Skip to main content
9,000+ open opportunities indexed

Search Grants — Free, No Account Required

Search federal, state, and foundation grants by keyword, state, or focus area. When you find a match, apply with our AI-assisted application builder.

957 grants foundClear search

24 grants worth up to $13.4M match your search

Enter your email to see grant names, funders, and application links

Nothing about us without us: Integrating the voices of people who use drugs into HIV resource allocation using large language models

open

NIDA - National Institute on Drug Abuse

This project will develop and apply a novel, data-driven modeling approach to guide HIV and hepatitis C virus (HCV) prevention resource allocation among people who use drugs (PWUD) in the United States. Despite advances in HIV prevention and treatment, including long-acting injectable ART, the United States continues to fail to meet the needs of PWUD, a population central to intersecting HIV, HCV, and overdose crises. A key reason is the absence of a rapid, scalable, and comprehensive way to capture and act on the preferences and behaviors of PWUD. Revolutionary advances in large language models (LLMs) now make it possible to create highfidelity “digital twins” — artificial-intelligence powered simulations of individuals that reflect their intervention preferences and even behaviors. Using a community-based participatory process, we will train an LLM on data from multiple PWUD cohorts to generate PWUD digital twins that simulate locally-specific intervention preferences. These digital twins will be integrated into an epidemic and economic model that simulates HIV and HCV transmission, overdose, and related complications, across numerous jurisdictions in the United States. The integrated modeling framework will be used to evaluate the impact and cost-effectiveness of different HIV/HCV prevention and treatment strategies, including responses to potential funding constraints. Epidemic model outputs will be shared through an interactive dashboard designed in consultation with public health departments. Ultimately, our project aims to improve intervention implementation and reduce HIV, HCV, and overdose. Our project includes the following activities: 1) Co-design, development, and validation of a PWUD-informed LLM. 2) Digital twin simulations within a HIV/HCV transmission and overdose model to inform resource allocation. 3) Dissemination and implementation of the epidemic and resource allocation dashboard to county health departments. The proposed research will enable rapid, data-driven evaluation of prevention strategies and resource allocation options. It aligns with the NIH Office of AIDS Research priority to reduce new HIV infections and address HIV coinfections.

Up to $1.1M
2031-03-31
health research

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

Novel Approaches for Gestational E-Cigarette Vaping-Induced Neuronal Adaptations

open

NIEHS - National Institute of Environmental Health Sciences

PROJECT SUMMARY Electronic cigarette (e-cig) use during pregnancy has become a major health concern in recent years and is perpetuated by the perception that e-cigs are less harmful than traditional combustible cigarettes. Recent estimates show 7% of women use e-cigs in pregnancy, and 45% view them as less harmful and may help them quit or reduce combustible cigarettes in pregnancy. An extensive knowledge gap persists regarding their health impact when aerosolized, especially during pregnancy. Using our well-established pregnant rat model, we obtained preliminary data utilizing a state-of-the-art e-cig system with a commercial e-cig unit and atomizer that offered a translational inhalation delivery and generated vapor profiles directly comparable to human vaping. Our preliminary data demonstrated that a cardinal outcome of e-cig use was a significant fetal and neonatal growth deficit. Concomitant with growth restriction, our exciting preliminary data provides direct evidence that e-cig vaping significantly alters developmental brain hippocampal mTOR system. As a critical node, mTOR regulates essential brain metabolic activities, including protein synthesis and autophagy. Interestingly, our new preliminary data indicate that these mTORC1 and mTORC2 signaling adaptations were accompanied by altered fetal hippocampal dendritic morphology and hippocampal-dependent long term memory deficits. We subsequently generated critical preliminary data that demonstrated that optimizing mTORC1/C2 activity via in vivo administration of the 3rd gen mTORC1/C2 blocker (RapaLink-1) concomitant with e-cig aerosol exposure reversed specific e-cig-induced fetal developmental phenotypes. Thus, we hypothesize that the mTOR system plays a central role in e-cig induced alterations in fetal brain hippocampal adaptations. To test this hypothesis, we will (1) seek to answer fundamental questions about the impact of e-cig aerosol exposure on hippocampal mTORC1/C2 system using novel mechanistic in vivo studies, (2) assess the role of mTOR in e-cig-induced fetal brain hippocampal developmental adaptations using morphometric, stereological and behavioral approaches, and (3) identify e-cig-induced protein signal propagation pathways leading to activation of mTOR and signal propagation downstream of mTORC1/C2 utilizing mass spectrometry- based phosphoproteomics followed by stochastic optimization and reinforcement learning algorithms. We will then compare and interpret the signature pathways impacted by e-cig vaping with and without mTOR blocker using machine learning models. Upon successful completion of these aims, we will have comprehensively characterized the mTOR signaling cascade as it transduces cues from e-cig vaping into molecular action, enabling the identification of potential strategies to mitigate e-cig-induced neurodevelopmental deficits in the hippocampus. The proposed studies develop a strong etiological framework and directly address a “major research area” of developmental impacts under Theme One of NIEHS Strategic Plan 2018-2023, titled “Advancing Environmental Health Sciences”.

