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

Columbia University

NCT06790394

/ 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 Date21 Oct 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

387

Literatures (Medical) associated with Florbetapir F-18

01 Oct 2025·European Journal of Nuclear Medicine and Molecular Imaging

Evaluating gray matter heterotopia with Florbetapir and Flortaucipir pet: a case report

Article

Author: Shu, Qiaoqiao ; Xu, Zhenchun ; Xiang, Xiaojiao ; Cai, Liang ; Feng, Yue

01 Sep 2025·Alzheimers & Dementia

Birth weight, incident dementia risk, and PET amyloid burden: The ARIC study

Article

Author: Dean F. Wong ; Mark Lee ; Marco Egle ; Kevin J. Sullivan ; Pamela L. Lutsey ; Andrea L. C. Schneider ; Renée C. Groechel ; Rebecca F. Gottesman ; Thomas H. Mosley ; Olivia M. Emanuel

Abstract:

INTRODUCTION:

The relationships among birth weight (BW), incident dementia, and amyloid beta (Aβ) are unknown.

METHODS:

Ten thousand four hundred seventy‐six Atherosclerosis Risk in Communities (ARIC) study participants without dementia reported their BW (1996–1998; low [< 5.5 lbs], medium [5.5–9.0 lbs], or high [> 9.0 lbs]), if premature (yes/no), and were followed for incident dementia ( N dementia = 2550) through 2019. A subset ( N = 312) had florbetapir positron emission tomography (2011–2014). BW was evaluated in association with dementia (Cox proportional hazards) and Aβ (logistic regression), adjusted for demographics, apolipoprotein E ε4, and vascular risk. Effect modification by race was explored.

RESULTS:

Neither low BW nor prematurity were associated with dementia. Dementia risk was elevated in Black (adjusted hazard ratio 1.95, 95% confidence interval 1.33, 2.86) but not White participants reporting high (versus medium) BW ( P‐ interaction = 0.001). BW was not associated with Aβ.

DISCUSSION:

Low BW was not associated with dementia or Aβ. High BW was associated with dementia in Black participants only. Further research should evaluate the role of BW in dementia etiology.

Highlights:

Low birth weight was not associated with an increased risk of incident dementia.The association between birth weight and incident dementia was modified by race.High birth weight was associated with dementia in Black adults.Odds of elevated standardized uptake value ratio was lower for those who were low birth weight.

01 Sep 2025·JAMA Neurology

Concordance Between Amyloid-PET Quantification and Real-World Visual Reads

Article

Author: Gatsonis, Constantine ; Soleimani-Meigooni, David N. ; Carrillo, Maria C. ; Schonhaut, Daniel R. ; Whitmer, Rachel A. ; Yadollahikhales, Golnaz ; Romanoff, Justin ; Hanna, Lucy ; Smith, Karen ; Iaccarino, Leonardo ; Apgar, Charles ; Koeppe, Robert A. ; Mundada, Nidhi S. ; Ranasinghe, Kamalini G. ; Cho, Hanna ; Rabinovici, Gil D. ; March, Andrew ; Windon, Charles ; Siegel, Barry A. ; Zeltzer, Ehud ; Blazhenets, Ganna ; Hillner, Bruce E. ; La Joie, Renaud

Importance:

With increased payer coverage and the advent of antiamyloid therapies, clinical use of amyloid positron emission tomography (PET) is likely to increase to help guide the diagnosis and treatment of patients with cognitive impairment. However, unlike most previous research studies, in clinical practice, scan acquisition is less standardized, interpretation typically relies purely on visual reads rather than scan quantification, and patients have more frequent comorbidities, all of which might compromise test accuracy.

Objective:

To compare visual interpretation of amyloid-PET in real-world clinical settings to scan interpretation based on central quantification, in order to assess the accuracy of clinical reads.

