Grace Science Foundation
Public records show a registered, tax-exempt organization in good standing.
What it says it does
THE MISSION OF THE FOUNDATION IS TO SUPPORT AND FUND THE DEVELOPMENT OF LIFE-SAVING TREATMENT FOR PATIENTS THAT ARE DEFICIENT IN THE N-GLYCANESE ENZYME AND THOSE SUFFERING FROM RELATED GENETIC DISEASES. THE ACTIVITIES OF THE FOUNDATION WILL INVOLVE PROVIDING GRANT FUNDING TO HOSPITALS AND MEDICAL RESESARCH FACILITIES WHICH ARE CONDUCTING MEDICAL RESEARCH IN VARIOUS FIELDS RELATING TO THE SEARCH FOR UNDERSTNADING AND TREATMENT OF THIS CONDITION, FOSTERING COLLABORATION BETWEEN ACADEMIA, RESEARCH INSTITUTIONS, HOSPITALS, PRIVATE COMPANIES, AND GOVERNMENTAL AGENCIES.
- Income
- $943,011
- Spending
- $1.5 million
- Spent on programs
- 92%
- Reserves
- 17.6 months of spending
- Largest source of income
- donations and private grants, 92%
- Employees
- 0
- Volunteers
- 0
Source: Form 990 for the year ending December 31, 2024, filed with the Internal Revenue Service. Rating method 2026.2. How we rate
Financial health
Good: 85 out of 100. Higher than 47% of charities in its peer group (medical research, $250k to $1m).
Reserves
35 of 35Spendable reserves would cover 17.6 months of spending.
Debt
20 of 20It owes 0% of what it owns.
Living within its means
0 of 15Spending exceeded income by 61% of income.
Income trend
15 of 15Income rose 14% on the year before.
Spending floor
15 of 1592% of spending went to programs and raising each dollar of donations cost 0 cents.
Source: Form 990 for the year ending December 31, 2024, filed with the Internal Revenue Service. Rating method 2026.2. How we rate
Governance
Fair: 59 out of 100. Higher than 27% of charities in its peer group (medical research, $250k to $1m).
Independent board
25 of 257 of 7 voting board members are independent.
Conflict of interest policy
15 of 15Has a written conflict of interest policy.
Whistleblower policy
0 of 8Reports no written whistleblower policy.
Record keeping policy
0 of 7Reports no written policy on keeping and destroying records.
Board minutes
0 of 5Reports that it does not keep minutes of board meetings.
Board sees the tax return
0 of 10Did not give the board a copy of this return before filing it.
Independent check of accounts
6 of 15Its accounts were not audited or reviewed by an independent accountant.
No reported misuse
10 of 10Reports no diversion of assets, excess benefits or loans to insiders.
Source: Form 990 for the year ending December 31, 2024, filed with the Internal Revenue Service. Rating method 2026.2. How we rate
Impact evidence
Describes programs. Its tax return describes what it does but we have found no measurable results in it.
Programs described in its return (31)
- $452,697 spent. Baylor College of Medicine NGLY1 Natural History Study (Bernhard Suter) Team is conducting a natural history study to define the clinical spectrum of the disease and its progression, and define biomarker endpoints for use in therapeutic trials. This study is led by Dr. Bernhard Suter, MD, a child neurologist and medical geneticist. The study is collecting longitudinal measures of movement concurrently with clinical and biomarker measures to define aspects of gait and movement that are most affected in the disorder, characterize progression of the disease, select clinical features for performing longitudinal assessments, and inform clinical endpoint development for therapeutic trials.
- $352,945 spent. Psychogenics Inc. Team has imported and is analyzing mouse and rat models of NGLY1 Deficiency for testing of candidate therapies. Team has conducted several studies using an NGLY1 knockout rat model to test phenotypic rescue using candidate small molecule therapies (both novel and approved drugs).
- $203,574 spent. THE UNIVERSITY OF TEXAS SOUTHWESTERN MEDICAL CENTER (YAN LAB) Team continues work generating and characterizing several mouse models of NGLY1 Deficiency, including models in which the gene is inactivated in certain tissues and conditionally after birth. These mouse models have allowed them to characterize neurological phenotypes including neuronal loss, neuropathological changes, inflammation, sensory and motor defects, and disease associated biomarkers, all of which are also observed in NGLY1 Deficiency patients These animal models provide a foundation for testing candidate therapies, including gene therapies and small molecule drugs. The team has also found that NGLY1 Deficiency in mice triggers a specific innate immune pathway mediated by the cGAS/STING pathway. Using genetic and pharmacological approaches, the team has uncovered three different targets that can be modulated to reduce disease associated phenotypes and improve survival.
