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.

Start Date01 Aug 2026

Sponsor / Collaborator-

NCT06790394

/ Not yet recruitingPhase 1

A Test-retest Study to Evaluate the Reproducibility of [18F]Florbetaben PET Imaging in Patients With Cardiac Amyloidosis and Control Patients

This study is an open-label study to evaluate and characterize test-retest reliability of [18F]florbetaben PET in subjects with AL-CA and ATTR-CA compared to non-CA subjects. Quantification of the [18F]florbetaben parameters related to the deposition of amyloid in the heart (such as Myocardial Tracer Retention (MTR) or Retention Index (RI)), and the variability in these parameters after repeated imaging will be evaluated. Measurement of blood metabolites and comparison of invasive with non-invasive quantification of [18F]florbetaben uptake in the heart will be performed.

Start Date01 Jun 2025

Sponsor / Collaborator

Life Molecular Imaging Ltd.

[+1]

NCT07012993

/ RecruitingPhase 2IIT

Evaluation of Ultralow Dose PET Imaging for Detecting Amyloid Tracer Uptake

The goal of this clinical trial is to evaluate an investigational ultralow dose PET imaging technique for Alzheimer's disease, mild cognitive impairment, other forms of dementia detection and monitoring. The main question it aims to answer is:
Can the investigators optimize the timing, scan duration, and image reconstruction to reduce the radiation dose 10-100 fold of the current clinical standard? Participants will be injected with a radioactive tracer called 18F-Florbetapir or 18F-Flutemetamol and be imaged on a new type of high-sensitivity PET scanner for up to 3 hours

Start Date20 May 2025

Sponsor / Collaborator

Nuclear Energy Institute

100 Clinical Results associated with Florbetapir F-18

100 Translational Medicine associated with Florbetapir F-18

100 Patents (Medical) associated with Florbetapir F-18

436

Literatures (Medical) associated with Florbetapir F-18

01 Jul 2025·JACC-Cardiovascular Imaging

Established and Emerging Fluorine-18–Labeled Cardiac PET Radiotracers

Review

Author: Malhotra, Saurabh ; Pelletier-Galarneau, Matthieu ; Packard, René R Sevag ; Dilsizian, Vasken ; Dorbala, Sharmila ; Chen, Wengen

Positron emission tomography (PET)/computed tomography is a major imaging strategy for cardiovascular disease characterization. Whereas multiple radioisotopes can be used for PET imaging of cardiac disease processes, fluorine-18 (¹⁸F) presents key advantages. These include availability as a unit dose given a favorable half-life of 109.7 minutes and a short positron range leading to a high spatial resolution. In this context, there is growing interest in the development of novel ¹⁸F-labeled probes applied to cardiac PET imaging, which in turn provide clinicians with new methods to evaluate disease pathways of interest. Beyond ¹⁸F-fluorodeoxyglucose, used in routine clinical practice to scrutinize myocardial viability, cardiac sarcoidosis, as well as prosthetic valve and cardiac device infection, new ¹⁸F-labeled radiopharmaceuticals have undergone clinical evaluation. These include ¹⁸F-flurpiridaz, which was recently approved by the U.S. Food and Drug Administration for myocardial perfusion imaging and that is also amenable to accurate myocardial blood flow quantitation, ¹⁸F-sodium fluoride to detect metabolically active epicardial coronary atherosclerotic lesions, and the ¹⁸F-labeled amyloid radiotracers florbetapir, flutemetamol, and florbetaben. This review will further explore emerging ¹⁸F-labeled probes applied to cardiac sarcoidosis, myocardial innervation, and ongoing fibrosis/fibroblast activation.

22 Jun 2025·EJNMMI Research

Head to head comparison of two PET/CT imaging agents, [¹⁸F]D3FSP ([¹⁸F]P16-129) and [¹⁸F]AV45, in patients with alzheimer's disease.

Article

Author: Kung, Hank F ; Alexoff, David ; Ploessl, Karl ; Wong, Dean F ; Kuwabara, Hiroto ; Dannals, Robert F

BACKGROUND:

A new β-amyloid (Aβ) targeting radiotracer, [¹⁸F]D3FSP ([¹⁸F]P16-129), for diagnosis of Alzheimer's disease (AD) is reported. This radiotracer is a deuterated N-methyl derivative of Amyvid (AV-45, florbetapir f18) which was FDA-approved in 2013. Deuteration may alter a tracer's PK such that imaging performance is improved. A head-to-head comparison between these two imaging agents was conducted in AD patients. A separate biodistribution study was conducted on six healthy subjects, and radiation dosimetry estimation was obtained.

