Avid Radiopharmaceuticals is an American company, founded by Dr. Daniel Skovronsky, and based at the University City Science Center research campus in Philadelphia, Pennsylvania. The company has developed a radioactive tracer called florbetapir . Florbetapir can be used to detect beta amyloid plaques in patients with memory problems using positron emission tomography scans, making the company the first to bring to market an FDA-approved method that can directly detect this hallmark pathology of Alzheimer's disease. Venture investors include Alta Partners, Osage University Partners, and Safeguard Scientifics.Eli Lilly and Company announced on November 8, 2010, that they would acquire Avid for $800 million, with $300 million paid out up front and the balance paid later on. Wikipedia.
Landau S.M.,University of California at Berkeley |
Landau S.M.,Lawrence Berkeley National Laboratory |
Landau S.M.,Avid Radiopharmaceuticals |
Mintun M.A.,Avid Radiopharmaceuticals |
And 7 more authors.
Annals of Neurology | Year: 2012
Objective: Using data from the Alzheimer's Disease Neuroimaging Initiative (ADNI) population, we examined (1) cross-sectional relationships between amyloid deposition, hypometabolism, and cognition, and (2) associations between amyloid and hypometabolism measurements and longitudinal cognitive measurements. Methods: We examined associations between mean cortical florbetapir uptake, mean 18F-fluorodeoxyglucose-positron emission tomography (FDG-PET) within a set of predefined regions, and Alzhiemer's Disease Assessment Scale (ADAS-cog) performance in 426 ADNI participants (126 normal, 162 early mild cognitive impairment [EMCI], 85 late MCI [LMCI], 53 Alzheimer disease [AD] patients). For a subset of these (76 normal, 81 LMCI) we determined whether florbetapir and FDG-PET were associated with retrospective decline in longitudinal ADAS-cog measurements. Results: Twenty-nine percent of normal subjects, 43% of EMCI patients, 62% of LMCI patients, and 77% of AD patients were categorized as florbetapir positive. Florbetapir was negatively associated with concurrent FDG and ADAS-cog in both MCI groups. In longitudinal analyses, florbetapir-positive subjects in both normal and LMCI groups had greater ongoing ADAS-cog decline than those who were florbetapir negative. However, in normal subjects, florbetapir positivity was associated with greater ADAS-cog decline than FDG, whereas in LMCI, FDG positivity was associated with greater decline than florbetapir. Interpretation: Although both hypometabolism and β-amyloid (Aβ) deposition are detectable in normal subjects and all diagnostic groups, Aβ showed greater associations with cognitive decline in normal participants. In view of the minimal cognitive deterioration overall in this group, this suggests that amyloid deposition has an early and subclinical impact on cognition that precedes metabolic changes. At moderate and later stages of disease (LMCI/AD), hypometabolism becomes more pronounced and more closely linked to ongoing cognitive decline. ANN NEUROL 2012;72:578-586 Copyright © 2012 American Neurological Association.
Landau S.M.,University of California at Berkeley |
Landau S.M.,Lawrence Berkeley National Laboratory |
Lu M.,Avid Radiopharmaceuticals |
Joshi A.D.,Avid Radiopharmaceuticals |
And 6 more authors.