Design, Setting, and Participants:

This cross-sectional quality improvement study used data from the Imaging Dementia—Evidence for Amyloid Scanning study, collected between February 2016 and January 2018 and analyzed between December 2021 and April 2023. The setting included 294 imaging facilities in the US. Medicare beneficiaries 65 years or older with cognitive decline for whom Alzheimer disease was a diagnostic consideration were recruited by dementia specialists from their clinical practices.

Exposures:

Amyloid-PET with [18F]florbetapir, [18F]florbetaben, or [18F]flutemetamol.

Main Outcomes and Measures:

PET scans were visually interpreted as positive or negative by local radiologists or nuclear medicine physicians following approved guidelines. Independently, scans were centrally processed and quantified using the standardized Centiloid (CL) scale. We applied an a priori autopsy-based threshold of 24.4 CL to quantitatively define scan positivity.

Results:

Of 18 293 participants included in the parent study, scan images were available for 10 774 (59%), of which Centiloids were successfully calculated for 10 361 (96%). Median (IQR) patient age was 75 (71-80) years; 5245 patients (51%) were female, 6500 (63%) had mild cognitive impairment, and 3861 (37%) had dementia). Participants self-reported the following races and ethnicities: 1 Alaska Native (0%), 23 American Indian (0.2%), 188 Asian (1.8%), 316 Black (3.1%), 449 Hispanic or Latino (4.3%), 8 Native Hawaiian or Other Pacific Islander (0.1%), and 9125 White (88.2%). A total of 6332 scans (61%) were visually read as positive, and 6121 (59%) were quantitatively positive. Agreement between visual reads and quantitative classification was 86.3% (95% CI, 85.7%-87.0%; Cohen κ = 0.72; 95% CI, 0.70-0.73). A total of 5519 (53%) scans were positive visually and quantitatively (V+/Q+), 3416 (33%) were negative by both (V−/Q−), 813 (8%) were V+/Q−, and 602 (6%) were V−/Q+. Female sex (female: 4581/5241 [87.4%]; male: 4354/5109 [85.2%]; P =.001), White race (White race: 7900/9125 [86.6%]; non-White race: 1035/1225 [84.5%]; P =.046), and use of [18F]flutemetamol and [18F]florbetaben ([18F]flutemetamol: 559/628 [89.0%]; [18F]florbetaben: 2664/3032 [87.9%]; [18F]florbetapir: 5712/6690 [85.4%]; P &lt;.001), compared with [18F]florbetapir, were associated with higher visual-quantitative concordance. Scans within a 10- to 40-CL borderline positivity zone were more likely to be discordant.

Conclusions and Relevance:

This cross-sectional study found high concordance between local visual reads and central quantification of clinical amyloid-PET scans, supporting the validity of amyloid-PET visual reads in real-world clinical practice.

News (Medical) associated with Florbetapir F-18

09 Dec 2025

·pmlive.com

Novo Nordisk presents new findings on semaglutide in Alzheimer’s disease

Novo Nordisk has presented new findings from its phase 3 Evoke and Evoke+ trials on using semaglutide as part of Alzheimer’s disease (AD) treatment. The trials did not meet their primary endpoints; however, they still highlighted important biomarker findings. Semaglutide demonstrated reductions of up to 10% in biomarkers linked to AD and neuroinflammation that, despite not being a large enough change to have clinical impact, is still a notable result. Semaglutide is a glucagon-like peptide-1 (GLP-1) drug currently used in the treatment of type 2 diabetes, and as a weight management medication. Research into other possible indications of GLP-1 drugs is ongoing. There is high unmet medical need for treatment in AD, a progressive neurodegenerative disease which currently has no cure. The Alzheimer’s Drug Discovery Foundation (ADDF) made early investments in the science that led to the Evoke trials, stressing that the full pathophysiology of AD needs to be addressed in order to discover possible treatment. From 2011, the ADDF provided nearly $1m to Paul Edison’s phase 2 study of liraglutide, another injectable GLP-1 drug. Edison, a professor of neuroscience in the Faculty of Medicine at Imperial College London, said: “The metabolic pathway remains a compelling area of investigation, and we will continue to pursue rigorous studies to determine how therapies targeting these mechanisms can be optimised and combined to achieve greater impact for patients.” Founded in 1998, the ADDF is a foundation focused on accelerating the discovery and development of drugs to treat AD. It is the only public charity with this focus, and its funding has assisted in bringing to market the first Alzheimer’s PET scan (Amyvid) and blood test (PrecivityAD). “With more than 70% of the Alzheimer’s drug pipeline now focused on non-amyloid targets, the field is moving steadily toward an era of precision medicine and combination therapies,” said Howard Fillit, co-founder and chief science officer of the ADDF. “The Evoke trials are an important part of this progress, demonstrating how large-scale studies of novel pathways can deepen our understanding of Alzheimer’s biology.”

