REGENERATIVE RESEARCH FOUNDATION

LLCNGSLHHLJ5

4S6G0

2024-06-13

http://www.neuralsci.org

2023-06-16

2007-06-01

4S6G0

Active

Non-Manufacturer

2024-05-16

2029-05-16

2025-05-14

TOM IRWIN

+1 518-694-8189

+1 518-694-8187

203654626

2023

47

5186948188

View File

2022

44

5186948188

View File

2021

38

5186948188

View File

2020

38

5186948188

View File

2019

33

5186948189

View File

HHSN263201000954P

View Award on USAspending website

AWARD

PO

Department of Health and Human Services

2010-08-16

T25 FLASK OF HUMAN IPS DERIVED RPE CELLS (STANDING ORDER , 1 FLASK PER MONTH) LAB POC SHELDON MILLER

424210: DRUGS AND DRUGGISTS' SUNDRIES MERCHANT WHOLESALERS

6505: DRUGS AND BIOLOGICALS

2022-02-22

View on USAspending

Department of Health and Human Services

DEVELOPING ANTIBODY-OLIGONUCLEOTIDE BRIDGES TO SIMPLIFY SINGLE CELL SPATIAL TRANSCRIPTOMICS - PROJECT SUMMARY SINGLE CELL RNA-SEQUENCING (SCRNA-SEQ) HAS ENABLED RESEARCHERS TO INVESTIGATE A WIDE ARRAY OF BIOLOGICAL PROCESSES AND HOW TISSUE HETEROGENEITY CONTRIBUTES TO FUNCTION. THESE TECHNOLOGIES HAVE LED TO THE DEVELOPMENT OF PROGRAMS, SUCH AS THE NIH HUMAN BIOMOLECULAR ATLAS PROGRAM, TO UNDERSTAND HOW CELLS INTERACT IN AN ORGANISM TO DRIVE ITS FUNCTION. THE DEVELOPMENT OF SPATIAL TRANSCRIPTOMIC TECHNOLOGIES HAS ALLOWED RESEARCHERS TO INVESTIGATE HOW CELL-CELL INTERACTIONS AFFECT CELLULAR GENE EXPRESSION WITHIN A TISSUE. CURRENT APPROACHES GENERALLY RELY IN SITU RNA BASED METHODOLGIES OR SLIDE-BASED SEQUENCING IN COMBINATION WITH SCRNA-SEQ (E.G. SLIDE-SEQ) TO GENERATE SPATIAL MAPS OF INTERACTING CELLS. THESE TECHNOLOGIES HAVE HELPED DEMONSTRATE THE POWER OF COMBINING THE TISSUES STRUCTURAL DATA WITH TRANSCRIPTIONAL DATA TO BETTER UNDERSTAND CELL BEHAVIOR IN A TISSUE AND GOING FORWARD IMPROVING THE INTERFACE BETWEEN THESE TECHNOLOGIES WILL BE KEY TO UNCOVERING HOW STRUCTURE AND CELL TRANSCRIPTION DRIVES FUNCTION. HOWEVER, MULTIPLE BARRIERS IMPEDE THE WIDESPREAD ADOPTION OF THE CURRENT METHODS FOR PERFORMING SPATIAL TRANSCRIPTOMICS, INCLUDING SIGNIFICANT FINANCIAL COST, TIME REQUIREMENTS, AND A LACK OF SUFFICIENT EXPERTISE. HEREIN, WE PROPOSE TO DEVELOP A SIMPLE REAGENT COMPATIBLE WITH CURRENT PROTOCOLS FOR DROP-BASED AND PIPETTE-BASED SCRNA-SEQ TECHNOLOGIES. THIS REAGENT WILL BE ABLE TO GENERATE SPATIAL DATA IN THE NORMAL COURSE OF SCRNA-SEQ EXPERIMENTS WITHOUT SIGNIFICANTLY INCREASING COST OR TIME COMMITMENTS. WE PROPOSE TO INVENT “ANTIBODY-OLIGONUCLEOTIDE BRIDGES” AND BUILD SOFTWARE CAPABLE OF BIOINFORMATICALLY GENERATING A NETWORK OF CELL-CELL CONTACTS ACROSS THE TISSUE TO RECAPITULATE THE SPATIAL RELATIONSHIPS OF THE CELLS IN A TISSUE. IN THIS PROPOSAL, WE WILL CARRY OUT A PROOF-OF- PRINCIPAL EXPERIMENT FOR THE AO BRIDGE SCRNA-SEQ APPROACH FOR GENERATING THE SPATIAL RELATIONSHIPS BETWEEN CELLS.

