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 2027

Sponsor / Collaborator

Columbia University

NCT07843459

/ Not yet recruitingPhase 1

A Placebo-Controlled, Single- and Multiple-Ascending Dose, Phase 1 Study to Evaluate the Safety, Tolerability, Pharmacokinetics, and Pharmacodynamics of LY4560736 in Healthy Participants and Participants With Alzheimer's Disease

The purpose of this study is to see how safe LY4560736 is and to see how much and how quickly LY4560736 gets into the bloodstream. For healthy participants, the study also looks at how much LY4560736 gets into the brain. This part of the study lasts up to 13 weeks which includes staying in the Clinical Research Unit (CRU) for at least 4 days. This group will include Japanese participants, and the Sponsor may choose to enroll Chinese participants. For participants with Alzheimer's Disease, the study will also look at levels of a specific Alzheimer's-related protein in the brain and will last up to 13 weeks which includes staying in the CRU twice, each lasts about 1 to 2 days. Japanese participants, and potentially Chinese participants, may also be enrolled in this group.

Start Date01 Oct 2026

Sponsor / Collaborator

Eli Lilly & Co.

NCT07787169

/ RecruitingPhase 1

A Master Protocol for Phase 1 Clinical Trials of Multiple Amyloid-Targeting Therapies for the Treatment of Alzheimer's Disease

The purpose of this Master Protocol is to support multiple studies looking at safety and tolerability of different drugs in healthy participants and participants with Alzheimer's disease, and if they remove clumps of protein (amyloid plaque) in the brain in participants with Alzheimer's Disease. Participants will enroll into either A1D-MC-AT01 (NCT07787182) or A1D-MC-AT02 (upcoming).

Start Date09 Sep 2026

Sponsor / Collaborator

Eli Lilly & Co.

100 Clinical Results associated with Florbetapir F-18

100 Translational Medicine associated with Florbetapir F-18

100 Patents (Medical) associated with Florbetapir F-18

385

Literatures (Medical) associated with Florbetapir F-18

01 Oct 2026·NUCLEAR MEDICINE COMMUNICATIONS

Quantitative AV-45 PET imaging for assessing treatment response to lecanemab and deep cervical lymphatic–venous anastomosis in Alzheimer’s disease

Article

Author: Jin, Luqiang ; Wang, Xu ; Song, Fahuan ; Hou, Jie ; Cheng, Aiping ; Bi, Yueqian ; Wen, Xuehua ; Lai, Fangyuan ; Wang, Xinyu

Objectives:

This study aimed to validate the clinical utility of visual and software-based quantitative AV-45 PET analyses and compare treatment effects between lecanemab and deep cervical lymphatic–venous anastomosis (dcLVA).

Methods:

This retrospective cohort study included Alzheimer’s disease patients who received 6-month lecanemab therapy or dcLVA surgery between July 2024 and 2025. AV-45 PET was performed 1 week before and 6 months after treatment. Standardized uptake value ratios (SUVRs) and centiloids (CLs) were obtained using visual and quantitative analyses. Agreement was assessed using Cohen’s κ and intraclass correlation coefficients (ICC). Receiver operating characteristic (ROC) analysis evaluated diagnostic performance. Logistic regression used Informant Questionnaire on Cognitive Decline in the Elderly score greater than or equal to 3.3 as the outcome.

Results:

Baseline characteristics were comparable between groups (all P > 0.05). Visual assessment showed good agreement with centiloid quantification ( κ = 0.72, ICC = 0.663). ROC analysis identified ΔCL as the optimal marker (area under the curve = 0.764, P = 0.026), with a cutoff of −11.5%. ΔCL ≥ −11.5% independently predicted cognitive decline in the lecanemab group (odds ratio = 10.281, 95% confidence interval = 1.289–82.005; P = 0.028). Cognitive decline was less frequent in the lecanemab group (23.5 vs. 81.8%; P < 0.001). ΔCL differed significantly between groups ( P = 0.006), whereas ΔSUVR did not.