Annals of Neurology | Year: 2013
Objective We examined agreement and disagreement between 2 biomarkers of β-amyloid (Aβ) deposition (amyloid positron emission tomography [PET] and cerebrospinal fluid [CSF] Aβ1-42) in normal aging and dementia in a large multicenter study. Methods Concurrently acquired florbetapir PET and CSF Aβ were measured in cognitively normal, mild cognitive impairment (MCI), and Alzheimer's disease participants (n = 374) from the Alzheimer's Disease Neuroimaging Initiative. We also compared Aβ measurements in a separate group with serial CSF measurements over 3.1 ± 0.8 years that preceded a single florbetapir session. Additional biomarker and cognitive data allowed us to further examine profiles of discordant cases. Results Florbetapir and CSF Aβ were inversely correlated across all diagnostic groups, and dichotomous measurements were in agreement in 86% of subjects. Among subjects showing the most disagreement, the 2 discordant groups had different profiles: the florbetapir+/CSF Aβ- group was larger (n = 13) and was made up of only normal and early MCI subjects, whereas the florbetapir-/CSF Aβ+ group was smaller (n = 7) and had poorer cognitive function and higher CSF tau, but no ApoE4 carriers. In the longitudinal sample, we observed both stable longitudinal CSF Aβ trajectories and those actively transitioning from normal to abnormal, but the final CSF Aβ measurements were in good agreement with florbetapir cortical retention. Interpretation CSF and amyloid PET measurements of Aβ were consistent in the majority of subjects in the cross-sectional and longitudinal populations. Based on our analysis of discordant subjects, the available evidence did not show that CSF Aβ regularly becomes abnormal prior to fibrillar Aβ accumulation early in the course of disease. Ann Neurol 2013;74:826-836 © 2013 American Neurological Association.
Wolk D.,University of Pennsylvania |
Zhang Z.,Brown University |
Boudhar S.,The American College |
Clark C.M.,Avid Radiopharmaceuticals |
And 2 more authors.
Journal of Neurology, Neurosurgery and Psychiatry | Year: 2012
Background: Amyloid imaging provides in vivo detection of the fibrillar amyloid-β (Aβ) plaques of Alzheimer's disease (AD). The positron emission tomography (PET) ligand, Pittsburgh Compound-B (PiB-C11), is the most well studied amyloid imaging agent, but the short halflife of carbon-11 limits its clinical viability. Florbetapir-F18 recently demonstrated in vivo correlation with postmortem Aβ histopathology, but has not been directly compared with PiB-C11. Methods: Fourteen cognitively normal adults and 12 AD patients underwent PiB-C11 and florbetapir-F18 PET scans within a 28-day period. Results: Both ligands displayed highly significant group discrimination and correlation of regional uptake. Conclusion: These data support the hypothesis that florbetapir-F18 provides comparable information with PiB-C11.
Jennings D.,Institute for Neurodegenerative Disorders |
Siderowf A.,Avid Radiopharmaceuticals |
Stern M.,University of Pennsylvania |
Seibyl J.,Institute for Neurodegenerative Disorders |
And 3 more authors.
Neurology | Year: 2014
Objectives: The purpose of this study is to evaluate the relative risk of abnormal dopamine transporter (DAT) imaging for subjects with and without hyposmia and the feasibility of acquiring a large, community-based, 2-tiered biomarker assessment strategy to detect prodromal Parkinson disease (PD). Methods: In this observational study, individuals without a diagnosis of PD, recruited through 16 movement disorder clinics, underwent tier 1 assessments (olfactory testing, questionnaires). Tier 2 assessments (neurologic examination, DAT imaging, and other biomarker assessments) were completed by 303 subjects. The main outcome of the study is to compare age-expected [123I]b-CIT striatal binding ratio in hyposmic and normosmic subjects. Results: Tier 1 assessments were mailed to 9,398 eligible subjects and returned by 4,999; 669 were hyposmic. Three hundred three subjects (203 hyposmic, 100 normosmic) completed baseline evaluations. DAT deficit was present in 11%of hyposmic subjects compared with 1% of normosmic subjects. Multiple logistic regression demonstrates hyposmia (odds ratio [OR] 12.4; 95% confidence interval [CI] 1.6, 96.1), male sex (OR 5.5; 95% CI 1.7, 17.2), and constipation (OR 4.3; 95% CI 1.6, 11.6) as factors predictive of DAT deficit. Combining multiple factors (hyposmia, male sex, and constipation) increased the percentage of subjects with a DAT deficit to .40%. Conclusion: Subjects with DAT deficit who do not meet criteria for a diagnosis of PD can be identified by olfactory testing. Sequential biomarker assessment may identify those at risk of PD. Selecting hyposmic individuals enriches the population for DAT deficit, and combining hyposmia with other potential risk factors (male sex, constipation) increases the percentage of subjects with a DAT deficit compatible with prodromal PD. © 2014 American Academy of Neurology.
