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Assay-Ready iPSC-Derived
DM1 Skeletal Muscle Myoblasts

Patient-specific human myoblasts and CRISPR-corrected isogenic control — optimized for 3D engineered muscle tissue research and therapeutic discovery

iPSC-Skeletal Muscle Line Genetic Mutation Clinical Disease Price
DM1-716
(Disease)
35 y.o. male 		CTG trinucleotide repeat expansion in 3′ UTR of DMPK
716 CTG repeats (~2,100 nt)		 Myotonic Dystrophy Type 1 $3,295
6 million cells
$5,995
12 million cells
*10 day supply of media included
DM1-473
(Disease)
18 y.o. male 		CTG trinucleotide repeat expansion in 3′ UTR of DMPK
473 CTG repeats (~1,500 nt)		 Myotonic Dystrophy Type 1
DM1-0
(Isogenic Control) 		0 CTG repeats (CRISPR-corrected) · WGS confirmed Isogenic control to DM1-716
24-WT
(Unrelated Wild-Type) 		Normal CTG repeat length Healthy reference control $2,550
6 million cells
$4,750
12 million cells
*10 day supply of media included
💡 Bundle & Save: Full 4-line bundles available. Contact us for volume pricing.
Request a Quote to Order
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 Enabling DM1 Therapeutic Discovery

Myotonic Dystrophy Type 1 (DM1) is the leading cause of adult-onset muscular dystrophy and a pervasive, multi-systemic disorder. Characterized by progressive muscle wasting, myotonia, and life-threatening cardiac complications, symptoms typically emerge in early adulthood and worsen over time. Despite its profound and life-altering impact, there is currently no cure for this degenerative condition.

DM1 is caused by an unstable expansion of CTG trinucleotide repeats in the 3′ UTR of the DMPK gene on chromosome 19. The expanded DMPK transcript forms toxic RNA foci that accumulate in the nucleus and sequester critical RNA-binding proteins, particularly Muscleblind-like splicing regulators (MBNL1/2). This triggers widespread splicing dysregulation across hundreds of transcripts, contributing to nearly all aspects of DM1 pathology.

Validated Phenotypes, Clinical Relevance

Curi Bio's DM1 myoblasts recapitulate hallmark molecular and cellular features of DM1 disease, providing a biologically relevant platform for target validation and therapeutic testing. The model includes two patient-derived disease lines spanning a range of CTG repeat lengths, one CRISPR-corrected isogenic control, and one unrelated wild-type line. This enables precise dose-response profiling and ensures that every insight is rooted in disease biology, not genetic noise.

 

Force Deficit Inversely Correlates with CTG Length

Nuclear RNA Foci bind MBNL1

 

Emergent Relaxation Prolongation Indicative of a Nascent Myotonic Phenotype

Impaired Calcium Handling

 
 

 More DM1 Resources

Read the App Note

Modeling Myotonic Dystrophy Type 1 in 3D – Functional Characterization of Curi Bio's DM1 Isogenic Skeletal Muscle Model

Learn how Curi Bio's iPSC-derived DM1 myoblasts recapitulate hallmark disease phenotypes in 3D engineered muscle tissues, including force deficits, prolonged relaxation, and impaired calcium handling — measured across an isogenic cell line panel.

Download App Note
 
 

Begin Your DM1 Research Today

With Curi Bio's DM1 Skeletal Muscle Model, you gain the industry's only commercially available isogenic iPSC-derived DM1 model — fully validated, assay-ready, and backed by expert scientific support.

  • Genetic Precision: CRISPR/Cas9 isogenic control with WGS-confirmed 0 CTG repeats eliminates background genetic variation for high-confidence results.

  • Biological Accuracy: 3D Engineered Muscle Tissues (EMTs) recapitulate hallmark DM1 phenotypes including force deficits, myotonia, and impaired calcium handling over a 46-day window.

  • Translational Framework: CTG repeat-stratified model enables dose-response profiling of disease severity, supporting target validation, lead optimization, and compound screening for DM1 therapeutics.

Request a quote today or speak to a specialist to integrate the DM1 model into your research workflow.

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