Grants

National Institutes of Health

In Vivo High-Resolution Imaging for Inner Ear Visualization (R01 Clinical Trial optional)

2026-10-01

general

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In vivo imaging of the immune response in human uveitis: linking cellular level optical biomarkers to the immune environment of the living eye

NEI - National Eye Institute

Uveitis is responsible for up to 10% of blindness in the US and is a leading cause of vision loss worldwide. Associated with diverse mechanisms of inflammation driven by a range of causes, diagnosis is challenging because it often relies on serological testing or systemic assessments rather than direct ocular measurements. Microglia and other retinal cells and circulating immune cells, as well as the cytokines they produce such as IFN- γ, TNF-α, IL-1, IL-6, and IL-12 influence uveitis pathophysiology as they shape the immune environment within the eye. However, there is a major gap in the understanding of how these key players of the immune response differ across the myriad forms of uveitis. Most of our knowledge comes from animal models due to a lack of tools for real time assessment of immune responses in the eye. We recently showed, for the first time, how adaptive optics ophthalmoscopy (AOO) methods can assess the immune response in posterior uveitis (PU), which affects the retina and/or choroid, in real time in the living eye. Our non-invasive, label-free approach offers promise to revolutionize the diagnostic toolkit for PU and may provide rigorous new biomarkers for evaluating treatment efficacy in the clinic and in clinical trials. It is known that the immune environment differs in infectious and non- infectious uveitis, so we will begin by defining these immunological differences quantitatively using conventional immunological assays including flow cytometry and cytokine analysis in a case-control study of well characterized patients (Aim 1). Next, we will test the hypothesis that these differences allow the use of AOO to detect morphological and dynamic changes of immune cells associated with the retina. Our preliminary findings suggest that AOO can also detect certain pathogens, and we will define the types of microbes that are causing infectious uveitis. We will also determine the other inflammatory biomarkers accessible to AOO in PU, such as vascular changes. Finally, in longitudinal study of a subset of patients, we will track the changes of these biomarkers over time in response to treatment. We predict that imaging will reveal distinct and significant differences between infectious and non-infectious uveitis, specifically: 1) the morphology and dynamic activity of immune cells moving in and through the retina, 2) the profiles of specific microbes related to infectious uveitis pathology, and 3) vascular and other microscopic retinal changes. To realize our goal of transforming the clinical toolkit for real-time monitoring of inflammation, we also need rigorous tools to generate quantitative metrics from the inflammatory biomarkers. We will develop these quantitative tools and generate new imaging protocols for uveitis (Aim 2). This will allow us to establish a novel analytical pipeline to analyze the retina in real-time to increase diagnostic efficiency and improve treatment monitoring. Together, the knowledge and tools developed here will lay the foundation needed to use these new technologies to improve patient care, including rapid diagnosis and real-time treatment monitoring.

Up to $680K

2030-05-31

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In vivo Investigation of KOR availability in hoarding disorder and clinically meaningful endophenotypic correlates

NIMH - National Institute of Mental Health

The purpose of this mentored career development award is to provide the candidate with rigorous and comprehensive training in preparation for an independent academic research career in molecular neuroimaging. Specifically, the completion of individualized training activities and proposed research over the course of the five-year award term will allow the candidate to develop the requisite expertise for a research career utilizing positron emission tomography (PET) in individuals with severe compulsive and impulsive behaviors, such as hoarding disorder (HD). The three career goals outlined in this training program include intensive, focused training in 1) Neurobiology and pathology of compulsive behaviors (emphasizing HD and relationships to functional outcomes and risk); 2) Intensive training in PET methodology and data acquisition; and 3) Advanced training in biostatistics for integration of PET and behavioral data. Integral to these goals is essential training in responsible conduct of research. The training plan will be executed with oversight from experts in neurobiology, molecular imaging, and psychiatry and performed in a rich academic environment (Yale School of Medicine), offering optimal resources and facilities for the proposed training and research. The proposed research consists of an innovative PET study in individuals diagnosed with DSM-5 HD. HD is a devastating and understudied psychiatric condition characterized by severe and compulsive difficulties with discarding and excessive acquisition, resulting in debilitating levels of clutter. HD is associated with profound personal and public health issues, including medical and psychiatric comorbidity, vast functional impairment, and increased risk for suicide. Alarmingly, studies report that fewer than one-third of patients achieve clinically significant change in treatment due in part to factors such as attrition and low treatment motivation. Currently, no FDA-approved pharmacological therapies for HD are available. Research into novel treatments is necessary to provide symptom relief, reduce risk, and improve quality of life. Moreover, pharmacological interventions addressing acute distress and increasing treatment retention may be needed to impart long-term behavior change. Evidence implicates kappa opioid receptors (KOR) in motivation, emotion regulation, compulsive behaviors, and in pre-clinical models of hoarding. Our promising pilot data show significantly lower KOR availability in subjects with hoarding behaviors (n=5) relative to healthy controls (HC). Here, we aim to extend these exciting findings by examining 1) KOR availability in-vivo using [11C]EKAP PET in individuals with HD relative to demographically matched HC; 2) relationships between KOR availability and clinically meaningful endophenotypes of HD; and 3) associations between KOR and functional outcomes in individuals with HD. Results have potential to significantly impact HD treatment development. Completion of the proposed training plan and research study will optimally position the candidate for a successful career conducting impactful research in psychiatric populations with severe compulsive behaviors.