RESULTS:

Eight patients, clinically diagnosed with Alzheimer's disease, had an average age of 61.1 ± 10.0 years, and an average MMSE score of 21 ± 4. Each patient underwent paired 90-minute dynamic PET/CT scans separately within a few weeks (323 ± 31 MBq of [¹⁸F]D3FSP or [¹⁸F]AV45; florbetapir f18). SUVR (50-70 min) and Distribution Volume Ratio (DVR) of 43 brain regions were evaluated. The average SUVR across cortical gray matter was 1.65 ± 0.21 for [¹⁸F]AV45 and 1.65 ± 0.23 for [¹⁸F]D3FSP, while global DVRs were 1.36 ± 0.14 and 1.37 ± 0.13 for [¹⁸F]AV45 and [¹⁸F]D3FSP respectively. Strong correlations (R² = 0.8-0.9) were observed between tracers for both SUVR and DVR, with slopes of ~ 0.9 (SUVR) and ~ 1 (DVR). No image artifacts or confounds influenced the visual interpretation of [¹⁸F]D3FSP compared to [¹⁸F]AV45.

CONCLUSIONS:

Results showed no difference between [¹⁸F]D3FSP and [¹⁸F]AV45 and no benefit of deuteration at the N-methyl site. Even so, [¹⁸F]D3FSP may be a useful alternative for PET/CT imaging of Aβ deposits in the brain as its binding characteristics were very similar to its non-deuterated analog, the FDA-approved drug [¹⁸F]AV45.

TRIAL REGISTRATION:

Clinicaltrials.org, NCT03902548. Registered 01/07/2018.

04 May 2025·Journal of Sulfur Chemistry

Small molecule heterocycles: design and synthesis of novel fluorescent Benzothiazoles for early detection of Alzheimer’s disease

Author: Sharma, Vijay ; Sundaram, G.S.M.

Diagnostic agents capable of imaging β-amyloid (Aβ) plaques at prodromal stages could provide noninvasive tools to assess plaque burden and assist in determining efficacy of disease-modifying therapeutic interventions in vivo.To accomplish this goal, FDA approved 18F-incorporated tracers, such as Florbetapir, Flutemetamol, and Florbetaben may allow quant. anal. of therapeutic efficacy of disease-modifying treatments that attenuate Aβ pathophysiol. in vivo.Although promising, these tracers show high off-target binding.Importantly, current anti-amyloid therapy also targets diffuse amyloid plaques (included in revised NIAAA criteria for detecting AD) and other forms of amyloid plaques.Therefore, mols. capable of detecting both diffuse and fibrillar plaque pathol. can potentially offer better quant. tools for interrogating efficacy of anti-amyloid therapy.To achieve this goal, herein, we report synthesis and characterization of new small organic mols.: ((Z,E)-4-(2-(6-(2-Fluoroethoxy)benzo[d]thiazol-2-yl)vinyl)-N,N-dimethylaniline), ((Z)-4-(2-(6-(2-(2-(3-Fluoropropoxy)ethoxy)ethoxy)benzo[d]thiazol-2-yl)vinyl)-N,N-dimethylaniline) and ((E)-4-(2-(6-(2-(2-(3-Fluoropropoxy)ethoxy)ethoxy)benzo[d]thiazol-2-yl)vinyl)-N,N-dimethylaniline) We also report preliminary investigations on binding affinity in vitro.While demonstrated a relatively higher affinity, both and showed moderate affinity for Aβ1-42 aggregates in vitro.Furthermore, all 3 agents showed ability to detect Aβ fibrillar and diffuse plaque pathol. in brain sections of APP/PS1 transgenic mice and post-mortem confirmed AD human brain tissue sections.