Conclusion:

Visual and centiloid-based AV-45 PET analyses show good concordance for monitoring Alzheimer’s disease treatment response. ΔCL is a robust marker of lecanemab efficacy, which is superior to dcLVA in reducing amyloid-β burden and delaying cognitive decline.

01 Jul 2026·Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring

Visual read performance of ¹⁸ F‐Florbetapir and ¹⁸ F‐NAV4694 Aβ PET compared against Centiloid reference standard in a paired cohort

Article

Author: Feizpour, Azadeh ; Sutherland, Antony ; Toh, H. B. ; Doré, Vincent ; Poon, Aurora ; Gillman, Ashley G. ; Huang, Kun ; Kaewchur, Tawika ; Rowe, Christopher C. ; Villemagne, Victor L. ; Thientunyakit, Tanyaluck ; Fripp, Jurgen ; Bourgeat, Pierrick ; Paranawithana, Ishara

Abstract:

INTRODUCTION:

Visual assessment remains standard practice to rule out amyloid‐β (Aβ) pathology. 18 F‐NAV4694 (NAV) has high affinity for Aβ potentially detecting lower levels than other F‐18 Aβ tracers.

METHODS:

One hundred fifty participants in the AIBL study underwent both 18 F‐Florbetapir (FBP) and NAV Aβ PET scans. PET scans were assessed by six nuclear medicine physicians against Centiloid (CL) quantification. An optimized reference region was utilized for FBP as it improved CL–visual read correlations. Inter‐reader agreement of visual assessment was measured using Fleiss’ Kappa.

RESULTS:

Mean peak accuracy for visual read exceeded 95% for both NAV and FBP. However, peak accuracy for NAV visual reads was achieved at 14–15CL compared to 38–46CL for FBP. Higher inter‐reader agreement was observed for NAV compared to FBP.

DISCUSSION:

For mild to moderate elevation in Aβ, visual read of NAV is more sensitive and consistent than visual read of FBP by both experienced and novice readers.

01 May 2026·JPAD-Journal of Prevention of Alzheimers Disease

Discordance in amyloid positivity between visual reads and Centiloids: Impact of white matter uptake

Article

Author: Devanarayan, Viswanath ; Charil, Arnaud ; Reyderman, Larisa ; Kramer, Lynn D ; Irizarry, Michael C ; Reilhac, Anthonin ; Dhadda, Shobha ; Nelson, Todd M

BACKGROUND:

The visual interpretation of amyloid PET scans, or visual read (VR), is the most common technique used in clinical practice to identify the presence of cerebral amyloid plaques. Amyloid status (positive or negative) determined by VR or using a Centiloid (CL) cut-off shows high overall concordance. However, discordant cases can occur where the VR is positive, but the CL is below the positivity cut-off, or vice versa.

OBJECTIVES:

The objective of this analysis was to evaluate the rate of discordance and explore potential causes, particularly the role of amyloid tracer uptake in the white matter (WM), when determining amyloid status using VR and CL in screening for the elenbecestat phase 3 studies in early Alzheimer's disease (AD).

DESIGN:

Amyloid PET scans using either Florbetapir (Amyvid™), Florbetaben (Neuraceq™) or Flutemetamol (Vizamyl™) from 3,232 participants (1507 VR- and 1725 VR+) with cognitive impairment screened for the elenbecestat phase 3 studies in early AD were visually interpreted at screening by trained neuroradiologists and quantified using CL values.

SETTING:

Academic and clinical centers INTERVENTION/MEASUREMENTS: Quantitatively, amyloid positivity was defined as CL > 32.21. The number of positive cortical regions was determined by counting the number of regions with a standardized uptake value ratio (SUVr) that exceeded 1.17. PET SUVr levels in the cerebral WM were measured using an eroded WM region of interest (ROI). Statistical tests were conducted to detect differences among the four concordance groups, defined by the relationship of VR and CL status (positive or negative). Additionally, tests examined the relationship between uptake in the WM and rates and type of discordance. Receiver operating characteristic (ROC) analysis and DeLong's test were also used to examine the effect of different tracers on the discordant rates.