Up to $191K

2031-05-31

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In Vivo Metabolic Tagging and targeting of Long-Circulating Biomembranes

NIGMS - National Institute of General Medical Sciences

Project Summary The native biomembrane of red blood cells (RBCs) has long been considered an attractive engineering target for drug delivery, immune modulation, hemostasis, vaccination, and many other applications due to the natural abundance, long life-span, and excellent tissue accessibility of RBCs. However, current RBC membrane engineering approaches are only applicable to isolated RBCs under in vitro conditions, and there is a lack of effective methods for in vivo tagging or modification of circulating RBCs under physiological conditions. Here we propose to develop an innovative platform technology for in vivo metabolic tagging of RBC membrane and subsequent targeting of molecular imaging and therapeutic cargos via efficient click chemistry. The proposed work builds upon our preliminary data that RBCs can metabolize unnatural sugars and express chemical tags (e.g., azido groups) in the form of glycoproteins and glycolipids. This finding is somewhat counter-intuitive considering the RBC’s nucleus-free structure and low metabolic activities, but it is not surprising since glycoproteins and glycolipids are essential components of RBC membranes, so there must be some active pathways for metabolism and glyco-synthesis associated with RBCs. We further hypothesize that intravenous administration of unnatural sugars could also result in metabolic labeling of circulating RBCs with chemical tags, which would then allow direct conjugation and targeting of various imaging and therapeutic agents via click chemistry. Thus, the proposed work has three specific aims. In Aim 1, we will elucidate the fundamental mechanisms of metabolic glycan labeling, optimize its efficiency, evaluate the effects of metabolic glycan labeling on RBC structure and functions, and investigate the conjugation efficiency and membrane retention of cargos on chemically tagged RBCs. In Aim 2, we will explore metabolic glycan labeling in vivo, measure the in vivo conjugation efficiency of DBCO-molecules of different sizes to azido-labeled RBCs, and determine in vivo retention of the conjugated molecules. In vivo labeling of RBCs in dogs will also be studied. In Aim 3, we will demonstrate the promise of our membrane labeling and targeting technology to enable (1) long-term magnetic resonance imaging (MRI) with one dose of contrast agent, and (2) enhanced blood circulation and pharmacokinetics of drugs such as insulin. If successful, the proposed tagging technology is expected to have a broad range of biomedical applications including molecular imaging, long-acting drug delivery, and immune modulation.

Up to $1.4M

2030-03-31

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In vivo platforms for exploring co-evolution of ligands, receptors, and their targets