Up to $2.1M
2030-05-31
health research

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

Novel approaches to predict strength and breadth of influenza vaccine response

open

NIAID - National Institute of Allergy and Infectious Diseases

PROJECT SUMMARY Influenza vaccines remain the most cost-effective tool for reducing infection and disease burden. However, despite decades of research and development, the protection they provide is often suboptimal. A key challenge is the wide variability in vaccine induced immune responses among individuals, which is poorly understood. Addressing this knowledge gap is crucial for improving vaccine efficacy and vaccination strategies. Predictive modeling, with its demonstrated success in advancing medical research and public health, holds significant promise in this regard. By harnessing predictive models, we can tailor vaccination strategies to individuals, optimizing protection and improving outcomes. Current predictive models, however, suffer from critical limitations. Most rely solely on static, pre- vaccination data and focus narrowly on antibody responses to a single vaccine component (in current vaccines, these are H3N2, H1N1 and one or two of the B lineages). Existing models do not account for the dynamic nature of the immune system or the role of heterologous, non-vaccine-specific antibody responses, reducing their accuracy and practical utility. These shortcomings hinder the development of more comprehensive, adaptable models for predicting vaccine efficacy across diverse populations and viral strains. This project aims to overcome these limitations by developing and validating advanced predictive models for influenza vaccine responses. Our approach integrates systematically collected, longitudinal data with state-of-the-art statistical and machine-learning methods. Specifically, we will: 1. Develop predictive models that incorporate long-term antibody response trajectories and heterolo- gous strain data to improve predictions for vaccine strain responses. 2. Expand the scope of these models to predict heterologous breadth and overall antibody responses, offering a more complete understanding of vaccine-elicited immunity. 3. Generate and analyze high-throughput antibody landscape data to further refine and enhance our predictive models. By combining these innovations, we aim to establish a new framework for individualized vaccine re- sponse prediction. This framework will significantly improve upon existing models, enabling tailored vac- cination strategies designed to optimize protection for each individual. Ultimately, this work will provide a robust scientific foundation for guiding future influenza vaccination efforts, contributing to better public health outcomes worldwide.

Up to $806K
2031-04-30
health research

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

Novel pathways and mechanisms underlying disorders of platelet count and/or function

