, Erin ; Betthauser, Tobey J ; Bendlin, Barbara B ; Carlsson, Cynthia M

Importance:

It is unclear whether the duration of amyloid-β (Aβ) pathology is associated with neurodegeneration and whether this depends on the presence of tau.

Objective:

To examine the association of longitudinal atrophy with Aβ positron emission tomography (PET)-positivity (Aβ+) and the estimated duration of Aβ+ (Aβ+ duration), controlling for tau-positivity.

Design, Setting, and Participants:

Data for this longitudinal cohort study were drawn from the Wisconsin Registry for Alzheimer Prevention and the Wisconsin Alzheimer Disease Research Center Clinical Core Study. Participants who had 2 or more magnetic resonance imaging (MRI) visits, 1 Pittsburgh compound B (PiB) PET visit, and 1 MK-6240 PET visit with other covariates available were included. A replication analysis was conducted using data from the OASIS-3 dataset. All data were collected between June 1, 2009, and January 22, 2025. Follow-up times ranged from 1.0 to 13.0 years (median [IQR], 8.8 [5.9-10.6] years).

Exposures:

Sampled iterative local approximation (SILA)-estimated PiB PET uptake at baseline MRI was used to estimate Aβ+ and its duration at baseline MRI. MK-6240 PET uptake in the entorhinal cortex was used to create tau-positive and tau-negative groups using a threshold of 1.27 standardized uptake value ratio.

Main Outcomes and Measures:

SILA-based modeling of PiB PET data was used to obtain estimated Aβ+ duration at baseline MRI age. Linear mixed-effects models tested differences in atrophy between Aβ+ vs Aβ- individuals and with Aβ+ duration, controlling for individuals who were tau-positive (measured via MK-6240 tau PET) at their most recent PET scan within their MRI visits. Z-scored volumes in temporo-parietal regions of interest associated with AD dementia were assessed via a robust normative approach.

Results:

A total of 95 Aβ+ (median [IQR] age, 66.4 [61.1-70.4] years; 59 female [62.11%]) and 275 Aβ- (median [IQR] age, 60.2 [55.7-64.6] years; 183 [66.55%] female) individuals were included. Aβ+ (partial η2, 0.015-0.043) and tau-positivity (partial η2, 0.018-0.100) were independently associated with neurodegeneration, with generally small effect sizes. Aβ+ duration was associated with atrophy in a greater number of regions of interest than Aβ+ status alone with somewhat larger effect sizes (partial η2, 0.013-0.056). Results were mostly similar in the OASIS-3 dataset.

Conclusions and Relevance:

In this longitudinal cohort study, subtle neurodegeneration was observed soon after the onset of Aβ pathology. These results may be consistent with Aβ pathology as a pathological state.

2025-08-05·BIOCHEMISTRY

A Cooperative Model for Symmetric Ligand Binding to Protein Fibrils

Article

作者: DeGrado, William F. ; Grabe, Michael ; Shoichet, Brian K. ; Smith, Matthew S.

A hallmark of neurodegenerative diseases like Alzheimer's Disease (AD) and chronic traumatic encephalopathy (CTE) is the presence of toxic protein aggregates in neurons. In AD and CTE specifically, the protein tau forms insoluble fibrils that are hundreds of nanometers in length. Intriguingly, recent experimental structures suggest that tau ligands like the disaggregator EGCG and positron emission tomography (PET) tracers like GTP-1 and MK-6240 bind to tau fibrils in long stacks reflecting the symmetry of the protein across many binding sites. In these stacks, each ligand makes more contact with its symmetry mates than it does with the protein. To interpret the binding of these molecules and new ligands, we must understand the effects of the cooperativity between sites and the entropy coming from the number of sites. Here, we investigate a nearest-neighbors model of cooperativity and use statistical mechanics to derive binding isotherms for saturation and competition experiments. This model allows us to relate measured EC₅₀ and IC₅₀ values to the intrinsic binding affinity to a single site and to cooperativity across sites in ways resembling the Cheng-Prusoff Equation. Depending on the degree of cooperativity between molecular species, this model permits solutions that lack the steep binding curves expected from cooperative systems and even solutions resembling 2-site systems. We finally consider conditions for a fibril's detection in a PET scan and practical matters of fitting this model's parameters to data.