478500.00

0.00

0.00

2021-07-27

View on USAspending

Department of Health and Human Services

CELL TYPE AND REGIONAL VULNERABILITY IN FRONTOTEMPORAL DEMENTIA - PROJECT SUMMARY/ABSTRACT A KEY QUESTION IN TAUOPATHY RESEARCH IS WHY SOME BRAIN CELL POPULATIONS ARE SIGNIFICANTLY AFFECTED WHILE OTHERS ARE RELATIVELY SPARED. THE LONG-TERM GOAL OF THIS STUDY IS TO UNDERSTAND THIS DIFFERENTIAL CELL VULNERABILITY AND USE THE KNOWLEDGE TO DEVELOP THERAPIES THAT PROTECT NEURAL CELLS FROM TAUOPATHY-RELATED DEGENERATION. MUTATIONS IN THE MAPT GENE THAT ENCODES TAU COMMONLY CAUSE EXTENSIVE PATHOLOGY IN THE FOREBRAIN, WITH SIGNIFICANT LOSS OF FRONTAL AND TEMPORAL LOBE CEREBRAL CORTICAL CELLS LEADING TO BEHAVIORAL, LANGUAGE AND COGNITIVE DEFICITS. HOWEVER, A SUBSET OF MAPT MUTATIONS ALSO CAUSE SIGNIFICANT DEGENERATION OF MIDBRAIN DOPAMINERGIC NEURONS IN THE SUBSTANTIA NIGRA CONTRIBUTING TO A PARKINSONISM PHENOTYPE. FURTHERMORE, THESE CELLS ARE CONNECTED: MIDBRAIN DOPAMINERGIC NEURONS WIDELY INNERVATE THE PREFRONTAL CORTEX AND ARE RECIPROCALLY INNERVATED VIA CORTICO-STRIATAL-NIGRAL CIRCUITS. WHY SPECIFIC MAPT MUTATIONS SIGNIFICANTLY AFFECT THE MIDBRAIN IN ADDITION TO CORTEX WHILE OTHERS DO NOT, AND HOW CONNECTIVITY BETWEEN THESE REGIONS WITH THE POTENTIAL FOR PATHOLOGICAL TAU SPREAD MAY BE INVOLVED, REPRESENT SIGNIFICANT GAPS IN KNOWLEDGE THAT WE WILL ADDRESS IN THIS PROPOSED STUDY. OVER THE PAST FEW YEARS, WE HAVE HELPED CREATE A LARGE IPSC LINE COLLECTION FROM PATIENTS WITH FAMILIAL DEMENTIA DUE TO MUTATIONS IN THE MAPT GENE, INCLUDING ISOGENIC CONTROLS. PHENOTYPIC ANALYSES SHOW MAPT MUTANT AND CONTROL IPSC-DERIVED CEREBRAL CORTICAL CELLS ARE INITIALLY PHENOTYPICALLY SIMILAR BUT DEVELOP DIFFERENCES WITH MATURATION THAT INCLUDE INCREASED TAU AGGREGATION, TAU HYPERPHOSPHORYLATION AND VULNERABILITY TO SEVERAL STRESSORS, ASSOCIATED WITH THE MUTATION. HOWEVER, TO DATE, STUDIES COMPARING FOREBRAIN AND MIDBRAIN CELL POPULATION RESPONSES TO MAPT MUTATIONS THAT DIFFERENTIALLY AFFECT THESE BRAIN REGIONS HAVE NOT BEEN DONE. SUCH COMPARISONS HAVE THE POTENTIAL TO REVEAL COMMON AND UNIQUE MOLECULAR MECHANISMS THAT UNDERLIE CELL VULNERABILITY. OUR APPROACH IS TO USE HUMAN IPSC-DERIVED 3D ORGANOIDS, WHICH RECAPITULATE COMPLEX CELL-CELL INTERACTIONS IN A HUMAN CELL SYSTEM AND ENABLE LONG-TERM CULTURE OVER SEVERAL MONTHS. WE WILL CREATE CORTICAL AND MIDBRAIN ORGANOIDS FROM TWO MAPT MUTATIONS THAT PRIMARILY AFFECT CORTEX AND TWO THAT AFFECT BOTH CORTEX AND MIDBRAIN, VERSUS RESPECTIVE ISOGENIC CONTROLS. IN AIM 1 WE WILL EXAMINE THE IMPACT OF THESE MAPT MUTATIONS ON CELL POPULATIONS AND GENE EXPRESSION OVER TIME USING SINGLE CELL TRANSCRIPTOMICS TO DEFINE HOW DIVERSE CELL TYPES RESPOND TO EACH MUTATION. IN AIM 2, WE WILL CREATE ASSEMBLOIDS OF CORTICAL AND MIDBRAIN ORGANOIDS TO MODEL THE CIRCUITRY BETWEEN THE REGIONS AND DETERMINE WHETHER THIS CONNECTIVITY ALTERS PATTERNS OF CELL VULNERABILITY AND ENABLES THE SPREAD OF PATHOLOGICAL TAU FROM ONE REGION TO ANOTHER, DEPENDING ON SPECIFIC MAPT MUTATION. IN AIM 3 WE WILL PROBE THE IMPACT OF STIMULATING TAU DEGRADATION ON DIFFERENTIAL CELL VULNERABILITY IN CEREBRAL CORTEX AND MIDBRAIN.