- $80,637 spent. The University of North Carolina (Hantman Lab)
- $68,025 spent. Charles River Laboratories
- $49,108 spent. Boston Children's Hospital (Yu Lab)
- $27,695 spent. Hilltop Lab Animals Inc.
- $24,241 spent. Albert Einstein College of Medicine (Kaushik Lab)
- $23,869 spent. Purdue University (Rochet Lab)
- $20,356 spent. Pharmaron, Inc
- $19,321 spent. Universitry of Utah (Chow Lab)
- $10,115 spent. Standford University
- $9,747 spent. University of Houston
- $19,000 spent. Bioagilytix Labs
- $13,904 spent. Transnetyx
- $10,481 spent. Wuxi Apptec
- $5,369 spent. MedChem Express LLC
- Baylor College of Medicine NGLY1 Natural History Study (Bernhard Suter)Team is conducting a natural history study to define the clinical spectrum of the disease and its progression, and define biomarker endpoints for use in therapeutic trials. This study is led by Dr. Bernhard Suter, MD, a child neurologist and medical geneticist. The study is collecting longitudinal measures of movement concurrently with clinical and biomarker measures to define aspects of gait and movement that are most affected in the disorder, characterize progression of the disease, select clinical features for performing longitudinal assessments, and inform clinical endpoint development for therapeutic trials. EXPENSES $452,697. INCLUDING GRANTS OF $452,697. REVENUE $0.
- Psychogenics Inc. Team has imported and is analyzing mouse and rat models of NGLY1 Deficiency for testing of candidate therapies. Team has conducted several studies using an NGLY1 knockout rat model to test phenotypic rescue using candidate small molecule therapies (both novel and approved drugs). EXPENSES $352,945. INCLUDING GRANTS OF $352,945. REVENUE $0.
- The University of Texas Southwestern Medical Center (Yan Lab) Team continues work generating and characterizing several mouse models of NGLY1 Deficiency, including models in which the gene is inactivated in certain tissues and conditionally after birth. These mouse models have allowed them to characterize neurological phenotypes including neuronal loss, neuropathological changes, inflammation, sensory and motor defects, and disease associated biomarkers, all of which are also observed in NGLY1 Deficiency patients These animal models provide a foundation for testing candidate therapies, including gene therapies and small molecule drugs. The team has also found that NGLY1 Deficiency in mice triggers a specific innate immune pathway mediated by the cGAS/STING pathway. Using genetic and pharmacological approaches, the team has uncovered three different targets that can be modulated to reduce disease associated phenotypes and improve survival. EXPENSES $203,574. INCLUDING GRANTS OF $203,574. REVENUE $0.
- The University of North Carolina (Hantman Lab) Team has utilized a mouse model on NGLY1 Deficiency to analyze directed movement behavior and identify the affected brain circuits responsible for the movement phenotypes charcateristic of NGLY1 Deficiency. The studies involve training wild type and Ngly1-deficient mice to perform a "reach-grab" task, comparing the task performance and movement dynamics between typical and affected animals, and recording from specific brain circuits while the animals perform the task. Identified changes will help to better understand the neural basis of the NGLY1 Deficiency movement disorder, define the neural circuits that must be targeted to treat the disease, and establish a platform to test potential therapies. EXPENSES $80,637. INCLUDING GRANTS OF $80,637. REVENUE $0.
- Charles River Laboratories Team has imported and is maintaining a colony of Ngly1 knockout rats for use in evaluating therapies to treat NGLY1 Deficiency. This knockout model has been a key foundation to test adeno-associated virus (AAV)-mediated gene delivery for rescue of disease-associated phenotypes and has supported an investigational new drug (IND) application to the FDA for an NGLY1 Deficiency gene therapy clinical study. Team has also conducted a study to monitor clinical phenotypes and collect biological samples in homozygous mutant and heterozygous (carrier) NGLY1 knockout rats across the lifespan from birth to eighteen months of age, and has continued to produce Ngly1 KO animals for use in in vivo drug testing studies. EXPENSES $68,025. INCLUDING GRANTS OF $68,025. REVENUE $0.
- Boston Children's Hospital (Yu Lab) TEAM HAS CONCEIVED AND TESTED METHODS TO USE DESIGNER ANTISENSE OLIGONUCLEOTIDES (ASOS) TO INHIBIT POTENTIAL TARGETS FOR NGLY1 THERAPY DEVELOPMENT. THIS RESEARCH HAS DEVELOPED CELLULAR MODELS TO MEASURE INHIBITION OF A SPECIFIC GENE TARGET WHOSE INACTIVATION HAS BEEN SHOWN TO R ESCUE NGLY1 LOSS. PILOT SCREENS WERE CONDUCTED AND OPTIMIZED ASOS HAVEBEEN IDENTIFIED. TEAM IS RESEARCHING METHODS TO ASSESS RESCUE OF NGLY1 DEFICIENCY PHENOTYPES UPON ASO TREATMENT. EXPENSES $49,108. INCLUDING GRANTS OF $49,108. REVENUE $0.