2025-05-01·ANNALS OF NUCLEAR MEDICINE

Highly specific amyloid and tau PET ligands for ATN classification in suspected Alzheimer’s disease patients

Article

作者: Ogura, Masato ; Kaneko, Chikako ; Hanyu, Haruo ; Yamao, Tensho ; Matsuda, Hiroshi

Abstract:

Objective:

This study aims to accurately classify ATN profiles using highly specific amyloid and tau PET ligands and MRI in patients with cognitive impairment and suspected Alzheimer’s disease (AD). It also aims to explore the relationship between quantified amyloid and tau deposition and cognitive function.

Methods:

Twenty-seven patients (15 women and 12 men; age range: 64–81 years) were included in this study. Amyloid and tau PET scans were performed using 18F-NAV4694 and 18F-MK6240, respectively. For each patient, amyloid and tau PET images were visually assessed and classified as either amyloid-positive or amyloid-negative, and as 18F-MK6240 Braak stage 0 (tau-negative) or Braak stages I–VI (tau-positive). Voxel-based morphometry of three-dimensional T1-weighted MRI was used to evaluate neurodegeneration. Amyloid and tau depositions were quantified using the Centiloid scale and standardized uptake value ratio (SUVR), respectively. Global cognitive function was assessed with the Mini-Mental State Examination (MMSE).

Results:

Patients were categorized into seven ATN profiles. Six patients (22%) exhibited a normal AD biomarker profile, 15 patients (56%) fell within the Alzheimer’s continuum, and 14 patients (52%) were diagnosed with AD. Additionally, six patients (22%) displayed non-AD pathological changes. Positive and negative findings of amyloid and tau PET were concordant in 24 patients (89%). Among the 14 patients diagnosed with AD, the Centiloid scale for amyloid deposition did not show a significant negative correlation with MMSE scores (r = 0.269, p = 0.451). In contrast, the SUVR for tau deposition in the neocortex exhibited a significant negative correlation (r = −0.689, p = 0.014), while tau deposition in the mesial temporal region did not show a significant correlation (r = 0.158, p = 0.763).

Conclusion:

Highly specific amyloid and tau PET scans, along with MRI, can be utilized to accurately classify ATN profiles in patients with cognitive impairment and suspected AD. The discordance in amyloid and tau PET findings in three patients allowed for a more precise AD diagnosis. Furthermore, tau PET imaging provided insight into the propagation of tau deposition in the neocortex beyond the mesial temporal region, which is associated with cognitive decline.

