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The HUGO-GT™ Grant Awards aims to support high impact preclinical research – in the fields of rare disease, ultra-rare disease, ophthalmology, neurology, and oncology − to develop next-generation humanized mouse models for effective disease R&D and gene therapy evaluations. If you are conducting research that could use humanized mouse models to substantiate your studies, we invite you to apply for a grant from the HUGO-GT™ Grant Awards!

Cyagen launched the HUGO-GT™ (Humanized Genomic Ortholog for Gene Therapy) program to develop full-length genomic sequence humanized mouse models with a broader range of intervention targets relevant to human genetic diseases. We employ our proprietary TurboKnockout-Pro technology to perform in-situ replacement of the targeted mouse endogenous gene, creating full-length genomic sequence humanized mouse models with a broader range of intervention targets.

The HUGO-GT™ Grant Awards offers researchers the opportunity to apply for a FREE pair of wild-type (wt) humanized mice from our standard HUGO-GT™ model service ($76,000 value). All applicants will also qualify for $15,000 off CRISPR point mutation (PM) services to investigate mutations of clinical significance based on our preexisting wt HUGO-GT™ humanized mouse strains.

Submit an online application form (below) to receive 50% off CRISPR PM services on existing wt HUGO-GT™ models ($15,000 value) and have a chance to win any of the wt HUGO-GT™ mouse model research grants ($76,000 value) offered by Cyagen Biosciences across the following award categories:

Research Grant Award Categories:
Ophthalmology
Neurology
Oncology
Rare diseases
Ultra-rare diseases
Grant Status - Apply Now!
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Applications will be reviewed on a rolling basis until all awards are selected, so early submissions have a greater chance for selection! As the awards for each Research Grant Award Category are granted, the application form for the respective category will close. Feel free to contact us if you have any questions regarding your submission.

Awards

One (1) Grand Prize (per Category, 5 total): Free standard wild-type (wt) HUGO-GT™ model service with up to 3 rounds of gene targeting with TurboKnockout-Pro ($76,000 value)

Research Categories
  • Ophthalmology
  • Neurology
  • Oncology
  • Rare diseases
  • Ultra-rare diseases

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*All eligible grant applications will receive 50% off CRISPR PM services on existing wt HUGO-GT™ models ($15,000 value)!

The grant award can be used as store credit towards Cyagen’s HUGO-GT™ model services and related downstream CRO services and/or CGT development platforms for model validation within 6 months of the award date of the grant. The award may be used for one (1) single standard HUGO-GT™ mouse model generation project (up to 3 rounds of gene targeting with TurboKnockout-Pro, $76,000 value) as described in the winning application(s). It cannot be used in combination with other coupons, discounts, or promotional offers.

All professionals in academic, non-profit, and not-for-profit biological research are eligible to apply, including graduate students, post-docs, principal investigators, and staff scientists. Please read the HUGO-GT™ Grant Awards Official Rules for full details regarding the grant competition.

Apply Now

Please visit our Application Guidelines for a quick outline of the requested materials and judging criteria for entries. Submit your application for the HUGO-GT™ Grant Awards by completing the following form:

■ HUGO-GT™ Grant Application Form
Choose the files
Application Documents include:
  • Research Proposal (Need help? Check out this Sample Application)
  • Biosketch (Covering research from 2022-present)
  • Optional supporting documents (e.g. PI Letter of Support)
Note: Multiple files can be attached. 20 MB size limit per file.
“The HUGO-GT program provides valuable insights into the translation of gene therapies from bench to bedside, aiding in the development of targeted and effective treatments for various genetic diseases. I think it has the potential to reshape preclinical model selection, since these mice own the highest level of humanization that you could find from the market, which will be more accurately recapitulate the disease state you’re trying to address.”
——Dr. Marvin Ouyang, CSO of Cyagen Bioscience
HUGO-GT™: Wild-Type Humanized Mouse Models
Product Number Product Strain Background Application
C001396 B6J-hRHO C57BL/6JCya Retinitis Pigmentosa (RP), Congenital Stationary Night Blindness (CSNB), and other retinal diseases.
C001410 B6-htau C57BL/6JCya Frontotemporal Dementia (FTD), Alzheimer's Disease (AD), and other neurodegenerative diseases.
C001418 B6-hTARDBP C57BL/6JCya Amyotrophic Lateral Sclerosis (ALS), Frontotemporal Dementia (FTD), and other neurodegenerative diseases.
C001427 B6-hSNCA C57BL/6NCya Parkinson's Disease (PD).
C001437 B6-hIGHMBP2 C57BL/6NCya Spinal Muscular Atrophy with Respiratory Distress Type 1 (SMARD1) and Charcot-Marie-Tooth Disease Type 2S (CMT2S).
C001495 B6-hRHO-P23H C57BL/6JCya Retinitis pigmentosa (RP), congenital stationary night blindness (CSNB), and other retinal diseases research
C001504 B6-hSMN2(SMA) C57BL/6NCya Spinal muscular atrophy (SMA)
I001128 B6-hMECP2 C57BL/6NCya Rett Syndrome (RTT)
I001124 B6-hLMNA C57BL/6NCya Hutchinson-Gilford Progeria Syndrome (HGPS)
C001398 B6-hATXN3 C57BL/6NCya Spinocerebellar Ataxia Type 3 (SCA3)
C001512 B6-hTTR C57BL/6NCya Transthyretin Amyloidosis (ATTR)
I001131 B6-hSCN2A C57BL/6NCya Epilepsy
I001132 B6-hCFTR C57BL/6NCya Cystic Fibrosis (CF)
C001525 H11-Alb-hTTR*V50M C57BL/6NCya Transthyretin Amyloidosis (ATTR)
I001130 B6-hATP7B C57BL/6NCya Hepatolenticular Degeneration (HLD)
IR1019 SD-hGFAP Rat Sprague-Dawley Alexander disease (AxD), traumatic brain injury
C001533 B6-hINHBE C57BL/6NCya Obesity, metabolic disorders associated with improper fat distribution and storage
C001538 B6-hCOL7A1*c.6527dupC C57BL/6NCya Dystrophic Epidermolysis Bullosa (DEB)
C001428 B6-hCOL7A1 C57BL/6NCya Epidermolysis Bullosa (EB)
C001546 B6-hTGFBI C57BL/6JCya Corneal Dystrophy (CD)
C001551 B6-hABCA4 C57BL/6JCya Stargardt Disease (STGD)
C001554 B6-hUSH2A(E10-15) C57BL/6JCya Usher Syndrome (USH)
C001555 B6-hVEGFA C57BL/6JCya Age-related Macular Degeneration (AMD); Diabetic Retinopathy (DR); Corneal Neovascularization; Mechanisms of Tumorigenesis and Development, and Development of Antitumor Drugs.
I001191 B6-hFUS C57BL/6JCya Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal Lobar Degeneration/Dementia (FTLD)
I001181 B6-htau*P301L C57BL/6JCya Frontotemporal Dementia (FTD), Alzheimer's Disease (AD), and other neurodegenerative diseases.
I001182 B6-htau*P301S C57BL/6JCya Frontotemporal Dementia (FTD), Alzheimer's Disease (AD), and other neurodegenerative diseases.
I001203 B6-hELP1 C57BL/6NCya Familial Dysautonomia (FD)
I001179 B6-hPCSK9 C57BL/6NCya Research on metabolic diseases such as hypercholesterolemia, atherosclerosis, and coronary heart disease; neurodegenerative diseases such as stroke and Alzheimer's disease; and tumor immunotherapy and autoimmune disease treatment.
I001217 B6-hCEP290 C57BL/6JCya Leber Congenital Amaurosis (LCA)
I001218 B6-hC5 C57BL/6JCya Age-related Macular Degeneration (AMD)
I001133 B6-hDMD (E49-53) C57BL/6NCya Duchenne Muscular Dystrophy (DMD)
I001204 B6-hDMD(E44-45) C57BL/6NCya Duchenne Muscular Dystrophy (DMD)
I001208 B6-hDMD(E44-45)*Del E44 C57BL/6NCya Duchenne Muscular Dystrophy (DMD)
I001210 B6-hABCA4*c.5461-10T>C C57BL/6JCya Stargardt disease (STGD); Cone-Rod Dystrophy (CRD); Retinitis Pigmentosa (RP)
I001195 DBA/1-hTNF DBA/1 Research on rheumatoid arthritis (RA); studies on the TNF-α signaling pathway; research on the pathogenesis and treatment of other TNF-α-related diseases
I001190 B6-hMECP2*T158M C57BL/6NCya Rett Syndrome (RTT)
I001216 B6-hSCN9A C57BL/6NCya Research on erythromelalgia, Dravet syndrome, small fiber neuropathy, and congenital insensitivity to pain; research on the pathogenesis of other neurological diseases and analgesic drugs.
I001221 B6-htau/hGLP-1R C57BL/6Cya Research on neurodegenerative diseases such as frontotemporal dementia (FTD) and Alzheimer's disease (AD); research on metabolic diseases such as obesity and type 2 diabetes; evaluation of the potential efficacy of GLP-1 receptor agonists (GLP-1RA) in Alzheimer's disease (AD).
Why Humanized Mice?
Compared to traditional transgenic (Tg) animal models, the humanized mouse model is a powerful tool that excels in replicating human physiological and pathological characteristics. This makes humanized mice the preferred choice for studying human diseases and assessing the safety and effectiveness of potential therapeutics. Humanized mice provide improved alignment with human biology, leading to more precise predictions of drug responses and disease mechanisms – potentially streamlining the translation from preclinical research to clinical applications.
What are the shortcomings of current humanized mouse models?
Despite their popularity, common humanized models — including transgenic (Tg) mice, coding sequence (CDS), and single-exon humanized mice — fall short in achieving full human gene integration into the mouse genome. These current-generation models come with notable limitations such as random insertion, complex genetic backgrounds, and inadequate humanized regions.
How can humanized models be improved for preclinical research?
One of the key requirements during preclinical study is selection of appropriate animal models, which help translate basic study into clinical applications. To advance our understanding of disease mechanisms and drug development, there is a pressing need for full-length genomic DNA humanized mice. These models can faithfully replicate human gene expression patterns, regulations, and functional properties in a mouse model. However, replacing the entire genomic DNA sequence poses technical challenges as introducing large exogenous sequences may impact the expression and regulation of endogenous genes, presenting a significant obstacle.
“Current commonly used humanized models can only achieve partial insertion of the human gene, which exhibit notable limitations, including random insertion, complex genetic background and line establishment, as well as inadequate humanized regions. To facilitate further advancement of disease mechanistic study and related drug development, full-length genomic DNA humanized mice — that can faithfully recapitulate the expression pattern, regulation, and functional properties of human gene in a mouse model — are urgently needed to replace the existing animal models and reshape the translational research framework for drug development.”
------ Lance Han, CEO of Cyagen Biosciences
Full-Length Genomic Sequence Humanized HUGO-GT™ Mouse Models