- HILLTOP LAB ANIMALS, INC. TEAM HAS IMPORTED AND ESTABLISHED A COLONY OF NGLY1 KNOCKOUT MICE FOR USE IN TESTING THERAPIES TO TREAT NGLY1 DEFICIENCY. A BREEDING COLONY HAS BEEN ESTABLISHED, AND MUTANT PHENOTYPES HAVE BEEN CHARACTERIZED. THIS MODEL SYSTEM HAS BEEN USED TO TEST DRUG CANDIDATES FOR THEIR ABILITY TO RESCUE NGLY1 DEFICIENCY-ASSOCIATED NEUROLOGICAL SYMPTOMS AND FOR GENETIC STUDIES TO TEST WHETHER BLOCKING OTHER PATHWAYS (INCLUDING FBXO6) HAS POTENTIAL TO TREAT NGLY1 DEFICIENCY. EXPENSES $27,695. INCLUDING GRANTS OF $27,695. REVENUE $0.
- ALBERT EINSTEIN COLLEGE OF MEDICINE (KAUSHIK LAB) TEAM IS TESTING THE HYPOTHESIS THAT DEFECTS IN NGLY1 FUNCTION LEADS TO THE IMPAIRMENT OF CELLULAR PROTEOSTASIS PATHWAYS THAT RECOGNIZE AND CLEAR MISFOLDED AND AGGREGATED PROTEINS AND DEFECTIVE ORGANELLES. USING NGLY1 KNOCKOUT RAT AND MOUSE TISSUES, NGLY1 MUTANT CELL LINES, AND NGLY1 DEFICIENCY PATIENT FIBROBLASTS, THE TEAM HAS OBSERVED SIGNIFICANT IMPAIRMENT IN MACRO- AND CHAPERONE MEDIATED-AUTOPHAGY AND DEFECTS IN LYSOSOMAL BIOGENESIS. THESE RESULTS HIGHLIGHT THE POTENTIAL OF DRUGS THAT TARGET THE AUTOPHAGY-LYSOSOME PATHWAY TO REVERSE CELLULAR DEFECTS ASSOCIATED WITH NGLY1 DEFICIENCY. THE TEAM HAS BEGUN EVALUATING DRUG-LIKE CHEMICAL MODULATORS OF THE AUTOPHAGY-LYSOSOMAL SYSTEM FOR THEIR ABILITY TO REDUCE CELLULAR PROTEOTOXICITY IN NGLY1 DEFICIENCY MODELS. EXPENSES $24,241. INCLUDING GRANTS OF $24,241. REVENUE $0.
- PURDUE UNIVERSITY (ROCHET LAB) TEAM IS DEVELOPING AND EMPLOYING CELLULAR MODELS TO TEST WHETHER NGLY1 AND ITS SUBSTRATE NFE2L1 HAVE A ROLE IN MODULATING CELLULAR STRESS AND PREVENTING OR CLEARING PROTEIN AGGREGATES IN THE BRAIN. THESE STUDIES ARE TESTING WHETHER LOSS OR DYSFUNCTION OF THE NGLY1-NFE2L1 PATHWAY MAY SENSITIZE NERVE CELLS TO OXIDATIVE OR PROTEIN MISFOLDING STRESS, LEADING TO NEURONAL DAMAGE AND NEURODEGENERATION. IN ADDITION, THE TEAM IS TESTING THE IDEA THAT ENHANCING NGLY1-NFE2L1 ACTIVITY CAN PREVENT OR SLOW NEURONAL LOSS USING CELLULAR MODELS OF PARKINSON'S DISEASE, A NEURODEGENERATIVE DISORDER ASSOCIATED WITH OXIDATIVE STRESS AND PROTEIN AGGREGATION. THESE STUDIES AIM TO UNDERSTAND THE CAUSE OF NEUROTOXICITY IN RARE AND COMMON NEURODEGENERATIVE DISORDERS, EXPLORE MECHANISMS SHARED BETWEEN NGLY1 DEFICIENCY AND PARKINSON'S DISEASE, AND PROVIDE INSIGHTS FOR THE DEVELOPMENT OF DISEASE-MODIFYING NEUROPROTECTIVE THERAPIES. EXPENSES $23,869. INCLUDING GRANTS OF $23,869. REVENUE $0.
- PHARMARON, INC TEAM HAS CONDUCTED PHARMACOLOGY STUDIES TO SUPPORT IN VIVO TESTING OF SMALL MOLECULE THERAPIES FOR NGLY1 DEFICIENCY. EXPENSES $20,356. INCLUDING GRANTS OF $20,356. REVENUE $0.