RESULT:

Discordance was observed in 6.53% of cases (n=211), with VR+/CL- in 4.61% (n=149) and VR-/CL+ in 1.92% (n=62). VR+/CL- discordant cases had significantly fewer amyloid-positive cortical regions compared to both VR+/CL+ and VR-/CL+ cases. VR-/CL+ cases had a significantly higher WM uptake than VR-/CL- and VR+/CL- cases. Our findings revealed a relationship between WM uptake and rates and types of discordance. High WM uptake can erroneously lead to CL+, due to gray matter (GM) contamination from the WM, and VR- status, due to reduced contrast between WM and GM, resulting in VR-/CL+ cases. Conversely, low WM uptake can result in an underestimation of CL values, inaccurately classifying a scan as CL-, and at the same time, the increased contrast may result in a VR+, thereby increasing the occurrence of discordant VR+/CL- cases.

CONCLUSION:

Variations in WM uptake significantly contribute to discordances by introducing positive or negative bias in CL values and altering the GM to WM contrast, which forms the basis of the VR. Nevertheless, the rates of discordant cases are low and VR represents a robust and validated method to determine the presence of amyloid deposition. VR enables enrolling patients with amyloid beta pathology, as seen on amyloid PET scans, whereas CL scaling was developed to provide standardized units that more consistently characterize longitudinal amyloid‑β change. These findings reflect the complementary roles of VR and CL in amyloid PET evaluation, with implications for refining diagnostic accuracy and disease monitoring in AD clinical trials and practice.

News (Medical) associated with Florbetapir F-18

20 Aug 2026

·www.prnewswire.com

FDA Clearance of C2N Diagnostics' PrecivityAD2 Blood Test Advances Precision Medicine for Alzheimer's, Building on Groundwork Laid by Early ADDF Investment

First Alzheimer's blood test cleared for patients as young as 40, advancing the ADDF's long-standing push to close the gap between early pathology and early detection Milestone reflects nearly two decades of sustained ADDF investment, expanding access to scalable blood-based diagnostics to bring about a new era of clinical care NEW YORK, Aug. 20, 2026 /PRNewswire/ -- The U.S. Food and Drug Administration announced today that it has cleared C2N Diagnostics' PrecivityAD2 blood test for use in adults as young as 40 who are experiencing signs of cognitive impairment, making it the first FDA-cleared Alzheimer's blood test available to patients this young. The clearance builds on nearly 20 years of ADDF investment in C2N's science and reflects the growing momentum of blood-based diagnostics in bringing earlier, more accurate detection into mainstream care and moving the field toward a new era of precision medicine. "Today's clearance reflects how rapidly the field is advancing. Just over a year ago, there were no FDA-cleared blood tests for Alzheimer's and now we have three," said Isobel Coleman, Chief Executive Officer of the ADDF. "This is a proof point that sustained, early investment in translational science plays a catalytic role in moving promising ideas from the lab to patients. The ADDF first invested in C2N nearly two decades ago and has stayed committed as the technology matured into a diagnostic that is now transforming how Alzheimer's is detected and diagnosed. As PrecivityAD2 and tools like it move further into clinical practice, they will enable earlier detection, sharpen clinical trials, and build the foundation for precision medicine and combination therapies." The field has long recognized that Alzheimer's pathology can begin 15 to 20 years before symptoms appear. Closing that gap has been a key focus of the ADDF's work, and validated tools that reach patients earlier, including those in their 40s and 50s, help pave the way for earlier detection and, ultimately, earlier treatment. The ADDF's partnership with C2N Diagnostics began in 2008 with early seed funding that catalyzed the development of PrecivityAD, the first blood test to help diagnose Alzheimer's. This support has continued, including a $7 million investment through the ADDF's Diagnostics Accelerator (DxA), helping to establish blood-based biomarkers as a cornerstone of modern Alzheimer's research and care. Today's decision follows the FDA's clearance of Fujirebio's Lumipulse blood test, another ADDF-funded diagnostic, underscoring how early investment is driving a new generation of Alzheimer's blood tests for clinical use. The FDA's clearance of PrecivityAD2 comes at a pivotal moment, with the Alzheimer's field advancing at an unprecedented pace. PrecivityAD2 is part of the ADDF's robust diagnostics portfolio, which includes 47 active programs spanning seven different pathways. The ADDF is focused on advancing the next generation of biomarkers, including blood tests for tau and other mixed pathologies, multi-marker panels, AI-driven approaches, and diagnostics that reflect the broader pathobiology of the disease, which are key to enabling more precise treatment strategies tailored to individual patients. "PrecivityAD2 reflects how far biomarker science has come, and it points to an even bigger opportunity ahead," said Laura Nisenbaum, PhD, Interim Chief Science Officer at the ADDF. "Tests like this don't just help to diagnose Alzheimer's, they can also identify the right patients for a clinical trial and confirm whether a drug is engaging its target. That kind of precision is already reshaping trial design: 83% of active Alzheimer's trials now incorporate a biomarker. As we validate the next generation of tools, we will move closer to the same transformative approach already common in cancer care: being able to match the right drugs to the right patient at the right time." 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 nearly $400 million to fund 792 Alzheimer's drug development, biomarker, and prevention programs in 21 countries. To learn more, please visit: . SOURCE Alzheimer's Drug Discovery Foundation 21% more press release views with Request a Demo