News (Medical) associated with Florbetapir F-18

28 Jul 2025

·www.prnewswire.com

Next Era of Alzheimer's Care Will be Defined by Precision Prevention

New U.S. study reflects growing role of lifestyle interventions, further highlighting need to study lifestyle and drugs in combination NEW YORK, July 28, 2025 /PRNewswire/ -- Results from the U.S. Study to Protect Brain Health Through Lifestyle Intervention to Reduce Risk (U.S. POINTER) released today strengthen the case for precision prevention, a strategy set to revolutionize Alzheimer's care by combining lifestyle changes with targeted therapeutics based on individual risk factors. "The future lies in precision prevention," said Dr. Howard Fillit, Co-Founder and Chief Science Officer of the Alzheimer's Drug Discovery Foundation. "We have seen this model succeed in cancer and heart disease, and with a growing body of evidence showing neither lifestyle nor drugs can stop Alzheimer's alone, now is the time to double down on studying the two in combination, which will lay the path for precision medicine." The ADDF is driving a new era of clinical trials that look at lifestyle and therapeutic interventions in tandem, including Dr. Miia Kivipelto's MET-FINGER study, which has created a blueprint for combination therapy studies going forward. The U.S. POINTER study, released during the Alzheimer's Association International Conference (AAIC) and published simultaneously in the Journal of the American Medical Association (JAMA), found multidomain lifestyle interventions supported cognitive health in aging populations. This builds on previous findings from Dr. Miia Kivipelto's original FINGER trial, the first to show the critical role of lifestyle changes in preventing dementia. U.S. POINTER showed its structured high-intensity lifestyle interventions benefitted participants regardless of their APOE4 carrier status, a genetic risk factor for Alzheimer's disease. This contrasts findings from the FINGER study, which showed benefit especially in carriers of APOE4, and further highlights the wide-reaching impacts of lifestyle changes. "The U.S. POINTER results validate the findings of the FINGER study in a more diverse U.S. population," said Dr. Kivipelto. "This is yet another proof point that lifestyle can have a tremendous impact on the brain. By developing personalized scientific approaches to match each patient's unique biomarker profile with a combined drug and prevention plan, we are redefining how we treat and prevent 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 development 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 development, biomarker, and prevention programs 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

Clinical Study

09 Jul 2025

·www.prnewswire.com

Transposon Receives Investment from the Alzheimer's Drug Discovery Foundation to Support Advancement of TPN-101 for the Treatment of Alzheimer's Disease

Building on the positive results of Phase 2 clinical trials in PSP and ALS, Transposon plans to initiate a Phase 2 clinical trial of TPN-101 for the treatment of Alzheimer's disease in Q4 2025 Concurrently, Transposon is advancing TPN-101 in the Phase 2/3 HEALEY ALS Platform trial SAN DIEGO, July 9, 2025 /PRNewswire/ -- Transposon Therapeutics, a biotechnology company focused on developing novel, orally administered therapies for the treatment of neurodegenerative and aging-related diseases, including amyotrophic lateral sclerosis (ALS), progressive supranuclear palsy (PSP), and Alzheimer's disease (AD), today announced that it has secured an investment from the Alzheimer's Drug Discovery Foundation (ADDF) to advance the development of TPN-101 for the treatment of AD. The company expects to initiate a Phase 2 clinical trial to study the effect of TPN-101 in patients with AD by the end of 2025. "We are delighted to be partnering with the Alzheimer's Drug Discovery Foundation to rapidly advance the development of TPN-101 for the treatment of Alzheimer's disease," said Dennis Podlesak, Chairman and Chief Executive Officer of Transposon Therapeutics. "Based on the positive results of our recently completed Phase 2 studies of TPN-101 in both PSP and ALS, we believe TPN-101 has the potential to provide a critically needed treatment option for a wide range of neurodegenerative diseases, including Alzheimer's, ALS, and PSP." In the Phase 2 clinical trial of TPN-101 in patients with PSP, TPN-101 was the first treatment to reduce CSF levels of neurofilament light chain (NfL) compared to placebo, a key biomarker of neurodegeneration in tauopathies such as PSP and Alzheimer's disease. TPN-101 also showed dose-related reductions in interleukin 6 (IL-6) cytokine levels, a biomarker of neuroinflammation that is elevated in PSP and correlates with disease progression and severity. In the Phase 2 clinical trial of TPN-101 in patients with C9orf72-related ALS and/or frontotemporal dementia (FTD), treatment with TPN-101 also reduced levels of NfL and IL-6 in the ALS population and showed a slowing of ALS disease progression as measured by the Revised ALS Functional Rating Scale (ALSFRS-R). "The ADDF has a long history of supporting and investing in approaches to combat the underlying pathology of aging including novel pathways like inflammation," said Howard Fillit, MD, Co-Founder and Chief Science Officer at the ADDF. "Transposon's advancement of TPN-101 to target neuroinflammation and the abnormally activated immune system is one of the many exciting new therapeutic approaches in development for Alzheimer's." Concurrent with the Phase 2 clinical trial to study the effect of TPN-101 in patients with AD, Transposon is advancing TPN-101 in the Phase 2/3 HEALEY ALS Platform trial. Further information about the HEALEY ALS Platform Trial can be found at HEALEY ALS Platform Trial. About the Alzheimer's Drug Discovery Foundation 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: . About Transposon Transposon Therapeutics, Inc. is a clinical-stage biopharmaceutical company focused on developing transformational therapies for the treatment of neurodegenerative and aging-related diseases, including PSP, ALS, and Alzheimer's disease. The company's lead clinical compound, TPN-101, is first-in-class to address LINE-1 reverse transcriptase for the treatment of neurodegenerative and autoimmune diseases. The company also has a discovery platform supporting a deep pipeline of novel therapies to address additional indications. About TPN-101 TPN-101 specifically inhibits the LINE-1 reverse transcriptase that promotes LINE-1 replication. LINE-1 elements are a class of retrotransposable elements that in humans are uniquely capable of replicating and moving to new locations within the genome. When this process becomes dysregulated, LINE-1 reverse transcriptase drives the overproduction of LINE-1 cDNA, triggering innate immune responses that contribute to the pathology of neurodegenerative, neuroinflammatory, and aging-related diseases. Contact: Rick Orr Transposon Therapeutics, Inc. (858) 535-4821 [email protected] SOURCE Transposon Therapeutics WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