Phase 2Phase 3Clinical Result

13 Nov 2025

·www.prnewswire.com

Landmark JPAD Special Issue Highlights How Combination Therapies, Underpinned by New Era of Research, Are Poised to Redefine Alzheimer's Treatment

Innovative science convened by the Alzheimer's Drug Discovery Foundation is paving the way for a new, revolutionary era of precision care NEW YORK, Nov. 13, 2025 /PRNewswire/ -- The Journal of Prevention of Alzheimer's Disease (JPAD) today published a special edition in collaboration with the Alzheimer's Drug Discovery Foundation (ADDF), titled, "Combination Therapies for Alzheimer's Disease: Charting the Future of New Treatments and Prevention." This landmark issue builds upon the rapidly growing evidence that combination therapies will be essential to effectively treating Alzheimer's and provides a roadmap for advancing this critical research. "This JPAD issue arrives at a pivotal moment for the field," said Howard Fillit, MD, Co-Founder and Chief Science Officer at the ADDF. "The drug development landscape is changing, with multiple anti-amyloid therapies available and more than 70% of the Alzheimer's pipeline now aimed at novel targets informed by the disease's pathobiology. Alzheimer's is a complex condition that will ultimately require a precision approach, and it is crucial that we offer guidance to chart the path forward for a new generation of biomarker-powered clinical trials to evaluate drugs in combination." Combination therapies are already the gold standard in cancer care. The new JPAD edition provides a blueprint for expanding this approach to Alzheimer's disease and designing the next wave of combination trials – whether that be combining novel drugs with anti-amyloids, multiple novel drugs, or drugs with lifestyle interventions – to accelerate progress toward effective, personalized treatments. "With Alzheimer's science advancing at an unprecedented speed, this JPAD issue is especially timely," said Bruno Vellas, MD, PhD, President and Founder of IHU HealthAge in Toulouse. "The field is at a turning point – we now have the tools and the science to design the combination trials that will define the next era of Alzheimer's treatment. This issue provides the framework to do just that." Key highlights of the JPAD special issue include: Drug repurposing opportunities: Existing therapies from other disease areas, such as metabolic disease and schizophrenia, are being evaluated for use in Alzheimer's, opening new avenues for treatment. Integration of lifestyle interventions: Growing evidence from studies such as the landmark FINGER trial, led by Goodes Prize recipient Dr. Miia Kivipelto, demonstrates how combining drugs with diet, exercise, and other lifestyle changes can further prevent or slow disease progression. Emerging role of artificial intelligence: AI is increasingly being leveraged to identify promising drug combinations, optimize trial design, and accelerate discovery. Biomarker innovation: Developing and validating new biomarkers is essential to enable precision medicine and ensure patients receive the therapies most likely to benefit them as early as possible. "A critical next step is to further build out our biomarker guidance, as these tools will be vital to designing and running rigorous combination trials," said Suzanne Schindler, MD, PhD, Associate Professor of Neurology at the Washington University School of Medicine in St. Louis. "We now have multiple blood tests approved by the FDA to aid in Alzheimer's diagnosis, and this is only the beginning. Continuing to develop a diverse toolkit of biomarkers reflecting different pathologies and advancing digital technologies will be key to opening the door for precision care." There are already 20 ongoing trials evaluating combination therapy approaches in today's drug development pipeline, comprising 11% of all current trials. And many promising candidates remain on the horizon, including GLP-1 drugs like semaglutide. "We have entered a new era in Alzheimer's research, one that is embracing the complexity of the disease to build the foundations for personalized prevention and treatment," said Aaron Burstein, PharmD, Head of Search and Evaluation at the ADDF. "Combination therapy has already proven successful in other complex diseases, and this issue provides critical considerations for applying that strategy to Alzheimer's – offering hope for more effective treatments and better outcomes for patients worldwide." 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 21% more press release views with Request a Demo