- UNIVERSITRY OF UTAH (CHOW LAB) TEAM HAS DEVELOPED AND IMPORTED MODEL ORGANISM AND HUMAN CELLULAR MODELS OF NGLY1 DEFICIENCY, CHARACTERIZED THEIR ABNORMALITIES AND BEGUN TO USE THESE TO INVESTIGATE CANDIDATE THERAPEUTIC TARGETS OF THIS RARE DISEASE. IN PARTICULAR THE TEAM IS TESTING PREVIOUSLY IDENTIFIED DRUG HITS AND INHIBITORS OF GLYCOGEN SYNTHASE 3-BETA (GSK3B) IN CELLULAR MODELS OF NGLY1 DEFICIENCY, AND IN FLY AND MOUSE MODELS OF NGLY1 DEFICIENCY. EXPENSES $19,321. INCLUDING GRANTS OF $19,321. REVENUE $0.
- BIOAGILYTIX LABS - vendor has conducted biomarker and immune profiling of NGLY1 Deficiency patients in support of NGLY1 Deficiency natural history studies. EXPENSES $19,000. INCLUDING GRANTS OF $0. REVENUE $0. TRANSNETYX - vendor has provided genotyping services to support animal breeding and functional studies at Hilltop Lab Animals and Psychogenics, Inc. EXPENSES $13,904. INCLUDING GRANTS OF $0. REVENUE $0. WUXI APPTEC - vendor has synthesized and characterized small molecule drug candidates for in vivo studies. EXPENSES $10,481. INCLUDING GRANTS OF $0. REVENUE $0.
- STANFORD UNIVERSITY DIXON AND BERTOZZI LABORATORIES) TEAM HAS CHARACTERIZED THE ROLE OF FERROPTOSIS, A FORM OF CELL DEATH ASSOCIATED WITH OXIDATIVE STRESS, IN THE PATHOLOGIES ASSOCIATED WITH NGLY1 DEFICIENCY. THIS STUDY HAS ESTABLISHED THAT LOSS OF NGLY1 OR ITS SUBSTRATE NFE2L1 SENSITIZES CELLS TO FERROPTOSIS, AND THIS FERROPTOSIS SENSITIVITY CAN BE REVERSED BY EXPRESSION OF AN ACTIVATED FORM OF NFE2L1 MIMICKING THAT GENERATED BY NGLY1-CATALYZED PROTEIN MODIFICATION. THESE STUDIES MAY HELP EXPLAIN THE CAUSES OF CELL DYSFUNCTION AND LOSS IN NGLY1 DEFICIENCY AND SUGGEST POTENTIAL TARGETS FOR CANDIDATE THERAPY DEVELOPMENT. EXPENSES $10,115. INCLUDING GRANTS OF $10,115. REVENUE $0.
- UNIVERSITY OF HOUSTON - Team has conducted a pilot movement disorder study to systematically and quantitatively assess movement disorder characteristics of individual patients with NGLY1 Deficiency. EXPENSES $9,747. INCLUDING GRANTS OF $9,747. REVENUE $0. MEDCHEM EXPRESS LLC - vendor has provided small molecule compounds for in vivo and in vitro studies. EXPENSES $5,369. INCLUDING GRANTS OF $0. REVENUE $0.
Source: Form 990 for the year ending December 31, 2024, filed with the Internal Revenue Service. Rating method 2026.2. How we rate
Legitimacy checks
Is it registered with the IRS? Passed.
Listed in the IRS master file of tax-exempt organizations as a 501(c)(3) charitable organization.
Source: Exempt Organizations Business Master File, Internal Revenue Service, file dated September 7, 2026.
Has the IRS revoked its tax-exempt status? Passed.
Not on the IRS automatic revocation list.
Source: Automatic revocation of exemption list, Internal Revenue Service, file dated September 30, 2026.
Are donations tax-deductible? Passed.
On the IRS list of organizations eligible to receive tax-deductible contributions.
Source: Publication 78 data: organizations eligible for tax-deductible contributions, Internal Revenue Service, file dated September 10, 2026.
Is it keeping up with its IRS filings? Passed.
Most recent return on file covers the year ending December 2024.
Source: Exempt Organizations Business Master File, Internal Revenue Service, file dated September 7, 2026.
How long has it been tax-exempt? Passed.
Recognized by the IRS since July 2014.
Source: Exempt Organizations Business Master File, Internal Revenue Service, file dated September 7, 2026.
Is it in good standing with state regulators? Passed.
Not on California's list of charities barred from soliciting. Other states are not yet checked.
Source: May Not Operate or Solicit for Charitable Purposes list, California Attorney General, Registry of Charities and Fundraisers, file dated October 7, 2026.
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