Diagnostic Reagents

18 Aug 2026

·www.prnewswire.com

Cortechs.ai Announces FDA Clearance for NeuroQuant® PET: Advancing Molecular Imaging for Cognitive Impairment

COVINGTON, Ky., Aug. 18, 2026 /PRNewswire/ -- NeuroQuant ® PET has received FDA 510(k) clearance (K261916) for PET. NeuroQuant PET ® aids physicians in the evaluation of patient pathologies and the clinical interpretation of PET performed for the assessment of cognitive impairment and other neurological conditions. Continue Reading NeuroQuant ® PET by Cortechs.ai has received FDA 510(k) clearance (K261916) for PET. As molecular imaging plays an increasingly central role in the diagnosis and management of Alzheimer's disease and related neurodegenerative disorders, the demand for standardized, objective PET analysis continues to grow. NeuroQuant® PET is designed to deliver fully automated quantification, regional analysis, and structured reporting directly into routine clinical workflows. "Automated quantitative PET imaging represents the next frontier in precision and personalized medicine for Alzheimer's disease and related neurocognitive disorders. These new technological advancements are enabling the shift from phenotype-based assessment to a biological, biomarker-driven approach in assessing neurodegenerative disease. I am excited about the role NeuroQuant PET will play in shaping the future of how these conditions are understood and managed." said Dr. Ana Franceschi, M.D., Ph.D. The platform provides atlas-based quantification for amyloid PET tracers, generating standardized uptake value ratios (SUVRs) and structured reports to support consistent, data-driven interpretation. NeuroQuant® PET segments regions of interest and quantifies Centiloids for commonly used amyloid PET tracers flutemetamol, florbetaben, and florbetapir, enabling standardized comparison across tracers and imaging systems. Compatible with PET-CT, PET-MR, and PET-only workflows, NeuroQuant® PET features fully automated processing and PACS-ready outputs designed to integrate quantitative metrics into existing workflows. "NeuroQuant® PET reflects our commitment to advancing quantitative imaging in dementia care, giving clinicians objective, reproducible measurements they can trust, so patients get earlier answers and more confident treatment decisions" said Kyle Frye, CEO of Cortechs.ai. "With FDA 510(k)-clearance status, we look forward to expanding access to standardized PET quantification that supports precision medicine in Alzheimer's disease and related dementias." About Cortechs.ai Cortechs.ai is the leader in AI applications in radiology, leveraging advanced technologies in medical imaging to enhance disease screening and timely assessment, empowering healthcare providers to deliver better outcomes for patients. The company develops and markets innovative medical imaging solution software for assessing neurological disorders such as Alzheimer's disease, epilepsy, multiple sclerosis, brain trauma, tumors and prostate cancer, helping clinicians identify and monitor clinically significant cases. Cortechs.ai's industry-leading imaging solutions offer radiologists, oncologists, and urologists streamlined, cost-effective tools to assist in the assessment of brain and prostate health, including cancer evaluation. Visit  for additional insights and follow us on Twitter, LinkedIn, and Facebook. For more information, please contact: [email protected] +1 858 459 9700 SOURCE Cortechs.ai 21% more press release views with Request a Demo