1486445.66

0.00

0.00

2021-06-25

View on USAspending

Department of Health and Human Services

INVESTIGATING THE FUNCTIONAL IMPACT OF AD RISK GENES ON NEURO-VASCULAR INTERACTIONS - PROJECT SUMMARY/ABSTRACT CEREBROVASCULAR PATHOLOGY IS PRESENT THROUGHOUT STAGES OF ALZHEIMER’S DISEASE AND IS CORRELATED WITH COGNITIVE CHANGES. THERE IS STRONG EVIDENCE THAT VASCULAR DYSFUNCTION IS A SIGNIFICANT DRIVER OF NEUROPATHOLOGY. OUR LONG- TERM OBJECTIVE IS TO UNDERSTAND THE FUNCTION OF ALZHEIMER’S DISEASE-ASSOCIATED RISK GENES IN VASCULAR CELLS, THEIR CONTRIBUTION TO THE DEVELOPMENT OF CEREBROVASCULAR PATHOLOGY AND THE OPPORTUNITIES TO USE THIS INFORMATION IN THERAPEUTIC DEVELOPMENT. THERE ARE OVER 27 ALZHEIMER’S DISEASE-ASSOCIATED RISK (AD-RISK) LOCI ENCOMPASSING NUMEROUS GENETIC VARIANTS IN NON-CODING AND CODING REGIONS AND HUNDREDS OF LINKED GENES. OUR OVERARCHING HYPOTHESIS IS THAT A SUBSET OF AD-RISK GENES IMPAIRS VASCULAR FUNCTION, CAUSING RELEASE OF INFLAMMATORY FACTORS, BLOOD BRAIN BARRIER (BBB) IMPAIRMENT, AND REDUCED PERFUSION, THUS CONTRIBUTING TO NEURODEGENERATION. TO ADDRESS THIS, WE HAVE ASSEMBLED A MULTI-DISCIPLINARY TEAM WITH A PROVEN TRACK RECORD OF COLLABORATION, INCLUDING WITH ADSP AND ADGP MEMBERS, WHO BRING EXPERTISE IN VASCULAR PATHOLOGY IN DEMENTIA, ENDOTHELIAL CELL (EC) SIGNALING AND EC FUNCTIONAL TESTING, ALZHEIMER’S DISEASE GENOMICS, SINGLE CELL AND NUCLEAR TRANSCRIPTOMICS, BIOINFORMATICS, CRISPR-BASED GENE EDITING FOR LARGE SCALE SCREENING AND AD MOUSE MODELS FOR IN-DEPTH FUNCTIONAL ASSESSMENT IN VIVO. NOTABLY, WE WILL ADDRESS DIFFERENCES IN GENE EFFECTS RELATED TO THE IMPORTANT BIOLOGICAL VARIABLES, SEX AND METABOLIC DISEASE. MEN AND