NIGMS - National Institute of General Medical Sciences

Abstract: Cell signaling regulates information transfer across tissues through graded ligands that interact with receptors. Across evolution, ligand and receptor proteins co-evolve, with changes in one protein being counterbalanced by changes in its partner, thus preserving successful interactions that promote development rather than pathology. Despite the importance of co-evolution in speciation and disease, our understanding of these reciprocal processes primarily relies on bioinformatics predictive tools and in vitro systems like yeast two-hybrid assays. Currently, there is no robust in vivo system, at moderate cost, to validate the co-evolution of multiple cell-signaling components. Given the differences in physiological conditions across tissues that impact protein interactions, we will develop in vivo genetic and molecular platforms for investigating co-evolving proteins. Research using Drosophila melanogaster has greatly contributed to both basic and medical research at a low cost. Building on our extensive experience with Drosophila species, we plan to generate two new in vivo systems to study the co- evolution of Gurken (GRK), a TGF-alpha ligand that activates the epidermal growth factor receptor (EGFR), endogenously. Drosophila oogenesis is a powerful model system for studying EGFR-guided axis formation and eggshell morphology, providing simple phenotypic readouts. Although the pathway and the underlying mechanism, a localized source of GRK, are conserved among Drosophila species, we have observed dramatic variations in the ability of GRK orthologs to signal interchangeably across species, ranging from no signal to a striking overactivation of EGFR signaling. The new in vivo platforms will allow us to thoroughly explore the effects of a histidine-rich domain loss in GRK on EGFR activation across different subgenera. Additionally, we will investigate the causes of EGFR overactivation when both GRK and EGFR are substituted with their homologs. S2 culture cells will be engineered with biosensors for EGFR signaling, providing a robust system to prioritize computationally predicted co-evolving sequences in GRK and EGFR for in vivo studies. Furthermore, we will examine the evolution of EGFR signaling targets, including the Tbx-20 homologs, Midline (MID) and H15, in relation to changes in signaling intensity and duration. Finally, we will study the evolution of cis-regulatory modules (CRMs) that control the expression of Mid/H15 tandem paralogs in oogenesis and other fly tissues. Our comprehensive and multidisciplinary approach-- combining new in vivo systems, computational, biophysical, analytical, and CRISPR/Cas9 genome engineering tools-- provides an exciting new path for identifying the co- evolving domains in ligands and receptors that control signaling levels. By investigating these domains in vivo, under natural physiological conditions, we will advance our understanding of cell signaling mechanisms, which could lead to new strategies for addressing tissue pathologies. The research field will benefit from new in vivo platforms to explore co-evolving processes during development and homeostasis. The EGFR signaling field will gain high-resolution analyses of co-evolving sequences that control signaling levels and duration in vivo.

Up to $424K

2030-12-31

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In vivo profiling of a first-in-human study of chimeric autoantibody receptor T cells for MuSK myasthenia gravis

NIAID - National Institute of Allergy and Infectious Diseases

Project summary: Our laboratory invented a novel precision medicine approach for autoimmune disease treatment known as chimeric autoantibody receptor T cell (CAART) therapy, which aims to eliminate only the disease-causing autoimmune B cells while sparing healthy B cells, thus avoiding the risks of general immune suppression. We established initial efficacy of the approach in experimental autoimmune disease models and subsequently initiated a first-in-human clinical trial of DSG3-CAART in mucosal-dominant pemphigus vulgaris, a potentially fatal blistering disease caused by autoantibodies to the epithelial adhesion protein desmoglein 3 (DSG3), and more recently, MuSK-CAART in muscle-specific tyrosine kinase (MuSK) myasthenia gravis, in which autoantibodies to MuSK cause muscle weakness and potentially life-threatening respiratory crisis. DSG3- CAART was generally well-tolerated, although no consistent pattern of clinical or serologic improvement was observed. In contrast, 4 of the first 6 MuSK-CAART-treated patients experienced improvement in clinical disease activity scores, associated with MuSK-CAART expansion and persistence, and 2 of 4 subjects in the higher dose cohort experienced serious adverse events related to therapy. DSG3-CAART and MuSK-CAART are the first precision cellular immunotherapies for autoimmunity to enter clinical trials, which presents a unique opportunity to define the effects of these living drugs in human patients. In a separate line of studies we are investigating DSG3-CAART immune profiles; in this proposal, we will define immune profiles before and after infusion to evaluate pathways activated in MuSK-CAART and host immune cells that may identify biomarkers of safety and efficacy. Our studies will elucidate the cellular mechanisms of MuSK-CAART in vivo and may lead to new strategies for engineering the next generation of precision immunotherapies to achieve safe and durable autoimmune disease remission.