项与 Florquinitau F18 相关的新闻（医药）

2025-10-29

·搜狐新闻

mk6240前体;1841444-11-8;针对神经纤维缠结 (NFTs) 的正电子发射断层显像一种示踪剂、一种分子探针、靶向成像

MK6240前体相关信息一、基本性质简述英文名称：MK6240 Precursor中文名称：MK6240前体（注：该化合物无官方标准中文译名，科研领域常用英文名称或“MK6240前体”表述）CAS号：1841444-11-8核心特征：MK6240前体是合成正电子发射断层显像（PET）探针MK6240的关键中间产物，分子结构中含有可与放射性核素结合的活性官能团，具备良好的化学稳定性，可在特定实验条件下实现高效修饰，为后续放射性标记提供结构基础。其等电点、分子量等详细理化参数尚未在公开权威数据库中完整披露，需通过实验室检测或专项研究文献获取。二、应用原理MK6240前体的核心应用原理围绕“放射性标记-靶向显像”展开，以神经纤维缠结（NFTs）为检测目标，通过合成特异性PET探针实现病理特征的可视化，具体过程可分为三个关键环节：1. 放射性标记转化：MK6240前体分子结构中的活性基团（如含氟前体中的特定取代位点）可与正电子发射核素（常用氟-18，¹⁸F）发生亲核取代等特异性化学反应，在严格控制的实验条件（如适宜的反应温度、催化剂、反应时间）下完成放射性标记，生成具有放射性活性的MK6240显像探针。该过程需保障高标记效率（通常要求>50%）和高放射性比活度，以满足PET显像对灵敏度的要求，同时减少非标记杂质对显像结果的干扰。2. 体内靶向富集：经放射性标记的MK6240探针通过静脉注射进入人体后，可借助血脑屏障上的转运体或被动扩散作用进入中枢神经系统。由于MK6240分子通过结构设计实现了与NFTs核心成分——异常磷酸化tau蛋白的高度特异性结合，探针会在NFTs富集的脑区（如阿尔茨海默病患者的颞叶、顶叶等区域）特异性聚集，而在正常脑组织或无NFTs的区域分布较少，形成显著的“病灶-正常组织”放射性浓度差。3. PET显像检测：PET显像设备可捕捉MK6240探针发射的正电子与周围组织电子湮灭产生的γ光子，通过计算机断层扫描技术对γ光子信号进行重建，生成脑组织的三维放射性分布图像。医生可通过图像中高放射性信号区域的位置、范围及强度，直观判断NFTs的分布情况、聚集程度，进而为神经退行性疾病（如阿尔茨海默病）的诊断、病情分期及预后评估提供客观影像学依据。三、作用机理MK6240前体本身不直接发挥靶向显像作用，其作用机理核心体现为“前体-探针转化”及“探针-靶点结合”的协同效应，具体可从分子作用层面细化为以下两点：1. 前体的结构功能机理：MK6240前体的分子结构是实现放射性标记及后续靶向结合的基础。其分子骨架中不仅包含可与tau蛋白结合的核心母核结构，还引入了便于放射性核素标记的活性位点（如对氟-18标记友好的离去基团）。这种“靶向母核+标记位点”的双功能结构设计，使前体既能够通过标记反应转化为具有显像能力的探针，又能保障最终探针分子与tau蛋白的结合特异性，解决了“显像活性”与“靶向性”的协同问题。同时，前体的化学稳定性确保其在标记反应前可长期储存，且在反应过程中不易发生结构降解，保障标记产物的纯度。2. 探针的靶向结合机理：由前体转化而来的MK6240探针与NFTs中异常tau蛋白的结合遵循“锁钥模型”及“多重分子间相互作用”原理。MK6240分子的空间构象与tau蛋白纤维聚集体表面的特异性结合口袋高度适配，可通过氢键、疏水作用、π-π堆积及范德华力等多重非共价键相互作用形成稳定复合物。