open

NHLBI - National Heart Lung and Blood Institute

PROJECT SUMMARY Our overall vision and long-term goal are to obtain a more complete understanding for how cellular signaling pathways, in particular G proteins and integrin receptors, control platelet adhesion and plug formation in hemostasis and thrombosis. Furthermore, we aim to elucidate aspects of the signaling machinery that function differentially in hemostasis versus thrombosis (both arterial and venous). The conceptual framework is that human thrombotic diseases result from an otherwise protective mechanism gone awry, and that disease-induced changes to platelet reactivity (priming) are a major contributor to thrombotic disease. A detailed understanding of platelet activation pathways is critical for the development of novel antithrombotic therapies, and for the identification of new biomarker assays for a prothrombotic state. Over the last two decades, my lab has utilized state-of-the-art in vitro and in vivo approaches to redefine our understanding of the molecular mechanisms regulating platelet reactivity in circulation and at sites of vascular injury. Key findings include the identification of tightly balanced G protein networks, an integrin activation complex that is unique to platelets, and injury-specific contributions of platelets to vascular integrity and thrombotic complications. The proposed work will focus on several areas within the general conceptual framework outlined above: (1) studies on G protein networks and integrin affinity regulation in platelets; (2) studies on the role of platelets in venous thrombosis pathogenesis and novel antithrombotic strategies; (3) development of novel assays to measure levels of primed platelets in different diseases; and (4) studies to better understand and correct defects in platelet count and function associated with inherited and acquired platelet disorders. Exciting preliminary findings include the identification of a novel G protein network in platelets, the establishment of new assays to monitor an elusive intermediate affinity conformation in platelet integrins, and a critical role for intermediate affinity integrins in thrombocytopenia and/or thrombosis associated with platelet disorders and cancer. In summary, the proposed studies will investigate significant knowledge gaps in basic platelet biology and provide a new understanding for how disease states like cancer affect platelet reactivity and platelet plug formation. Our studies have high translational relevance in the areas of antithrombotic therapy, biomarker development, and transfusion therapy.

Up to $1.1M
2033-01-31
health research

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

Novel Preclinical Models of NeuroHIV with CART

open

NIMH - National Institute of Mental Health

Abstract Despite the effectiveness of antiretroviral therapies (ART) in reducing systemic HIV viral loads, central nervous system (CNS) dysfunction remains prevalent in 30-50% of people living with HIV (PWH). ART does not eliminate viral reservoirs in the CNS, leading to chronic neuroimmune dysfunction and conditions like HIV-associated neurocognitive disorder (HAND). Current preclinical research has primarily focused on models that simulate acute HIV infection, but there is a pressing need for models that accurately reflect CNS dysfunction in the context of chronic ART-suppressed infections. Recent advancements in immunodeficient mouse models with humanized immune systems have shown promise, allowing for natural HIV infection and crossing of the blood-brain barrier. These models have provided insights into HIV infection in the CNS and the role of human microglia cells. However, significant gaps remain, particularly in developing models that incorporate multiple human CNS cell types and accurately represent chronic infection dynamics. This proposal aims to develop preclinical NeuroHIV models that better mimic CNS-immune interactions in general and in particular during ART suppression. Specifically, our goal is to develop the next generation NeuroHIV model composed of autologous peripheral human immune cells, relevant human glial cell types, and an intact blood-brain barrier all in the context of ART-mediated HIV suppression.

Up to $1.8M
2028-06-04
health research

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

Novel selective allosteric modulators of PTHrP/PTH receptor to inhibit prostate cancer metastases

open

NCI - National Cancer Institute

The parathyroid hormone (PTH) receptor type 1 (PTH1R) is a G-protein coupled receptor (GPCR) and the only cell surface receptor for the PTH-related protein (PTHrP), which causes the “vicious” cycle of prostate cancer (PCa) bone metastases. Clinical trials to block PTHrP using neutralizing antibodies only showed palliative effects in cancer patients. We have identified a series of small molecules (referred to as Pitt molecules) that act as negative allosteric modulators of PTH1R signaling. We hypothesize that Pitt molecules have the potential to prevent PTH1R overactivity induced by PTHrP hypersecretion encountered in prostate cancer cells. As allosteric molecules, Pitt molecules have the key advantage over orthosteric antagonists to restore normal receptor activity when PTHrP is hypersecreted. Furthermore, PTH1R is recently identified as a target for enzalutamide resistance in PCa bone metastases. The goal of this project is to identify selective Pitt molecules targeting PTHrP- induced PTH1R overactivity as potential lead candidates for the development of drugs treating bone osteolysis induced by prostate cancer metastases. Specific Aim 1 will identify the most effective Pitt molecules for inhibition of PTH1R hyperactivation by PTHrP. We will use state-of- the-art optical analysis of receptor signaling in live cells expressing recombinant and native PTH1R. We will evaluate the toxicity and biostability of the Pitt molecules using assays in cell culture. Specific Aim 2 will determine the efficacy of selected Pitt molecules in prostate cancer metastases. We found that the selective deletion of PTH1R in mesenchymal lineage cells of a mouse model significantly inhibits prostate cancer metastases. We have successfully established cell culture and mouse models to longitudinally monitor prostate cancer tumor growth and metastases. We will use these models to test the efficacy of selected Pitt molecules, as a single agent or in combination with current clinical therapies such as enzalutamide, in inhibiting prostate cancer metastases. The significance of this research program lies in its premise to lay the groundwork for a future translational research program that will examine the development and therapeutic utility of Pitt molecules for treating prostate cancer bone metastases and overcoming enzalutamide resistance.