Up to $452K

2028-01-31

Free to search & build · $99 one-time to unlock the application pack · No subscription

In-cell analysis and elaboration of RNA-targeting fragment ligands

NIGMS - National Institute of General Medical Sciences

Project Summary The function and regulation of both coding and non-coding RNAs depend on their structures. A subset of RNAs contain pockets capable of binding ligands, and targeting RNA with small molecules can potentially modulate gene expression and cell state. To date, identifying and progressing these ligands within cells has posed a formidable challenge. I have developed a technology for transcript-specific detection of ligand binding in cells that is scalable for high throughput screens. This method simplifies the complex RNA ligand measurement into a manageable and efficient PCR-based strategy, which I used to discover a first-site fragment ligand that binds the 5’-UTR of MYC, a conventionally difficult-to-ligand target. In Aim 1, I propose to use my in-cell screening platform to discover molecules that exhibit enhanced binding to MYC mRNA when bound by the first-site ligand. Potential hits will be chemically linked to create ligands with substantially higher affinity than either ligand alone. My current first-site binder reduces c-MYC protein levels without affecting mRNA levels, suggesting translational regulation. In Aim 2, I will use functional studies to address a critical gap in our understanding of how small- molecule ligands can target RNA, to produce meaningful biological effects, focusing on how RNA structure affects ribosome recruitment to the mRNA. This project is designed to provide a comprehensive understanding of ligand-RNA interactions in cells, informing the development of RNA-targeted tool compounds and, ultimately, therapeutics. The overarching vision of this research and training program integrates RNA screening technologies, bioinformatics and cheminformatics, mechanistic studies, and mentoring opportunities. Through this program, I will gain a strong foundation for a career as an independent researcher and leader in RNA chemical biology and therapeutics.

Up to $75K

2028-12-31

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IN-PERSON FOREIGN LANGUAGE INTERPRETATION

Community DevelopmentHealth

READY MADE STAFFING

Editorial and Design and Graphic and Fine Art Services

2028-04-30

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In-vivo and Ex-vivo Analysis of Tissue S-nitrosothiols in Sepsis

NHLBI - National Heart Lung and Blood Institute

PROJECT SUMMARY Each year there is an estimated eight million deaths globally that are attributed to sepsis. Sepsis is one of the leading causes of death in the pediatric population. When children die it is often from refractory shock and development of multi-organ failure. A key driver of this refractory shock is vascular dysfunction. Nitrosative stress has been linked to the pathophysiology of sepsis and is associated with this vascular dysfunction. However, the role of nitrogen oxides is incompletely understood in sepsis. There is a need to define the role of nitrogen oxides to identify new and effective therapeutic targets. S-nitrosothiols are endogenous nitrogen oxides that are exquisitely bioactive in vascular physiology. Many circulating S-nitrosylated proteins have established physiological roles. In addition, certain low-mass S-nitrosothiols have important physiologic roles and have been recently demonstrated to be stored and released from extracellular vesicles (EVs). In adults S-nitrosothiol levels are high when measured ex-vivo in sepsis. Unfortunately, due to their lability, measurement can be very difficult, thus limiting clinical utility. Our team has recently designed and validated a device that allows for non-invasive measurement of tissue S-nitrosothiols in-vivo. Our objective is to define the role of S-nitrosothiols in blood and EVs and to establish their relationships in sepsis. Our hypothesis is that circulating concentrations of S- nitrosothiols, including those in EVs, are increased in sepsis and that these high levels are associated with worse outcomes. My long-term career goal is to develop a research portfolio studying the biology of these molecules and to leverage this understanding to develop new therapies for sepsis. This K08 proposal summarizes a 5-year program of mentored support tied to a research project to better determine the roles of S-nitrosylation signaling in sepsis. Our specific aims for this project are to: (1) test the hypothesis that EV cargo is enriched with S- nitrosothiols in a murine model of sepsis and to identify novel S-nitrosylated proteins associated with sepsis- related pathways and (2) test the hypothesis that S-nitrosothiols are elevated in EV cargo from pediatric patients with sepsis, and their levels correlate with device-based measurements and predict clinical outcomes. Through my career development plan and ongoing support and education from my mentors, I will develop expertise in a) bioinformatics and proteomics, b) mouse husbandry, and c) EV biology and research techniques. Together the research and career development aims of this proposal will provide me with the necessary skills and education to compete for additional funding as an independent investigator. Specifically, I plan to submit for an R01 application through the NHLBI in year 5 of this career development award period. This proposal will focus on investigating the mechanistic underpinnings for the differentially expressed S-nitrosothiols contained in EVs. Overall, this proposal is an important first step in establishing my career as an independent investigator with a focus on pediatric sepsis.