与其他tau蛋白显像探针相比，MK6240通过结构优化减少了与β淀粉样蛋白（Aβ）等其他脑内蛋白的非特异性结合，显著提升了对tau蛋白的选择性，其解离常数（KD）处于纳摩尔级水平，确保了在体内环境中与NFTs的高效结合及稳定滞留，为清晰显像提供了分子基础。四、药物研发相关进展MK6240前体的研发与应用始终围绕tau蛋白PET显像探针的临床转化展开，其研发历程及相关进展体现了“前体优化-探针开发-临床应用”的递进逻辑，具体可分为以下几个方面：1. 前体合成工艺优化研发：作为探针合成的关键原料，MK6240前体的合成工艺直接影响探针的生产成本、纯度及临床应用可行性。早期研发阶段，科研团队通过对反应路线的设计与筛选，确定了以廉价易得的起始原料（如取代苯胺、环状羧酸等）为基础的多步合成路线，重点解决了关键中间体的立体选择性合成问题（如手性中心的构建）。后续优化中，通过引入新型催化剂、调整反应溶剂体系及采用连续流反应技术，将前体的总收率从最初的不足10%提升至30%以上，同时通过柱层析纯化工艺的改进，使前体纯度达到99%以上，满足放射性标记对原料纯度的严苛要求。此外，研发过程中还建立了前体的质量控制标准，包括纯度检测（高效液相色谱法）、结构确证（核磁共振、质谱）及杂质限量控制，为探针的质量稳定性提供保障。2. 放射性标记工艺研发：针对MK6240前体的标记特性，研发团队开发了高效的氟-18标记工艺。早期采用传统的加热回流标记法，标记效率较低且反应时间较长（约60分钟）；后续通过优化反应条件，如使用极性非质子溶剂（如乙腈、二甲基亚砜）、提高反应温度（100-120℃）及加入相转移催化剂，将标记效率提升至60%-80%，反应时间缩短至20-30分钟。同时，研发了自动化标记模块，实现了前体标记、产物纯化（如高效液相色谱纯化、固相萃取）及无菌分装的一体化操作，不仅提高了标记过程的重复性和安全性，还满足了临床显像对探针快速供应的需求（氟-18半衰期仅109.8分钟）。3. 探针临床前与临床研发验证：以MK6240前体为原料合成的MK6240探针，已完成系统的临床前及临床研发验证。临床前研究中，在转基因小鼠模型（如PS19小鼠，可形成tau蛋白聚集）中证实，探针可特异性结合NFTs，且在脑内的清除速度适宜（半衰期约1-2小时），无明显脱氟现象（避免骨骼放射性干扰）。Ⅰ期临床研究（健康志愿者）显示，探针的药代动力学特征良好，安全性耐受性高，无严重不良反应；Ⅱ/Ⅲ期临床研究（阿尔茨海默病患者、轻度认知障碍患者及健康对照人群）进一步证实，探针可有效区分不同疾病状态人群的NFTs分布差异，与病理诊断结果的一致性较高，且可动态监测疾病进展过程中NFTs的变化，为疾病的早期诊断及治疗效果评估提供了可靠工具。目前，MK6240探针已在多个国家和地区获批用于临床tau蛋白显像，而前体的稳定供应及工艺优化是其临床转化的核心支撑。4. 衍生探针研发拓展：基于MK6240前体的结构优势，科研团队还开展了衍生探针的研发工作。通过对前体的分子母核进行修饰（如引入不同取代基）或改变标记核素（如尝试碳-11标记，半衰期20.4分钟，适用于短时间内多次显像），开发出一系列针对tau蛋白的新型显像探针。部分衍生探针在临床前研究中展现出更优的结合特异性或脑内药代动力学特征，为满足不同临床需求（如儿童患者显像、药物临床试验中的高频监测）提供了新的研发方向，而MK6240前体的合成经验为这些衍生探针的前体设计提供了重要参考。申明：仅实验室科研，不适应于人体，后果自负相关其他产品：AV1451 precursor OncoACP3 mk6240前体 NOTA-Pep-1L DOTA-Pep1-L供应商：上海楚肽生物科技有限公司返回搜狐，查看更多