In response to these demands, Cyagen has developed novel whole genomic DNA humanized mouse models for accelerating gene therapy drug development: Humanized Genomic Ortholog for Gene Therapy HUGO-GT™ mice. The HUGO-GT™ next-generation humanized mouse models feature the following technical improvements to provide clinically relevant humanized mouse models more closely aligned with real-world biological mechanisms:

Our proprietary TurboKnockout-Pro technology is used to perform in-situ replacement of the targeted mouse endogenous gene, creating full-length genomic sequence humanized mouse models with a broader range of intervention targets.
Incorporation of our highly efficient large-fragment vector fusion technology enables our wild-type (wt) HUGO-GT™ mice to serve as a versatile template for customized targeted mutagenesis.

In addition to our mouse models, we offer Contract Research Organization (CRO) services in various fields, including ophthalmology, neuroscience, tumor immunology, and other disease areas. Our aim is to empower research on genetic diseases and facilitate the development of gene therapy drugs.

How HUGO-GT Works

When replacing a mouse gene with the full genomic sequence of its human counterpart, the size of the DNA sequence can pose challenges for CRISPR-based approaches. In such cases, the use of homologous recombination in embryonic stem (ES) cells remains a viable and effective option.

Cyagen has leveraged the power of TurboKnockout-Pro, our proprietary high efficient ES targeting technology, to achieve in-situ replacement of the targeted mouse endogenous gene and successfully construct full-length genomic sequence humanized mouse models: HUGO-GT mice, that encompass a broader range of intervention targets.

Why HUGO-GT

HUGO-GT program is a comprehensive approach that combines the advantages of humanizing mouse genes through genomic replacement with the investigation of disease-causing mutations and potential gene therapy interventions.

Advantages of HUGO-GT™ Genomic DNA Humanized Model
  • In Situ Gene Replacement: Full genomic sequences (UTR, exon, intron) ensure accurate human gene function within the mouse genomic context and in vivo environment.
  • Minimal Gene Regulation Disruption: Maintains natural regulation and expression patterns, preserving different isoforms across tissues and cell types.
  • Flexible and Efficient: Initial wild-type humanization on mouse ES cells allows rapid introduction of disease-causing mutations, facilitating drug testing and research.
  • Superior Accuracy: Reduces artifacts seen in other models, providing phenotypes that closely resemble human conditions.
  • Comparative Superiority: Outperforms models with simple point mutations, CDS-only replacements, and BAC transgenes with random integration.