Up to $153K

2031-03-31

Free to search & build · $99 one-time to unlock the application pack · No subscription

In-Water Wave Energy Conversion (WEC) Device Testing Support - Notice of Intent (NOI)

Golden Field Office

The purpose of this Notice of Intent is to provide potential applicants advance notice of a proposed upcoming Funding Opportunity Announcement initially titled: In-Water Wave Energy Conversion (WEC) Device Testing Support. NO APPLICATIONS WILL BE ACCEPTED THROUGH THIS NOTICE. Prospective applicants should begin developing partnerships, formulating ideas, and gathering data in anticipation of the issuance of this FOA. It is anticipated that this FOA will be posted to EERE Exchange in FY12. Please do not respond or submit questions in response to this Notice of Intent. DOE intends to fund one industry-led project that will deploy a long-term (one year) in-water WEC device. The device will be deployed at the Navy Wave Energy Test Site (WETS) facility in Kaneohe Bay on the Hawaiian Island of Oahu. The full Notice of Intent (NOI) is posted on the EERE eXCHANGE website at https://eere-exchange.energy.gov. The applicant must first register and create an account on the EERE eXCHANGE website. A User Guide for the EERE eXCHANGE can be found on the EERE website http://eere.energy.gov/financing/exchangeExchange/Manuals.aspx after logging in to the system.

rolling

energyclean energy

Free to search & build · $99 one-time to unlock the application pack · No subscription

Inactivation of the ISR/ATF4 signaling pathway stabilizes HIV reservoirs

NIMH - National Institute of Mental Health

PROJECT SUMMARY Stable HIV reservoirs remain a significant challenge for the eradication of HIV-1 (HIV). While several anti- HIV latency strategies have been proposed to control HIV reservoirs, few have proven effective in reducing the size of the HIV reservoir in clinical settings. This suggests that our current understanding of how HIV achieves its persistent infection is limited and underscores the need for the development of alternative innovative tools for HIV cure. Recently, we and others characterized a unique integrated stress response (ISR)/ATF4 signaling pathway that is essential for HIV transcription and early seeding of HIV. Conversely, when ATF4 is knocked down, HIV transcription is inhibited. We further defined ATF4 as a new transcription factor of HIV, exploited by HIV for its own transcription after the recruitment of ATF4 to the ATF/CREB consensus site at the 5’ HIV long-terminal repeat. ATF4 induction leads to HIV activation from latency, indicating that ISR/ATF4 signaling activation promotes HIV transcription while the suppression of ISR signaling is associated with the establishment of HIV latency. Of note, prolonged activation of ISR/ATF4 signaling also induces cell death, mediated by ATF4 binding to the promoter of the CHOP gene, an essential protein driving apoptosis during persistent ISR/ATF4 activation. In a primary CD4+ T cell model of latency, prolonged ISR/ATF4 signaling activation disrupts latent HIV and selectively induces apoptosis in HIV+ CD4+ T cells, without affecting bystander HIV-negative CD4+ T cells. Notably, using viral outgrowth assays, we discovered that prolonged ISR/ATF4 signaling activation reduces replication-competent HIV by up to 2,300-fold in resting CD4+ T cells isolated from people with HIV receiving suppressive antiretroviral therapy (ART). Therefore, we hypothesize that the suppression of ISR/ATF4 signaling is essential for HIV persistence. This will be tested through three specific aims: Aim 1: Investigate how activation of the ISR/ATF4 signaling pathway eliminates HIV-latently infected T cells and brain microglia. Aim 2: Elucidate the unique mechanisms by which ISR/ATF4 signaling controls the stable HIV reservoir for the establishment of HIV latency. Aim 3: Determine the effectiveness of activating ISR/ATF4 signaling in eliminating HIV reservoirs in the hu-BLT mouse model of HIV latency in vivo.

Up to $793K

2031-01-31

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Inception Loops for Epilepsy