WOMEN DIFFER IN THEIR GENETIC RISK FOR ALZHEIMER’S DISEASE, WITH SEX-SPECIFIC POLYGENIC RISK SCORES PROVIDING BETTER PREDICTION OF ONSET, PROGRESSION, AND PATHOLOGY THAN POOLED-SEX SCORES. OVER 80% OF INDIVIDUALS WITH ALZHEIMER’S DISEASE HAVE CO-MORBID METABOLIC DISEASE, WHICH EXACERBATES VASCULAR PATHOLOGY. WE HAVE IDENTIFIED THE TOP 50 AD-RISK SNPS AND 600 AD-ASSOCIATED GENES, AND THESE WILL BE TARGETED FOR INDUCED PLURIPOTENT STEM CELL (IPSC)-DERIVED ENDOTHELIAL CELL (EC) SCREENS BY PRIME EDITING AND CRISPR-BASED GENE INHIBITION AND ACTIVATION APPROACHES RESPECTIVELY. IPSC-BASED PRODUCTION OF HUMAN ECS AND MURAL CELLS IN 2D AND 3D MODELS HAS BEEN OPTIMIZED AND SCALED TO ENABLE EFFICIENT FUNCTIONAL TESTING OF THE IMPACT OF GENE CHANGES, INCLUDING ON NEURO-VASCULAR INTERACTIONS IN CEREBRAL ORGANOIDS. DISCOVERIES MADE IN THESE HUMAN CELL SYSTEMS WILL BE VALIDATED BY AN IN-DEPTH INVESTIGATION OF GENE EXPRESSION CHANGES IN INDIVIDUAL ECS AND MURAL CELLS ACROSS A LARGE COLLECTION OF ALZHEIMER’S DISEASE BRAIN SAMPLES USING SINGLE NUCLEAR SEQUENCING. THE EC TRANSLATOME WILL ALSO BE OBTAINED FROM MOUSE ALZHEIMER’S DISEASE MODELS THAT INCORPORATE SEX AND METABOLIC DISEASE. THESE DIVERSE DATASETS WILL BE HARMONIZED AND INTEGRATED IN ORDER TO MAP VASCULAR PHENOTYPES OF AD-RISK GENES AND IDENTIFY CRITICAL MOLECULAR PATHWAYS THAT ARE TARGETABLE DRIVERS OF AD CEREBROVASCULAR PATHOLOGY. THESE DATA WILL ADD TO THE BREADTH OF KNOWLEDGE BEING GATHERED BY OTHER GROUPS TO FURTHER ELUCIDATE UNDERLYING NEURONAL, GLIAL, MICROGLIAL, ENDOTHELIAL AND MURAL CELL-CELL INTERACTIONS THAT CONTRIBUTE IN A SUBSTANTIAL WAY TO THE COMPLEX ARCHITECTURE OF ALZHEIMER DISEASE PATHOLOGY. 1

