Funded Projects

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Project # Project Title Research Focus Area Research Program Administering IC Institution(s) Investigator(s) Location(s) Year Awarded
1R43NS124421-01A1
Development of Nav1.7 Monoclonal Antibodies for Treating Pain Cross-Cutting Research Small Business Programs NINDS INTEGRAL MOLECULAR RUCKER, JOSEPH BENJAMIN Philadelphia, PA 2021
NOFO Title: HEAL INITIATIVE: Development of Therapies and Technologies Directed at Enhanced Pain Management (R43/R44 - Clinical Trial Not Allowed)
NOFO Number: RFA-NS-20-011
Summary:

Many current pain relief treatments rely on use of opioid drugs. This research is conducting preclinical development on a non-addictive, non-opioid therapeutic that uses antibodies to target the sodium channel Nav1.7. This channel is known to be one of the primary routes for generating pain signals – thus it is a target for reducing pain. The antibody approach offers potential for greater specificity than small molecule approaches, potentially resulting in fewer side effects.
3R01NS103350-02S1
REGULATION OF TRIGEMINAL NOCICEPTION BY TRESK CHANNELS Preclinical and Translational Research in Pain Management Discovery and Validation of Novel Targets for Safe and Effective Treatment of Pain NINDS WASHINGTON UNIVERSITY CAO, YUQING SAINT LOUIS, MO 2019
NOFO Title: Administrative Supplements to Existing NIH Grants and Cooperative Agreements (Parent Admin Supp Clinical Trial Optional)
NOFO Number: PA-18-591
Summary:

TWIK-related spinal cord K+ (TRESK) channel is abundantly expressed in all primary afferent neurons (PANs) in trigeminal ganglion (TG) and dorsal root ganglion (DRG), mediating background K+ currents and controlling the excitability of PANs. TRESK mutations cause migraine headache but not body pain in humans, suggesting that TG neurons are more vulnerable to TRESK dysfunctions. TRESK knock out (KO) mice exhibit more robust behavioral responses than wild-type controls in mouse models of trigeminal pain, especially headache. We will investigate the mechanisms through which TRESK dysfunction differentially affects TG and DRG neurons. Based on our preliminary finding that changes of endogenous TRESK activity correlate with changes of the excitability of TG neurons during estrous cycles in female mice, we will examine whether estrogen increases migraine susceptibility in women through inhibition of TRESK activity in TG neurons. We will test the hypothesis that frequent migraine attacks reduce TG TRESK currents.
3U24NS113844-03S1
EPPIC-NET DCC Clinical Research in Pain Management Early Phase Pain Investigation Clinical Network (EPPIC-Net) NINDS NEW YORK UNIVERSITY SCHOOL OF MEDICINE TROXEL, ANDREA B (contact); YU, CHANG New York, NY 2021
NOFO Title: Notice of Special Interest to Encourage Eligible NIH HEAL Initiative Awardees to Apply for PA-20-222: Research Supplements to Promote Diversity in Health-Related Research (Admin Supp - Clinical Trial Not Allowed)
NOFO Number: NOT-NS-20-107
Summary:

There is a clear public health imperative to improve the care and outcomes of people who experience severe acute and chronic pain. The Early Phase Pain Investigation Clinical Network (EPPIC-Net) is charged with conducting deep phenotyping and biomarker studies for specific pain conditions – and with conducting high-quality phase II clinical trials to test novel non-opioid pain treatments with academic and industry partners. This research will extend EPPIC-Net’s current portfolio to develop novel and efficient data-analytic methodologies for complex medical data, such as those that are expected to be generated by the clinical trials conducted by EPPIC-Net.
4R33NS114954-02
The Inflammatory Index as a Biomarker for Pain in Patients with Sickle Cell Disease Clinical Research in Pain Management Discovery and Validation of Biomarkers, Endpoints, and Signatures for Pain Conditions NINDS MEDICAL COLLEGE OF WISCONSIN BRANDOW, AMANDA M Milwaukee, WI 2023
NOFO Title: Discovery of Biomarkers, Biomarker Signatures, and Endpoints for Pain (R61/R33 Clinical Trial Optional)
NOFO Number: RFA-NS-18-041
1R61NS127285-01
Development of Therapeutic Antibodies to Target Sodium Channels Involved in Pain Signaling Preclinical and Translational Research in Pain Management Development and Optimization of Non-Addictive Therapies to Treat Pain NINDS University of California, Davis YAROV-YAROVOY, VLADIMIR M (contact); TRIMMER, JAMES S Davis, CA 2022
NOFO Title: HEAL Initiative: Planning Studies for Initial Analgesic Development [Small Molecules and Biologics] (R61 Clinical Trial Not Allowed)
NOFO Number: NS21-029
Summary:

Voltage-gated sodium channels such as Nav1.7, Nav1.8, and Nav1.9 transmit pain signals in nerve fibers and are molecular targets for pain therapy. While Nav channels have been validated as pharmacological targets for the treatment of pain, available therapies are limited due to incomplete efficacy and significant side effects. Taking advantage of recent advances in structural biology and computational-based protein design, this project aims to develop antibodies to attach to Nav channels and freeze them in an inactive state. These antibodies can then be further developed as novel treatments for chronic pain.