临床1期临床终止

2025-10-29

·搜狐新闻

AV1451 precursor;1533432-50-6;用于合成放射性标记的tau蛋白显像剂分子探针、靶向、示踪

AV1451前体相关信息一、基本性质英文名称：AV1451 precursor中文名称：AV1451前体CAS号：1533432-50-6等电点：目前公开的权威化学数据库及文献中，暂未明确记载AV1451前体的等电点数据。该参数通常需通过实验室电泳法等实验手段，结合化合物的分子结构特征（如氨基、羧基等带电基团的解离常数）进行测定，具体数值可参考相关专业研究文献或实验报告。其他关键性质：作为合成AV1451的关键中间产物，AV1451前体通常具备一定的化学稳定性，可在特定的温度、湿度及溶剂体系中储存。其分子结构中含有可修饰的活性基团，为后续放射性核素标记提供了反应位点，这一结构特征是其作为前体化合物的核心基础。二、应用原理AV1451前体的核心应用原理围绕tau蛋白显像剂的合成展开，具体可分为两个关键环节：前体修饰与靶向结合。在修饰环节，AV1451前体分子结构中的活性基团可与放射性核素（如氟-18等常用正电子发射核素）发生特异性化学反应，实现放射性标记，生成具有放射性的AV1451显像剂。这一标记过程需严格控制反应条件，确保标记效率及产物的放射性比活度，以满足后续影像学检测的灵敏度要求。在靶向结合环节，经放射性标记后的AV1451显像剂进入生物体内后，可通过血脑屏障进入中枢神经系统。由于AV1451分子与tau蛋白的异常聚集物（如神经纤维缠结，是阿尔茨海默病等神经退行性疾病的特征性病理改变）具有高度的特异性结合能力，显像剂会在tau蛋白聚集区域富集。通过正电子发射断层显像（PET）等影像学技术，可检测到显像剂发出的放射性信号，从而实现对脑组织中tau蛋白分布及聚集程度的可视化成像，为疾病的诊断提供依据。而AV1451前体作为合成该显像剂的关键原料，其纯度、结构完整性直接影响后续标记效率及显像剂的靶向结合性能。三、药物研发相关应用AV1451前体在药物研发领域的应用主要聚焦于tau蛋白靶向显像剂的研发，以及以tau蛋白为靶点的治疗药物的研发支持，具体体现在以下几个方面：1. tau蛋白显像剂的核心合成原料：在阿尔茨海默病等tau蛋白相关神经退行性疾病的研发过程中，明确疾病的病理进展、评估治疗效果均需可靠的影像学检测手段。AV1451作为经典的tau蛋白PET显像剂，其合成依赖于高纯度的AV1451前体。研发过程中，科研人员需对前体的合成工艺进行优化，提高前体的产量与纯度，以降低显像剂的合成成本、提升显像剂质量，为显像剂的临床转化及应用奠定基础。例如，通过优化前体合成的反应温度、催化剂种类、反应时间等参数，可有效减少副产物生成，提高目标前体的收率。2. 疾病诊断方法研发的支撑：基于AV1451前体合成的显像剂，为tau蛋白相关疾病的早期诊断方法研发提供了关键工具。在研发过程中，科研人员可利用该显像剂开展动物实验及临床研究，验证显像剂对疾病不同阶段tau蛋白聚集的检测灵敏度与特异性，探索其在疾病早期筛查、鉴别诊断中的应用价值。同时，通过对显像结果的分析，可深入了解疾病进展过程中tau蛋白聚集的时空规律，为揭示疾病发病机制提供影像学证据。3. 治疗药物研发的评估工具：在以tau蛋白为靶点的治疗药物（如tau蛋白聚集抑制剂、tau蛋白降解促进剂等）研发中，AV1451前体合成的显像剂可作为疗效评估的重要手段。在药物临床试验阶段，通过给受试者注射显像剂并进行PET成像，可动态监测药物干预后脑组织中tau蛋白聚集量的变化，直观评估药物对tau蛋白病理改变的调控效果，为药物的有效性评价提供客观依据。此外，借助显像剂还可筛选出对tau蛋白聚集具有显著调控作用的候选药物，加速研发进程。4. 研发过程中的质量控制关键：由于AV1451前体的质量直接决定显像剂的性能，在研发过程中需建立严格的前体质量控制标准。包括对前体的纯度检测（如采用高效液相色谱法）、结构确证（如采用核磁共振光谱、质谱等方法）、杂质限量控制等，确保每一批次的前体均符合合成显像剂的要求，保障研发数据的可靠性及后续产品的安全性。申明：仅实验室科研，不适应于人体，后果自负相关其他产品：AV1451 precursor OncoACP3 mk6240前体 NOTA-Pep-1L DOTA-Pep1-L供应商：上海楚肽生物科技有限公司返回搜狐，查看更多

放射疗法

2025-10-28

·Business Wire

Enigma Biomedical USA announces FDA Acceptance of New Drug Application for florquinitau F-18 (MK-6240), a Tau PET Alzheimer’s Disease radiodiagnostic