Phase 2Clinical Result

08 Jul 2025

·www.prnewswire.com

Circular Genomics Receives $250K Investment from the Alzheimer's Drug Discovery Foundation (ADDF) to Advance First-in-Class Circular RNA Blood-Based Biomarker Tests for the Early Detection of Alzheimer's Disease

SAN DIEGO, July 8, 2025 /PRNewswire/ -- Circular Genomics, Inc., a global leader in circular RNA (circRNA) biomarkers for precision neurology and psychiatry, today announced it has received a $250,000 investment from the Alzheimer's Drug Discovery Foundation (ADDF) through its Diagnostics Accelerator (DxA) program. The funding will support further studies of Circular Genomics' circRNA blood-based biomarkers for diagnosing and predicting the progression of Alzheimer's disease (AD). Circular Genomics is developing the first blood-based tests that harness the potential of circRNA to enable personalized diagnosis and treatment for complex neurological and psychiatric conditions, such as AD. The investment, titled Alzheimer's Disease Specificity and Sensitivity Analyses of circRNA Blood Markers, will support research conducted in partnership with Carlos Cruchaga, PhD, Director, NeuroGenomics and Informatics Center at Washington University of Medicine in St. Louis. The project will further study the potential of circRNA biomarkers to improve the diagnosis of AD and specifically distinguish it from other dementias, helping shift diagnostic uncertainty into clarity for patients and their healthcare providers. "We are honored to receive this investment from the ADDF as we continue to advance our suite of circRNA-based tools aimed at addressing the need for reliable diagnosis and prognosis for neurological conditions such as Alzheimer's and present several advantages over current protein-based biomarkers. Proper diagnosis and treatment of Alzheimer's can be challenging due to the complex nature of the disease, leading to misdiagnosis or delayed diagnosis, prolonging suffering for patients and their families," said Nikolaos Mellios, MD, PhD, Co-founder and Chief Scientific Officer of Circular Genomics. "Our goal is to transform the diagnostic and treatment journey for patients —enabling earlier detection, better patient stratification, and more personalized clinical management of the disease." Dr. Cruchaga, a renowned expert in neurogenomics and biomarker discovery, added, "CircRNA biomarkers offer an exciting and promising approach for improving diagnostic accuracy and advancing personalized care for Alzheimer's as they may present several advantages over current protein-based biomarkers. I'm looking forward to working with Circular Genomics to progress this innovative technology with the goal of improving outcomes for individuals at risk of AD through an earlier and more accurate diagnosis." CircRNAs have been shown to play important roles in brain development, maturation, function, and aging and have been linked to many neurological and psychiatric disorders. Their abnormal expression in pathological states positions them as novel diagnostic and predictive biomarkers for numerous brain disorders. CircRNAs are mainly expressed in brains but can also be measured in blood, representing a window into overall brain health. The research will further quantify and characterize blood brain-derived circRNA biomarkers to help create best-in-class tools for predicting AD's progression and enabling a more accurate diagnosis. "Circular Genomics' work represents the type of innovative science needed to transform how we detect and diagnose Alzheimer's disease," said Howard Fillit, MD, Co-Founder and Chief Science Officer at the ADDF. "By investing in accessible and scalable biomarker technologies, such as this one, we aim to accelerate earlier and more accurate diagnosis, which is a critical step towards moving to treating Alzheimer's with precision medicine, so the