Clinical Study

07 Oct 2025

·www.fiercebiotech.com

Lilly calls for \'urgent improvements\' in Europe to boost diagnostic testing for Alzheimer\'s

Eli Lilly says Alzheimer\'s disease experts are warning the disease “remains critically underdiagnosed\" across Europe. \n Eli Lilly is calling on European countries to make “urgent improvements” to their Alzheimer’s disease diagnostic testing practices just weeks after nabbing a new approval on the continent for its Alzheimer\'s therapy Kisunla.The Indianapolis Big Pharma has teamed up with leading Alzheimer\'s experts at this year\'s Alzheimer Europe Conference to call for “urgent improvements to diagnostic pathways to ensure people in Europe can benefit from new therapeutic innovation.”Lilly points to a recent survey, published in the Journal of Alzheimer’s Disease, that found 70% of clinicians believe biomarker tests, which can find evidence of Alzheimer\'s or dementia, are “important or extremely important.\" Still, such tests remain \"underutilized,\" according to Lilly\'s Oct. 7 release.The survey questioned clinicians who treat patients with mild cognitive impairment (MCI) and Alzheimer\'s in France, Germany, Italy, Spain, the U.K., Japan and the U.S. The team found that across these countries, fewer than 1 in 5 patients (15.2%) received biomarker testing to confirm the specific pathology, with those in Germany and the U.K. the least likely to receive these tests, according to the journal.As a result, experts warn Alzheimer\'s and dementia “remain critically underdiagnosed,” Lilly said in the release, which has the effect of \"denying patients the opportunity to access treatment and care options.\"Lilly markets Kisunla, which works as an amyloid-plaque-targeting therapy and has an FDA approval for early symptomatic Alzheimer\'s, which includes the MCI or the mild dementia stages of the disease.The drug was approved by the FDA last year and received a final European sign-off just last month.To qualify for the drugs, patients must have a confirmed amyloid pathology, which can be done via several routes including a PET scan, a blood test or an MRI.Lilly also markets Amyvid, which works as an injectable prescription imaging agent to find high level of plaques. These are a buildup of a protein called amyloid beta in the brain that, if found, can be ultimately used by patients or their doctors to help prescribe Alzheimer\'s meds such as Kisunla. More diagnoses of Alzheimer\'s also mean potentially more uptake for medicines. Rival drug Leqembi, marketed by Biogen and Eisai, was also approved in the EU earlier this year.“Emerging therapies that target the pathology of Alzheimer\'s disease offer hope to slow progression and delay the need for care services,” said Stéphane Epelbaum, M.D., Ph.D., associate vice president for international medical affairs at Eli Lilly, in a statement.“But this possibility hinges on early detection, as approximately one-third of individuals in early symptomatic stages of the disease will progress to more advanced clinical stages within one year. Timely and accurate diagnosis is essential to ensure patients can access the next generation of Alzheimer\'s disease care.”