NINDS - National Institute of Neurological Disorders and Stroke

PROJECT ABSTRACT Epilepsy is a debilitating and life-threatening condition, affecting 1% of the US population. A signiﬁcant portion of these patients have seizures that do not respond to medication therapy. Neurostimulation is often an effective treatment method for these patients, but only in an adjuvant capacity. The seizure reduction experienced by patients is far from curative, and stimulation treatments rarely result in seizure freedom. By contrast, resective surgery, the gold standard in care for drug-resistant epilepsy, reliably results in sustained seizure freedom and an improved quality of life. However, it is important to note that surgery, despite its potential beneﬁts, is a highly invasive procedure that carries certain risks and adverse effects. Moreover, its major limitation is that its use is restricted to brain regions that can be removed without causing a loss of essential neurological function. We believe that the limited effectiveness of current neurostimulation devices can be attributed to the crudeness of stimulation they provide. The brain, being a complex and non-linear system, requires a modulatory approach that matches its intricate nature when targeting networks involved in epilepsy. Achieving optimal control over these networks is likely to necessitate a complex approach. Therefore, we hypothesize that the generation of more complex patterns will allow for better engagement and modulation of these networks. Here we present a novel platform that offers an unprecedented ability to optimize the design of pulse sequences with complex spatiotemporal relationships for the control of epileptic activity. By combining a cutting-edge method for designing high-entropy stimuli and deep learning, we will demonstrate the ability to infer optimized stimulation for seizure control in a rat model. Our paradigm is based on adapting our Inception Loops paradigm, a deep learning framework for solving high-dimensional, non-linear optimization problems in neuroscience, for the pur- pose of constructing multi-patterned stimuli that are optimized to control epileptic activity. The ﬁrst step involves building data-driven neural predictive models of targeted brain areas, taking ongoing brain activity and stochastic, high-entropy electrical stimulation patterns as input to predict neural activity. Then, in silico optimization identiﬁes those dynamic stimulation patterns across many stimulation channels that suppress epileptic activity, which are then veriﬁed in vivo. The study detailed below will investigate the optimization of multi-pattern stimuli in two complementary rodent models. Finally, we will perform a ﬁrst-in-human study to investigate the ability of multi-pattern stimulation to con- trol interictal epileptiform discharges as a seizure likelihood proxy in patients undergoing intracranial evaluation.

Up to $50K

2029-02-14

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INCLUDE (INvestigation of Co-occurring conditions across the Lifespan to Understand Down syndromE) Predoctoral to Postdoctoral Fellow Transition Award (F99/K00 Clinical Trial Not Allowed)

income_security_and_social_servicesHealth

National Institutes of Health

<p>The purpose of the INvestigation of Co-occurring conditions across the Lifespan to Understand Down syndromE (INCLUDE) Predoctoral to postdoctoral Fellow Transition award (F99/K00) is to recruit exceptional graduate students from a variety of research fields to pursue postdoctoral training focused on Down syndrome related research. Talented graduate students from disciplines including, but not limited to, genetics, biochemistry, data science, imaging, engineering and neurobiology are invited to apply to this opportunity. Prospective applicants are strongly encouraged to contact the INCLUDE Program Staff prior to initiating plans for application submission.</p>

2026-07-01

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INCLUDE (INvestigation of Co-occurring conditions across the Lifespan to Understand Down syndromE) Predoctoral to Postdoctoral Fellow Transition Award (F99/K00 Clinical Trial Not Allowed)

National Institutes of Health

INCLUDE (INvestigation of Co-occurring conditions across the Lifespan to Understand Down syndromE) Predoctoral to Postdoctoral Fellow Transition Award (F99/K00 Clinical Trial Not Allowed)

2026-07-01

general

Free to search & build · $99 one-time to unlock the application pack · No subscription

INCLUDE (INvestigation of Co-occurring conditions across the Lifespan to Understand Down syndromE) Predoctoral to Postdoctoral Fellow Transition Award (F99/K00 Clinical Trial Not Allowed)

National Institutes of Health

The purpose of the INvestigation of Co-occurring conditions across the Lifespan to Understand Down syndromE (INCLUDE) Predoctoral to postdoctoral Fellow Transition award (F99/K00) is to recruit exceptional graduate students from a variety of research fields to pursue postdoctoral training focused on Down syndrome related research. Talented graduate students from disciplines including, but not limited to, genetics, biochemistry, data science, imaging, engineering and neurobiology are invited to apply to this opportunity. Prospective applicants are strongly encouraged to contact the INCLUDE Program Staff prior to initiating plans for application submission.