KNOXVILLE, Tenn. & BEDFORD, Mass.--(BUSINESS WIRE)--Enigma Biomedical USA (EB USA) today announced that the Food and Drug Administration (FDA) has accepted a New Drug Application (NDA) for MK-6240 (florquinitau F-18), their Tau Positron Emission Tomography (PET) Alzheimer’s disease radiodiaganostic. The FDA previously granted MK-6240 fast track status, which is a recognition of the potential to address an important unmet need. MK-6240 specifically targets a pathological form of tau called tau neurofibrillary tangles (NFTs), a key hallmark in Alzheimer’s disease. In April 2025 Lantheus announced that MK-6240 met its co-primary endpoints in two pivotal studies and has now delivered on its promise to file the MK-6240 NDA in 3Q 2025. The FDA has set a Prescription Drug User Fee Act (PDUFA) target action date of August 13, 2026. Lantheus acquired the rights to MK-6240 in 2023 and engaged the Enigma Biomedical team to work on the development of MK-6240. “EB USA is extremely excited about NDA acceptance of the MK-6240 NDA filing and congratulate our partners at Lantheus for this significant accomplishment. This milestone is an important step in our committed journey to address critical unmet needs in neurodegenerative disease as well as providing tools and technologies to support the development of disease modifying therapies,” said Rick Hiatt, President and CEO of EB USA. “We are pleased the FDA accepted our NDA for MK-6240,” said Brian Markison, CEO, Lantheus. “By enabling early and accurate identification of tau accumulation, MK-6240 has the potential to enhance diagnostic confidence, personalize patient care, and, through ongoing monitoring, transform our understanding of disease progression. We are deeply grateful for the continued support and expertise of the Enigma team, whose contributions have been instrumental to the development of MK-6240.” About MK-6240 (florquinitau F-18) MK-6240 is designed to target aggregated tau protein in the form of neurofibrillary tangles (NFTs), a key hallmark of several neurodegenerative diseases, including Alzheimer’s disease. MK-6240 has demonstrated a high affinity for tau and limited off-target binding in both preclinical and clinical studies.1,2 Acquired by Lantheus in 2023, MK-6240 has received Fast Track designation and is currently being used in nearly 100 active clinical trials. We anticipate that MK-6240 will support earlier disease detection, patient staging, therapy selection, and monitoring, and may help enable tau to serve as a surrogate endpoint for treatment efficacy. About Enigma Biomedical – USA Enigma Biomedical USA’s vision is to be the premier provider of imaging biomarkers for neurological pathologies, associated information technology, and related tools to accelerate the development, approval, and adoption of effective therapies to treat neurodegenerative diseases. EB’s neuroimaging biomarkers provide Pharma and Academic researchers with state-of-the-art tools for enabling Disease-Modifying Therapy development with the highest precision and accuracy. In pursuit of this vision, subsidiaries of EB have sold the best-in-class Tau and Amyloid PET imaging biomarkers, MK-6240 and NAV-4694, to our partners to enable their research efforts. EB also recently announced a partnership with AbbVie to explore their novel 4R Tau PET Imaging Biomarkers. About Lantheus Lantheus is the leading radiopharmaceutical-focused company, delivering life-changing science to enable clinicians to Find, Fight and Follow disease to deliver better patient outcomes. Headquartered in Massachusetts with offices in New Jersey, Canada, Germany, Switzerland, Sweden and the United Kingdom, Lantheus has been providing radiopharmaceutical solutions for nearly 70 years. For more information, visit www.lantheus.com. Safe Harbor for Forward-Looking and Cautionary Statements This press release contains “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995, as amended, that are subject to risks and uncertainties and are made pursuant to the safe harbor provisions of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended. Forward-looking statements may be identified by their use of terms such as "continue,” “expects,” “may,” “moving closer,” “plans,” “poised,” “position,”“potential,” “will,” and other similar terms. Such forward-looking statements are based upon current plans, estimates and expectations that are subject to risks and uncertainties that could cause actual results to materially differ from those described in the forward-looking statements. The inclusion of forward-looking statements should not be regarded as a representation that such plans, estimates and expectations will be achieved. Readers are cautioned not to place undue reliance on the forward-looking statements contained herein, which speak only as of the date hereof. The Company undertakes no obligation to publicly update any forward-looking statement, whether as a result of new information, future developments or otherwise, except as may be required by law. Risks and uncertainties that could cause our actual results to materially differ from those described in the forward-looking statements include: (i) a delay in obtaining, or failure to obtain, a positive regulatory outcome from the FDA for MK-6240; (ii) our ability to launch MK-6240 as a commercial product; (iii) the market receptivity to MK-6240 as a radiopharmaceutical diagnostic; (iv) the existence, availability and profile of competing products; (v) our ability to obtain and maintain adequate coding, coverage and payment for MK-6240; (vi) the safety and efficacy of MK-6240; (vii) the intellectual property protection of MK-6240; (viii) our ability to successfully develop and scale the manufacturing capabilities to support the launch of MK-6240; and (ix) the risks and uncertainties discussed in our filings with the Securities and Exchange Commission (including those described in the RiskFactors section in our most recently filed Annual Report on Form 10-K and Quarterly Reports on Form 10-Q). 1 Krishnadas N, Doré V, Robertson JS, Ward L, Fowler C, Masters CL, Bourgeat P, Fripp J, Villemagne VL, Rowe CC. Rates of regional tau accumulation in ageing and across the Alzheimer’s disease continuum: an AIBL 18F-MK-6240 PET study. EBioMedicine. 2023 Feb;88:104450. doi: 10.1016/j.ebiom.2023.104450. Epub 2023 Jan 27. PMID: 36709581; PMCID: PMC9900352. 2 Lohith TG, Bennacef I, Vandenberghe R, Vandenbulcke M, Salinas CA, Declercq R, Reynders T, Telan-Choing NF, Riffel K, Celen S, Serdons K, Bormans G, Tsai K, Walji A, Hostetler ED, Evelhoch JL, Van Laere K, Forman M, Stoch A, Sur C, Struyk A. Brain imaging of Alzheimer dementia patients and elderly controls with 18F-MK-6240, a PET tracer targeting neurofibrillary tangles. J Nucl Med. 2019 Jan;60(1):107-114. doi: 10.2967/jnumed.118.208215. Epub 2018 Jun 7. PMID: 29880509.