Up to $419K
2028-04-30
health research

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

NSF Scholarships in Science, Technology, Engineering, and Mathematics Program

open

U.S. National Science Foundation

The main goal of the S-STEM program is to enable academically talented, low-income students to pursue successful careers in promising STEM fields. Ultimately, the S-STEM program seeks to increase the number of academically promising low-income students who graduate with an S-STEM eligible degree and contribute to the American innovation economy with their STEM knowledge. Recognizing that financial aid alone cannot increase retention and graduation in STEM, the program provides awards to institutions of higher education (IHEs) not only to fund scholarships, but also to adapt, implement, and study evidence-based curricular and co-curricular[a] activities that have been shown to be effective in supporting recruitment, retention, transfer (if appropriate), student success, academic/career pathways, and graduation in STEM. To be eligible, scholars must be domestic low-income students with academic ability, talent, or potential and demonstrated unmet financial need who are enrolled in an associate, baccalaureate, or graduate degree program in an S-STEM eligible discipline. Proposers must provide an analysis that articulates the characteristics and academic needs of the population of students they are trying to serve. NSF is particularly interested in supporting the attainment of degrees in fields identified as critical needs for the Nation. It is up to the proposer to make a compelling case that such a field serves a critical need in the United States. [a] an activity at a school or college pursued in addition to the normal course of study. S-STEM Eligible Degree Programs Associate of Arts, Associate of Science, Associate of Engineering, and Associate of Applied Science Bachelor of Arts, Bachelor of Science, Bachelor of Engineering and Bachelor of Applied Science Master of Arts, Master of Science, and Master of Engineering Doctoral (Ph.D. or other comparable doctoral degree) S-STEM Eligible Disciplines Disciplinary fields in which research is funded by NSF, including technology fields associated with the S-STEM-eligible disciplines (e.g., biotechnology, chemical technology, engineering technology, information technology, etc.). The following degrees and disciplines areexcluded: Clinical degree programs, including medical degrees, nursing, veterinary medicine, pharmacy, physical therapy, and others not funded by NSF, are ineligible degrees. Programs for STEM teacher certification or licensure currently covered by the Robert Noyce Teacher Scholarship program (NOYCE) are ineligible for S-STEM funding. Business school programs that lead to Bachelor of Arts or Science in Business Administration degrees (BABA/BSBA/BBA) are not eligible for S-STEM funding. Masters and Doctoral degrees in Business Administration are also excluded. Proposers are strongly encouraged to contact Program Officers before submitting a proposal if they have questions concerning degree or disciplinary eligibility. The S-STEM program particularly encourages proposals from 2-year institutions, predominately undergraduate institutions, and urban, suburban, and rural public institutions.

$1M – $5M
2027-03-02
sciencetechnology

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

FindGrants Pro

Save unlimited matches with FindGrants Pro — $19/mo

Includes 1 application credit per month, weekly emailed grant alerts matching your org, and deadline reminders. Cancel anytime.

See Pro details

Found a grant that fits? Get matched to even more.

Answer a 2-minute questionnaire and our engine scores every grant in the database against your organization — surfacing opportunities you might miss browsing manually.

Get Personalized Matches — Free