7139996.00

0.00

0.00

2021-02-01

View on USAspending

Department of Health and Human Services

CHARACTERIZING HUMAN RPE CELL PROLIFERATION TO ADVANCE ENDOGENOUS REGENERATION - PROJECT SUMMARY / ABSTRACT DECADES OF STUDY HAVE DEMONSTRATED THAT ADULT HUMAN RETINAL PIGMENT EPITHELIUM (RPE) CELLS HAVE STRONG PROLIFERATIVE CAPACITY IN VITRO, WHICH INDICATES THAT THE RPE LAYER HAS THE POSSIBILITY OF SELF-REPAIR. WE HAVE SHOWN THAT ADULT RPE FROM ELDERLY DONORS OR DONORS WITH AGE-RELATED MACULAR DEGENERATION (AMD) CAN PROLIFERATE IN CULTURE AND PRODUCE A NEAR-NATIVE, RENEWED RPE MONOLAYER. DESPITE THIS, RPE CELLS IN VIVO DO NOT REGENERATE THE DAMAGED COBBLESTONE RPE LAYER IN PATIENTS WITH DEGENERATING CELLS, SUCH AS THOSE WITH DRY AMD. THE ENVIRONMENT IN VIVO MUST EFFECTIVELY PREVENT REPAIR OF THE COBBLESTONE RPE MONOLAYER, EITHER THROUGH LACK OF MITOGENS OR INHIBITORY MOLECULES OR A COMBINATION OF BOTH. THE OVERARCHING GOAL OF THESE STUDIES IS TO ACHIEVE SAFE, CONTROLLED PROLIFERATION OF ENDOGENOUS RPE CELLS TO ENABLE SELF-REPAIR OF THE RPE LAYER IN PATIENTS WITH AMD. THE OBJECTIVE OF THIS PROPOSAL IS TO CHARACTERIZE THE ENVIRONMENTAL FACTORS THAT POSITIVELY AND NEGATIVELY CONTROL THE PROLIFERATION OF ADULT HUMAN RPE CELLS. THE FIRST SPECIFIC AIM IS TO CHARACTERIZE THE ADULT HUMAN RPE CELL SURFACEOME ON DIVIDING AND NON-DIVIDING CELLS USING AN INNOVATIVE MASS SPECTROMETRY AND BIOINFORMATIC PLATFORM. THIS WILL PROVIDE THE FIRST COMPREHENSIVE ANALYSIS OF THE MOLECULES ON THE RPE PLASMA MEMBRANE AND REVEAL CELL SURFACE RECEPTORS AND SECRETED PROTEINS THAT RESPOND TO ENVIRONMENTAL FACTORS IMPACTING CELL DIVISION. INVESTIGATING BOTH NORMAL AND AMD RPE WILL PROVIDE A GREATER UNDERSTANDING OF HOW RPE CELLS CHANGE WITH DISEASE. THE SECOND SPECIFIC AIM IS TO EXAMINE A TRANSCRIPTIONAL NETWORK WE HAVE IDENTIFIED THAT IS ASSOCIATED WITH ADULT HUMAN RPE CELL PROLIFERATION TO DETERMINE WHICH MOLECULES ARE CRITICAL. TO DO THIS EFFICIENTLY, WE WILL FIRST EMPLOY CRISPRI, THEN ADDITIONAL FUNCTIONAL SCREENS. THE THIRD SPECIFIC AIM WILL EXAMINE WHETHER EXOGENOUS FACTORS CAN ACTIVATE PROLIFERATION OF QUIESCENT, COBBLESTONE HUMAN RPE, INCLUDING THOSE IN SITU ON BRUCH’S MEMBRANE EXPLANTS, AND THOSE FROM PATIENTS WITH AMD. IN ADDITION TO THE MAIN OBJECTIVE, THIS STUDY WILL GENERATE NEW KNOWLEDGE ABOUT RPE MOLECULES THAT CAN BE USED TO TARGET RPE IN VIVO. THE PROPOSED WORK ALSO HAS THE POTENTIAL TO IMPROVE RPE CELL PROLIFERATION EX VIVO FOR MORE EFFICIENT CELL MANUFACTURING. MOST IMPORTANTLY, THIS STUDY WILL CREATE A FOUNDATION FOR SAFELY STIMULATING RPE CELL PROLIFERATION IN VIVO. ENDOGENOUS ACTIVATION OF RPE CELL PROLIFERATION TO COUNTERACT RPE CELL LOSS IN AMD HAS THE POTENTIAL TO AVOID SURGERY AND IMMUNOSUPPRESSION INVOLVED IN RPE CELL TRANSPLANTATION, WHICH WOULD GREATLY BENEFIT THE ELDERLY AMD PATIENT POPULATION.