right patients get the right treatments at the right time." The DxA is a $100M global research initiative aimed at fast-tracking the development of biomarkers and diagnostic tools to aid in the detection and diagnosis of Alzheimer's and related dementias. About Circular Genomics Circular Genomics is the world-leading developer of circular RNA-based precision medicine tools, data and diagnostics for precision neurology and psychiatry. Leveraging exclusive licenses and pioneering technologies in circular RNA, Circular Genomics is aiming to reshape the standard of care for major depressive disorder and other neurological and psychiatric diseases such as like Alzheimer's disease, Parkinson's disease, and Bipolar disorder. Initial products include assays to assess and tailor optimal treatment protocols for individual patients, resulting in more personalized and effective care. For additional details, please visit . 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: . About The Diagnostic Accelerator (DxA) The Diagnostics Accelerator, created in July 2018, is a $100 million global research initiative from partners including ADDF Co-Founder Leonard A. Lauder, Bill Gates, Jeff Bezos, MacKenzie Scott, the Dolby family, the Charles and Helen Schwab Foundation, The Association for Frontotemporal Degeneration, among others, to develop novel biomarkers for the early detection of Alzheimer's disease and related dementias. This research initiative is dedicated to accelerating the development of affordable and accessible biomarkers to diagnose Alzheimer's disease and related dementias and advance the clinical development of more targeted treatments. Through translational research awards and access to consulting support from industry experts, this program will challenge, assist and fund the research community in both academia and industry to develop novel peripheral and digital biomarkers. About the Neurogenomics and Informatics Center (NGI) at Washington University The NGI was founded in 2020 with the goal of identifying new biomarkers, and causal and druggable targets for neurological diseases, by performing deep molecular profiling of human samples. NGI investigators use a data-driven approach and integrate multi-tissue and multi-omic data with AI/ML to understand the biological processes implicated on Alzheimer's disease, Parkinson's disease, stroke and other neurodegenerative diseases which will lead to personalize biomarkers and treatments. SOURCE Circular Genomics WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

Clinical Study

100 Deals associated with Florbetapir F-18

External Link

KEGG	Wiki	ATC	Drug Bank
D09617	Florbetapir F-18	V09AX05	DB09149

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Alzheimer Disease	European Union	Eli Lilly Nederland BV	14 Jan 2013
Alzheimer Disease	Iceland	Eli Lilly Nederland BV	14 Jan 2013
Alzheimer Disease	Liechtenstein	Eli Lilly Nederland BV	14 Jan 2013
Alzheimer Disease	Norway	Eli Lilly Nederland BV	14 Jan 2013
Contrast agents	United States	Avid Radiopharmaceuticals, Inc.	06 Apr 2012

Developing

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Dementia due to Alzheimer's disease (disorder)	Phase 3	China	JYAMS PET Research & Development Ltd.	20 Oct 2022
Cognitive Dysfunction	Phase 3	United States	Avid Radiopharmaceuticals, Inc.	01 Jul 2011
Mild cognitive disorder	Phase 3	-	Avid Radiopharmaceuticals, Inc.	01 Feb 2011
Chronic Traumatic Encephalopathy	Phase 2	United States	Avid Radiopharmaceuticals, Inc.	01 Jun 2014
Lewy Body Disease	Phase 2	United States	Avid Radiopharmaceuticals, Inc.	01 Mar 2010
Striatonigral Degeneration	Phase 2	United States	Avid Radiopharmaceuticals, Inc.	01 Mar 2010
Frontotemporal Dementia	Phase 2	United Kingdom	Avid Radiopharmaceuticals, Inc.	01 Sep 2009
Parkinson Disease	Phase 2	United States	Avid Radiopharmaceuticals, Inc.	01 Jan 2009