2026-07-01

Free to search & build · $99 one-time to unlock the application pack · No subscription

INCLUDE Project: Clinical Trials Phased Awards for Down syndrome Research (R61/R33 Clinical Trial Required)

National Institutes of Health

The NIH INvestigation of Co-occurring conditions across the Lifespan to Understand Down syndromE (INCLUDE) Project seeks to improve health and quality-of-life for individuals with Down syndrome. The purpose of this Notice of Funding Opportunity (NOFO) encourages Exploratory/Developmental Phased Innovation (R61/R33) grant applications to support development of clinical trials to treat critical and co-occurring health conditions in individuals with Down syndrome. The proposed research aims should be milestone-driven. The total project period for an application submitted in response to this NOFO may not exceed five years. This NOFO provides support for up to two years (R61 phase) for preliminary/developmental/planning studies, followed by possible transition to clinical trial support (R33) of up to three years, although the total duration of the award may not exceed five years. This NOFO requires measurable R61 milestones.

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INCLUDE Project: Clinical Trials Phased Awards for Down syndrome Research (R61/R33 Clinical Trial Required)

National Institutes of Health

Health

Free to search & build · $99 one-time to unlock the application pack · No subscription

INCLUDE Project: Clinical Trials Phased Awards for Down syndrome Research (R61/R33 Clinical Trial Required)

National Institutes of Health

INCLUDE Project: Clinical Trials Phased Awards for Down syndrome Research (R61/R33 Clinical Trial Required)

research

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INCLUDE Project: Exploratory/Developmental Research Awards for Down syndrome (R21 Clinical Trial Not Allowed)

National Institutes of Health

INCLUDE Project: Exploratory/Developmental Research Awards for Down syndrome (R21 Clinical Trial Not Allowed)

research

Free to search & build · $99 one-time to unlock the application pack · No subscription

INCLUDE Project: Exploratory/Developmental Research Awards for Down syndrome (R21 Clinical Trial Not Allowed)

National Institutes of Health

The NIH INvestigation of Co-occurring conditions across the Lifespan to Understand Down syndromE (INCLUDE) Project seeks to improve health and quality-of-life for individuals with Down syndrome. This Notice of Funding Opportunity (NOFO) invites researchers to submit applications for support of new exploratory and developmental research projects that address critical needs for Down syndrome projects, as articulated in the INCLUDE Project objectives. For example, such projects could assess the feasibility of a novel area of investigation or a new experimental system that has the potential to enhance health-related research. Another example could include the unique and innovative use of an existing methodology to explore a new scientific area. These studies may involve considerable risk but may lead to a breakthrough in a particular area, or to the development of novel techniques, agents, methodologies, models, or applications that could have a major impact on a field of biomedical, behavioral, or clinical research.

Up to $200K

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INCLUDE Project: Transformative Research Awards for Down syndrome (R01 Clinical Trial Not Allowed)

National Institutes of Health

The NIH INvestigation of Co-occurring conditions across the Lifespan to Understand Down syndromE (INCLUDE) Project seeks to improve health and quality-of-life for individuals with Down syndrome. The purpose of this Notice of Funding Opportunity (NOFO) is to solicit Transformative Research Award applications to support individual scientists or groups of scientists proposing groundbreaking, exceptionally innovative, original, and/or unconventional research that has the potential to create new scientific paradigms, establish entirely new and improved clinical approaches, or develop transformative technologies related to Down syndrome. Applications are welcome in all topics relevant to Down syndrome-related research or its co-occurring conditions. No preliminary data are required. Projects must clearly demonstrate, based on the strength of the logic, a compelling potential to produce a major impact in research related to Down syndrome.

Up to $500K

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INCLUDE Project: Transformative Research Awards for Down syndrome (R01 Clinical Trial Not Allowed)

National Institutes of Health

The NIH INvestigation of Co-occurring conditions across the Lifespan to Understand Down syndromE (INCLUDE) Project seeks to improve health and quality-of-life for individuals with Down syndrome. The purpose of this Notice of Funding Opportunity (NOFO) is to solicit Transformative Research Award applications to support individual scientists or groups of scientists proposing groundbreaking, exceptionally innovative, original, and/or unconventional research that has the potential to create new scientific paradigms, establish entirely new and improved clinical approaches, or develop transformative technologies related to Down syndrome. Applications are welcome in all topics relevant to Down syndrome-related research or its co-occurring conditions. No preliminary data are required. Projects must clearly demonstrate, based on the strength of the logic, a compelling potential to produce a major impact in research related to Down syndrome.

Up to $500K

Health

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INCLUDE Project: Transformative Research Awards for Down syndrome (R01 Clinical Trial Not Allowed)

National Institutes of Health

INCLUDE Project: Transformative Research Awards for Down syndrome (R01 Clinical Trial Not Allowed)

research

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Inclusive Gender Equality Champions