2286488.00

0.00

0.00

2021-09-10

View on USAspending

Department of Health and Human Services

PHASE1/2A CLINICAL TRIAL OF RPESC-DERIVED RPE TRANSPLANTATION AS THERAPY FOR NON-EXUDATIVE AGE-RELATED MACULAR DEGENERATION - PROJECT SUMMARY/ABSTRACT AGE-RELATED MACULAR DEGENERATION (AMD) IS A MAJOR CAUSE OF BLINDNESS IN OUR AGING POPULATION. EARLY AMD PATHOGENESIS INVOLVES ATROPHY OF THE RETINAL PIGMENT EPITHELIUM (RPE) WITH ACCOMPANYING LOSS OF RETINAL FUNCTION AND VISION. ALTHOUGH THERAPY IS AVAILABLE FOR EXUDATIVE (WET) AMD, AN EFFECTIVE TREATMENT IS NOT AVAILABLE FOR THE MORE COMMON NON- EXUDATIVE (DRY) AMD FORM. PLURIPOTENT STEM CELL (PSC)-DERIVED RPE (PSC-RPE) TRANSPLANTATION HAS SHOWN PROMISE FOR AMD IN EARLY CLINICAL TRIALS. DUE TO THE HIGHLY PROLIFERATIVE AND PLASTIC NATURE OF PSC, HOWEVER, EXTENSIVE DIFFERENTIATION TO RPE IS NEEDED PRIOR TO TRANSPLANTATION TO AVOID TUMOR GROWTH AND GENOTYPE INSTABILITY INHERENT TO THE PSC SOURCE. WE DISCOVERED AN ADULT RPE STEM CELL (RPESC) WITH RESTRICTED PROLIFERATIVE AND LINEAGE POTENTIAL. RPESC-DERIVED RPE (RPESC- RPE) DO NOT FORM TUMOR ENABLING TRANSPLANTATION OF LESS DIFFERENTIATED RPE AT THE PROGENITOR STAGE. WE FOUND THAT TRANSPLANTED RPE PROGENITOR CELLS WERE MORE EFFECTIVE THAN HIGHLY DIFFERENTIATED PROGENY AT VISION RESCUE IN THE ROYAL COLLEGE OF SURGEONS RAT MODEL OF AMD. RPESC-RPE DIFFERENTIATED FOR 4 WEEKS INTO AN INTERMEDIATE RPE PROGENITOR STAGE RESCUED VISION MORE EFFECTIVELY THAN CELLS DIFFERENTIATED FOR 8 WEEKS INTO THE MATURE RPE PHENOTYPE. THIS IMPROVED EFFICACY COMBINED WITH LACK OF TUMORGENICITY PROVIDES COMPELLING RATIONALE FOR THE PROPOSED PHASE 1/2A CLINICAL TRIAL OF RPESC-RPE TRANSPLANTATION AS THERAPY FOR DRY AMD. EXPERIENCED CLINICAL TRIAL TEAMS HAVE BEEN ASSEMBLED AT THE UNIVERSITY OF MICHIGAN KELLOGG EYE CENTER (KEC) AND STANFORD UNIVERSITY. THE KEC TEAM INCLUDES A VITREORETINAL SURGEON EXPERIENCED IN STEM CELL RESEARCH WHO WILL RECRUIT, PERFORM INTERVENTIONS, AND MANAGE PARTICIPANT CARE. ANOTHER RETINAL SPECIALIST WILL DIRECT POST-INTERVENTION ASSESSMENT AT THE KEC CLINICAL RESEARCH CENTER, AND A SENIOR KEC RETINAL SPECIALIST WILL SERVE AS ON-SITE MEDICAL MONITOR. A CLINICAL TRIALIST HIGHLY EXPERIENCED IN EARLY PHASE OPHTHALMIC TRIALS WILL PROVIDE REGULATORY, DESIGN AND STATISTICAL SUPPORT. THE NEURAL STEM CELL INSTITUTE (NSCI) AND THE STANFORD UNIVERSITY BYERS EYE INSTITUTE WILL WORK WITH KEC TO PROVIDE SCIENTIFIC AND CLINICAL GUIDANCE FOR THE PROPOSED TRIAL. SINGLE CELL TRANSCRIPTOMIC ANALYSES GENERATED AT NSCI WILL BE CORRELATED WITH CLINICAL OUTCOMES, WHICH WILL CONTRIBUTE TO THE RECOGNIZED NEED FOR IMPROVED CELL PRODUCT IDENTITY AND POTENCY MEASURES IN REGENERATIVE MEDICINE GENERALLY. WE PROPOSE TO COMBINE A STRONG PROGRAM IN STEM CELL BIOLOGY WITH AN EXPERIENCED TEAM IN THE CONDUCT OF OPHTHALMIC CLINICAL TRIALS SOUND CLINICAL TRIAL CONDUCT AIMS TO PRODUCE RELIABLE OUTCOMES RESULTS TO EVALUATE RPESC-RPE PROGENITOR CELL TRANSPLANTATION AS THERAPY FOR DRY AMD. OUTCOMES WILL BE CORRELATED WITH PRODUCT IDENTITY AND POTENCY MEASURES AT THE SINGLE CELL LEVEL. COMPLETION OF THE PROPOSED WORK WILL IMPROVE UNDERSTANDING OF RM PRODUCT CHARACTERIZATION AND ADVANCE A UNIQUE TYPE OF ADULT STEM CELL TO REPLACE RPE FOR DRY AMD PATIENT BENEFIT.