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT04118764 (CTgov)	Not Applicable	Alzheimer Disease	6	Neuronavigation-guided single-element focused ultrasound transducer+Amyvid+Definity	pdobrrlftd = nagseixgsa wmjgzaeyqi (iflkkghnmq, dnitlgrwtt - jiurgxlrsf) View more	-	26 Aug 2024
NCT01683825 (CTgov)	Phase 4	Senile cardiac amyloidosis	23	florbetapir	fcxocwnfjn(msvihvblpm) = embypkvusp fcwafxyuwm (jfkkuzxbig, iycfqbxele - lzolqnhlgw) View more	-	13 Apr 2022
NCT01767493 (CTgov)	Phase 4	Multiple Sclerosis, Relapsing-Remitting	19	[18F]Florbetapir PET imaging	kbwsshoxau = qutuekzxvh kpalrvxnao (lxuwurrctt, dsrrfcddrg - ikddxngykq) View more	-	27 Aug 2021
NCT01518374 (CTgov)	Phase 2	Alzheimer Disease \| Mild cognitive disorder	1,768	Florbetapir F 18	kfiqjryfmm = ljmzlwwavr artgutcfqp (pvaiddmodb, ztjzfssfny - bkykogzwkg) View more	-	14 Jun 2018
NCT02051790 (CTgov)	Phase 4	Alzheimer Disease	241	florbetapir F 18	rxeiwztwrj = lxwxhrqxbz mohzfqenbj (lbbvzlsqsy, iypposwfrh - mgbglmmfcb) View more	-	28 Sep 2015
NCT01890343 (CTgov)	Phase 2	Alzheimer Disease \| Frontotemporal Dementia	34	florbetapir 18F+18F-FDG (Frontotemporal Disorder)	uzgrpcvcwl = jifuqgzris hmfcemlgbf (omtdmphaun, rubouzorxk - lcjddkzvou) View more	-	17 Sep 2014
NCT01890343 (CTgov)	Phase 2	Alzheimer Disease \| Frontotemporal Dementia	34	florbetapir 18F (Cognitively Normal)	uzgrpcvcwl = qmxfvvmpdz hmfcemlgbf (omtdmphaun, bylidkkccx - hpsijxuxjd) View more	-	17 Sep 2014
NCT01662882 (CTgov)	Phase 2/3	Alzheimer Disease \| Mild cognitive disorder	48	florbetapir (18F) (AD Subjects)	ueusskjvqx = qlahyipvzd faudrsvsyb (kzgoqmngpy, awnroapsxt - cbbxkubeew) View more	-	19 Sep 2013
NCT01662882 (CTgov)	Phase 2/3	Alzheimer Disease \| Mild cognitive disorder	48	florbetapir (18F) (Healthy Controls)	ueusskjvqx = hbhfesfxyn faudrsvsyb (kzgoqmngpy, rnadncbphs - mygamyxxfv) View more	-	19 Sep 2013
NCT01447719 (Pubmed \| Lancet Neurol)	Phase 3	Plaque, Amyloid	59	Florbetapir PET imaging	zfzhhaopqw(lndyesyqnh) = bwmdrzdjvu ajwyvmpicc (yzecyjprpv, 78 - 98) View more	-	01 Aug 2012
NCT01447719 (Pubmed \| Lancet Neurol)	Phase 3	Plaque, Amyloid	59	florbetapir (Autopsy)	zfzhhaopqw(lndyesyqnh) = ghshgckvgo ajwyvmpicc (yzecyjprpv, 80 - 100) View more	-	01 Aug 2012
NCT01565382 (CTgov)	Phase 3	Alzheimer Disease \| Mild cognitive disorder	40	Florbetapir	bxkhedsuvt = jyatrrpufr yjhrsechud (jrgbgfhawv, cjglmqlfnw - aqrrgfeapy) View more	-	27 Jun 2012
NCT00857415 (CTgov)	Phase 3	Alzheimer Disease	226	florbetapir F 18 (Autopsy Cohort)	rvmgcshqjk = ermjzxmdnp spchpcvjow (mutqujulhy, dfcphwlytw - ifjhqgjoim) View more	-	07 May 2012
NCT00857415 (CTgov)	Phase 3	Alzheimer Disease	226	florbetapir F 18 (Specificity Cohort)	bpstlbzxqv = hjiwhohxyf dwphpdooie (eazguvcebf, cftalnvdrs - lmitqpincd) View more	-	07 May 2012

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