Hao J.,Eli Lilly and Company |
Xiong H.,Avid Radiopharmaceuticals
Current Topics in Medicinal Chemistry | Year: 2014
Metabotropic glutamate receptor 5 (mGlu5) is a class C G-protein-coupled receptor which possesses a large extracellular N-terminal domain (ATD) connected to the seven-transmembrane (7-TM) domain. In contrast to the glutamate and its close analogs binding at the orthosteric site on the ATD region, allosteric modulators bind at topographically distinct sites in the 7-TM region. Activation of mGlu5 receptors at either the orthosteric or allosteric sites results in enhancement of NMDA receptor function and represents a promising opportunity for the treatment of schizophrenia. Since the disclosure of the first mGlu5 positive allosteric modulators (PAM) in 2003, there have been intense industry-wide efforts to discover and develop safe and efficacious agents capable of selectively enhancing mGlu5 receptor function at the allosteric sites. Over the past decade, tremendous progress has been made, and multiple chemical scaffolds have been identified as mGlu5 PAMs, possibly binding to different allosteric sites on the 7-TM domain. These ligands have helped gain novel insights into the biology of mGlu5 receptor allosteric activation. Here we provide a comprehensive review on the structure-activity relationship (SAR) progress on the mGlu5 PAMs reported in the primary literature and include appropriate and complementary examples from the patent literature. Important in vivo studies of select compounds from individual scaffolds are highlighted, and challenges facing the clinical development of mGlu5 receptor PAMs are discussed. © 2014 Bentham Science Publishers
Pontecorvo M.J.,Avid Radiopharmaceuticals |
Mintun M.A.,Avid Radiopharmaceuticals
Alzheimer's Research and Therapy | Year: 2011
Current theory suggests that -amyloid accumulation may be an early step in the cascade that leads to cognitive impairment in Alzheimer's disease. -Amyloid targeted positron emission tomography (PET) imaging potentially provides a direct, relatively noninvasive estimate of brain -amyloid burden. This has recently been supported by demonstration that amyloid plaque binding on PET was strongly correlated with brain -amyloid burden at autopsy. Additionally, there is growing consensus that PET imaging can identify subjects with elevated -amyloid burden, even at early stages of disease. Finally, preliminary evidence suggests that abnormal -amyloid accumulation, as evidenced by PET imaging, has implications for both present nd future cognitive performance. Although large longitudinal studies like the ongoing ADNI trial will be required for definitive evaluation, present data suggest that PET amyloid imaging has the potential to promote earlier and more specific diagnosis of dementia. © 2011 BioMed Central Ltd.
Avid Radiopharmaceuticals | Date: 2013-10-14
Methods for simultaneously detecting dementia or cognitive impairment, such as Alzheimers Disease (AD), Parkinsons Disease (PD), Lewy Body Dementia (LBD) and Vascular Dementia (VaD) in a patient using dual or multiple radiopharmaceutical probes are provided herein.
Avid Radiopharmaceuticals | Date: 2014-09-18
Diagnostic agents, preparations and substances for medical purposes; diagnostic scanning agents for medical use, namely, diagnostic scanning agents for in vivo use; radiopharmaceutical diagnostic preparations for medical use; radiopharmaceutical diagnostic preparations for use in the diagnosis of neurodegenerative amyloid diseases.
Avid Radiopharmaceuticals | Date: 2016-12-12
Pharmaceutical preparations, namely, pharmaceutical preparations for the treatment of Alzheimers; Diagnostic agents, preparations and substances for medical purposes; diagnostic scanning agents for medical use, namely, diagnostic scanning agents for in vivo use; radiopharmaceutical diagnostic preparations for medical use; radiopharmaceutical diagnostic preparations for use in the diagnosis of neurodegenerative diseases.