14 Jul 2026

·www.prnewswire.com

Diranersen Results at AAIC Provide First Evidence That Targeting Tau May Slow Cognitive Decline, Signaling Momentum Toward Addressing the Full Pathobiology of Alzheimer's

New data show greater tau reduction at higher doses but strongest clinical signal at lowest dose, raising key questions about optimal dosing in further trials, says the ADDF NEW YORK, July 14, 2026 /PRNewswire/ -- Today at the Alzheimer's Association International Conference (AAIC), Biogen presented results from the phase 2 CELIA study of diranersen (BIIB080), an investigational therapy designed to target tau in people with early Alzheimer's disease. While the study failed to meet its primary endpoint of demonstrating dose response-related effects on change in Clinical Dementia Rating-Sum of Boxes (CDR-SB), the new data showed strong biomarker effects, including reductions in CSF tau and tau PET, as well as clinical effects at lower doses, raising important questions about the optimal dose and design of future trials. "These are the first data from a randomized trial to show a tau-targeting drug producing both a robust biomarker effect and a signal of clinical benefit," said Laura Nisenbaum, PhD, Interim Chief Science Officer at the Alzheimer's Drug Discovery Foundation (ADDF). "Tau is one of the two defining pathologies of Alzheimer's disease and has long been difficult to target, which makes these results all the more notable. But the dose-response discordance between the biomarker and clinical endpoints raises important questions about the optimal level of tau reduction and the right dose of diranersen to test in subsequent studies. Those questions will be central to designing the strongest possible phase 3 program." The central unanswered question from the study is the discordance between the biomarker and clinical findings. Higher doses led to greater tau reduction, while the lowest dose showed the strongest clinical signal. Biogen has said these results support advancing diranersen into further trials as it continues to analyze the full data to understand why the biomarker and clinical effects diverged and what that means for future trial design. With disease-modifying anti-amyloid therapies now available, tau represents an important opportunity to expand Alzheimer's treatment options beyond a single target. The Alzheimer's therapeutic pipeline continues to broaden, with 75% of current clinical trials aimed at pathways beyond amyloid and tau, including inflammation, neurotransmitters, and metabolic dysfunction. This growing range of potential therapeutic approaches is essential to the future of Alzheimer's care, as the field moves toward treatments that can be individualized and combined based on each person's underlying disease biology. "Alzheimer's is a complex disease, and these results are another signal that drug development is moving in the right direction: beyond a single target and toward a broader arsenal of therapies that address the full pathobiology," said Isobel Coleman, Chief Executive Officer of the ADDF. "Tau is one of the core pathologies we will need to tackle if we are going to make combination therapy a reality. There is still more to learn, but progress like this helps move the field closer to the precision medicine future the ADDF has championed for decades." 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 nearly $400 million to fund 792 Alzheimer's drug development, biomarker, and prevention programs in 21 countries. To learn more, please visit: . SOURCE Alzheimer's Drug Discovery Foundation 21% more press release views with Request a Demo

Phase 2Clinical Result

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
Aphasia, Primary Progressive	Phase 2	United Kingdom	Avid Radiopharmaceuticals, Inc.	23 Aug 2011
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

Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT03333551 (CTgov)	Phase 4	Senile cardiac amyloidosis	4	amyvid	vqxwempcck(geqdetylkf) = bqdzlpvlsh dzvfmfhwan (hfinbihmri, hxtccqlija - hbmdlobflm) View more	-	16 Jul 2026
NCT04118764 (CTgov)	Not Applicable	Alzheimer Disease	6	Neuronavigation-guided single-element focused ultrasound transducer+Amyvid+Definity	vawtjqmmxl = yzfrvyklsw nibwmitgyu (tewfhozcbn, mbruukgarh - jsuqllivpd) View more	-	26 Aug 2024
NCT03977584 (CTgov)	Phase 2	Alzheimer Disease	114	Crenezumab (Crenezumab - Mutation Carriers)	sskgoyiyxh(urmhqpkvst) = yhdnlsrism vdobitozcd (ldvxvhfajk, 0.00752) View more	-	15 Mar 2024
NCT03977584 (CTgov)	Phase 2	Alzheimer Disease	114	placebo+\[\^18F\]GTP1+crenezumab (Placebo - Mutation Carriers)	sskgoyiyxh(urmhqpkvst) = vedzuuatii vdobitozcd (ldvxvhfajk, 0.00768)	-	15 Mar 2024
NCT01683825 (CTgov)	Phase 4	Senile cardiac amyloidosis	23	florbetapir+F	uvebnapnjw(aumbsflezx) = booxryeqbo ymaebumnyv (nehsfwuvkj, yhoksysyhe - qyjheaiccl) View more	-	13 Apr 2022
NCT01767493 (CTgov)	Phase 4	Multiple Sclerosis, Relapsing-Remitting	19	[18F]Florbetapir PET imaging	gwtdvqnyua = epltlcvlip neigaixegf (qklbeelkyc, exxncuejis - megqhizwvb) View more	-	27 Aug 2021
NCT01518374 (CTgov)	Phase 2	Alzheimer Disease \| Mild cognitive disorder	1,768	Florbetapir F 18	hpkwoyupsl = zyyukyncde sgihnouakp (ibgjfxzlbm, ihrtquqbuz - brmpiquxtq) View more	-	14 Jun 2018
NCT02051790 (CTgov)	Phase 4	Alzheimer Disease	241	florbetapir F 18	ccmiazonbr = ifarwbayaz rbnbvqhukm (otubbdosie, bejhhzqboh - rstoxtfcyh) View more	-	28 Sep 2015
NCT01890343 (CTgov)	Phase 2	Alzheimer Disease \| Frontotemporal Dementia	34	florbetapir 18F+18F-FDG (Frontotemporal Disorder)	cktkdfgjkk = ymkhyhzfyy gjgjmmujbd (nbekzncxlp, przdbgpcvm - dixclajayj) View more	-	17 Sep 2014
NCT01890343 (CTgov)	Phase 2	Alzheimer Disease \| Frontotemporal Dementia	34	florbetapir 18F (Cognitively Normal)	cktkdfgjkk = mbozpcxunn gjgjmmujbd (nbekzncxlp, lsygmtdveg - rdxblpssqm) View more	-	17 Sep 2014
NCT01662882 (CTgov)	Phase 2/3	Alzheimer Disease \| Mild cognitive disorder	48	florbetapir (18F) (AD Subjects)	rxkmoxniey = wtnlzpulra lpaaofxpbw (mgsqpirmpr, ozzdqwytya - riwergosni) View more	-	19 Sep 2013
NCT01662882 (CTgov)	Phase 2/3	Alzheimer Disease \| Mild cognitive disorder	48	florbetapir (18F) (Healthy Controls)	rxkmoxniey = bqurprhwti lpaaofxpbw (mgsqpirmpr, rvcqgxmicx - sgnpxmcsto) View more	-	19 Sep 2013
NCT00857415 \| NCT01447719 (Pubmed \| Lancet Neurol)	Phase 3	Plaque, Amyloid	59	Florbetapir PET imaging	qgdtufkyhl(igxstqecnf) = ubrpvalnpa txfitgrjxm (wmjjlexxjt, 78 - 98) View more	-	01 Aug 2012
NCT00857415 \| NCT01447719 (Pubmed \| Lancet Neurol)	Phase 3	Plaque, Amyloid	59	florbetapir (Autopsy)	qgdtufkyhl(igxstqecnf) = nuiqoobgry txfitgrjxm (wmjjlexxjt, 80 - 100) View more	-	01 Aug 2012

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