2612955.28

0.00

0.00

20-3654626

Government Instrumentality, Title-Holding Corporation, Charitable Organization, Educational Organization, Local Association of Employees, Agricultural Organization, Horticultural Organization, Board of Trade, Business League, Pleasure, Recreational, or Social Club, Fraternal Beneficiary Society, Order or Association, Voluntary Employees' Beneficiary Association (Non-Govt. Emps.), Voluntary Employees' Beneficiary Association (Govt. Emps.), Domestic Fraternal Societies and Associations, Teachers Retirement Fund Assoc., Benevolent Life Insurance Assoc., Mutual Ditch or Irrigation Co., Burial Association, Cemetery Company, Credit Union, Other Mutual Corp. or Assoc., Mutual Insurance Company or Assoc. Other Than Life or Marine, Corp. Financing Crop Operations, Supplemental Unemployment Compensation Trust or Plan, Employee Funded Pension Trust (Created Before 6/25/59), Post or Organization of War Veterans, Legal Service Organization, Black Lung Trust, Multiemployer Pension Plan, Veterans Assoc. Formed Prior to 1880, Trust Described in Sect. 4049 of ERISA, Title Holding Co. for Pensions, etc., State-Sponsored High Risk Health Insurance Organizations, State-Sponsored Workers' Compensation Reinsurance, ACA 1322 Qualified Nonprofit Health Insurance Issuers, Apostolic and Religious Org. (501(d)), Cooperative Hospital Service Organization (501(e)), Cooperative Service Organization of Operating Educational Organization (501(f)), Child Care Organization (501(k)), Charitable Risk Pool, Qualified State-Sponsored Tuition Program, 4947(a)(1) - Private Foundation (Form 990PF Filer)

2007-11

Medical Research: Neurology, Neuroscience Research

Type of organization and use of contribution: A public charity. Deductibility Limitation: 50% (60% for cash contributions)

2020-04-28

Paid in Full

100

349840

349840

Unanswered

Unknown/NotStated

Unanswered

Unanswered

352332.01