$Lilly calls for \'urgent improvements\' in Europe to boost diagnostic testing for Alzheimer\'s$

Drug Approval

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

Clinical Result

Indication

Phase

Evaluation

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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	zjbtahnzgb = wbsdvzlbyh lbqymwweeh (pljxbuqnbx, eykbswyasv - vqgidxiqrp) View more	-	26 Aug 2024
NCT01683825 (CTgov)	Phase 4	Senile cardiac amyloidosis	23	florbetapir	psfarnhfmp(ivbcoztowa) = akbqxoqoao kdsrvztimo (iotvppjdsp, zllohoqxcr - xhvwxuoqay) View more	-	13 Apr 2022
NCT01767493 (CTgov)	Phase 4	Multiple Sclerosis, Relapsing-Remitting	19	[18F]Florbetapir PET imaging	njwtggkcye = vzlxmeqbrt lgvhvfoilw (vomjybdhus, evpzudehln - rzoyimkmcm) View more	-	27 Aug 2021
NCT01518374 (CTgov)	Phase 2	Alzheimer Disease \| Mild cognitive disorder	1,768	Florbetapir F 18	hnwwcmwqyg = iksudnhfyu smcuuyafiq (zvdnalkman, pdtijyaydw - gkcrtffndh) View more	-	14 Jun 2018
NCT02051790 (CTgov)	Phase 4	Alzheimer Disease	241	florbetapir F 18	glqcuwnuvg = fiisloeske ngmbyvbihg (hnqozskdrr, smmrvthtun - cyrzkksjso) View more	-	28 Sep 2015
NCT01890343 (CTgov)	Phase 2	Alzheimer Disease \| Frontotemporal Dementia	34	florbetapir 18F+18F-FDG (Frontotemporal Disorder)	xuovtrlgzz = knfnbumjno qykejqygxa (fjbhqlngwp, oxuagktgii - pjvysmpymx) View more	-	17 Sep 2014
NCT01890343 (CTgov)	Phase 2	Alzheimer Disease \| Frontotemporal Dementia	34	florbetapir 18F (Cognitively Normal)	xuovtrlgzz = ezyphwyvqf qykejqygxa (fjbhqlngwp, dfjeoykpdz - maoshsvqzn) View more	-	17 Sep 2014
NCT01662882 (CTgov)	Phase 2/3	Alzheimer Disease \| Mild cognitive disorder	48	florbetapir (18F) (AD Subjects)	ivjkvzjvut = fcarbybfia bhlzjottgy (munyenjldy, ldmoqxzmdq - muhcukemcr) View more	-	19 Sep 2013
NCT01662882 (CTgov)	Phase 2/3	Alzheimer Disease \| Mild cognitive disorder	48	florbetapir (18F) (Healthy Controls)	ivjkvzjvut = mwpzycdelb bhlzjottgy (munyenjldy, eshnrvrijb - adqrjisjpu) View more	-	19 Sep 2013
NCT00857415 \| NCT01447719 (Pubmed \| Lancet Neurol)	Phase 3	Plaque, Amyloid	59	Florbetapir PET imaging	uhcqqoypxp(fxpvkilarn) = yaawvsawum zbetzfjdjs (vaxlilxqwy, 78 - 98) View more	-	01 Aug 2012
NCT00857415 \| NCT01447719 (Pubmed \| Lancet Neurol)	Phase 3	Plaque, Amyloid	59	florbetapir (Autopsy)	uhcqqoypxp(fxpvkilarn) = mpdwrzhlnf zbetzfjdjs (vaxlilxqwy, 80 - 100) View more	-	01 Aug 2012
NCT01565382 (CTgov)	Phase 3	Alzheimer Disease \| Mild cognitive disorder	40	Florbetapir	zmeuvalrwm = wlqzgkwqkm aniunffqje (timfsouqvb, wlsasadops - orvviakrgq) View more	-	27 Jun 2012
NCT00857415 (CTgov)	Phase 3	Alzheimer Disease	226	florbetapir F 18 (Autopsy Cohort)	suemzqkcql = lmgbijxdqj hjnxgwgttk (eqhubzfbjv, dpajywzyws - ealoezjhvp) View more	-	07 May 2012
NCT00857415 (CTgov)	Phase 3	Alzheimer Disease	226	florbetapir F 18 (Specificity Cohort)	flkgakiggv = egwvcvbzyl vulojqargt (zfzpauhwic, vjduggrvew - rpsnxrrzzw) View more	-	07 May 2012

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