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100 项与 Florquinitau F18 相关的药物交易

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研发状态

10 条进展最快的记录,

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适应症	最高研发状态	国家/地区	公司	日期
阿尔茨海默症	申请上市	美国	Enigma Biomedical Group, Inc.	2025-10-28
轻度认知障碍	临床3期	中国	北京先通国际医药科技股份有限公司	2024-11-20
认知功能障碍	临床3期	美国	University of California	2018-05-01
神经变性	临床3期	美国	University of California	2018-05-01

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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


NCT03706261 (CTgov)	临床1期	阿尔茨海默症	145	18F-Florbetaben+18F-MK-6240	築簾鑰願蓋夢構膚糧鬱(構膚淵衊糧鑰膚餘選範) = 齋齋繭襯範齋鬱醖糧簾襯構構鹹鑰繭齋餘簾廠 (衊鏇夢顧願衊艱願網願, 0.23) 更多	-	2025-08-01
NCT03373604 (CTgov)	临床2期	阿尔茨海默症	71	Lumbar Puncture (optional)+18F-MK-6240 (No Cognitive Impairment)	壓獵選選膚襯艱鹹製憲(築築膚鏇鑰積簾築簾鬱) = 網築顧鹹衊膚鹹鹹顧憲網積糧構繭糧憲鑰願淵 (鬱夢憲壓繭鏇網鹹築範, 0.43) 更多	-	2025-05-08
NCT03373604 (CTgov)	临床2期	阿尔茨海默症	71	Lumbar Puncture (optional)+18F-MK-6240 (Cognitive Impairment)	壓獵選選膚襯艱鹹製憲(築築膚鏇鑰積簾築簾鬱) = 壓積鏇簾觸壓蓋製壓鹽網積糧構繭糧憲鑰願淵 (鬱夢憲壓繭鏇網鹹築範, 0.92) 更多	-	2025-05-08
NEWS 人工标引	N/A	阿尔茨海默症	-	MK-6240	廠構鹹廠積簾壓餘選壓(蓋憲簾鑰積繭網繭齋積) = successfully met its co-primary endpoints in two pivotal studies assessing its sensitivity and specificity 構憲壓鹹製築衊製積窪 (餘廠艱廠製廠壓願憲願 ) 达到	积极	2025-04-30
NCT02562989 (6240-001 \| MK-6240-001, CTgov)	临床1期	阿尔茨海默症 \| 轻度认知障碍	13	[18F]MK-6240, ~185 MBq (Part 1, Healthy Young Participants)	醖淵壓鹹夢鬱淵壓壓獵 = 醖艱簾觸網壓範網醖鏇鏇夢鏇獵壓蓋憲窪繭壓 (醖餘構鏇構鏇壓鏇築蓋, 蓋襯廠顧憲蓋網衊衊壓 ~ 鑰鏇築鬱構壓醖繭蓋艱) 更多	-	2018-07-23
NCT02562989 (6240-001 \| MK-6240-001, CTgov)	临床1期	阿尔茨海默症 \| 轻度认知障碍	13	[18F]MK-6240, ~160 MBq (Part 2, Healthy Elderly Participants)	醖淵壓鹹夢鬱淵壓壓獵 = 夢淵獵糧襯範鑰壓鏇艱鏇夢鏇獵壓蓋憲窪繭壓 (醖餘構鏇構鏇壓鏇築蓋, 觸積鏇膚憲觸壓積鑰範 ~ 膚壓網壓積淵鑰築獵遞) 更多	-	2018-07-23