EndoC-βH3®

A human beta cell with conditional immortalisation

ONE STEP CLOSER TO NATIVE HUMAN BETA CELLS

EndoC-βH3® human pancreatic beta cell line is an intermediate version of EndoC-βH® cells. EndoC-βH3® cells are conditionally immortalized and de-immortalization leads to an increase in insulin content and secretion. EndoC-βH3® cells thus represent a translational tool to study beta cell proliferation and apoptosis.

FUNCTIONALLY AND CONDITIONNALY IMMORTALIZED HUMAN BETA CELL

EndoC-βH3® is a conditional excisable high-quality functional human beta cell line

Glucose stimulated insulin secretion
Insulin content up to 20% that of native human beta cells
Insulin content about 20% of native human beta cells
Sensibility > 2 fold increase 20mM glucose
HTS compatible
Homogeneous cell line > 99%
Robust over 85 passages
Can be genetically engineered for assay development

ALREADY TESTED AND APPROVED BY MORE THAN

Academic & pharmaceutical laboratories worldwide

KEY BENEFITS

Unlimited supply
Conditionally quiescent
Compatible with High-Throughput Screening (HTS)
Compatible with genome editing and gene expression modulation strategies (CRISPR, lentiviral shRNA, siRNA…)
Genetic stability over 85 passages

APPLICATIONS

Beta cell de-differentiation and maturation
Beta cell apoptosis
Beta cell proliferation
Type I and II diabetes cell assay development
In vivo transplantation

TECHNOLOGY LIMITS

Implementation in your facility required
Lack of GSIS robustness
Lack of response to GLP1 analog Exendin-4
Lack of respone to GIP analog

DOWNLOADS

QUALITY ASSURANCE

Deposited cell line (Pasteur Institute CNCM)
Short Tandem Repeat analysis available
Batch Release Certificates available
Every batch negatively tested for mycoplasma
Every batch validated for thawing / amplification / GSIS

FUNCTIONAL VALIDATION

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Insulin content

Insulin content of de-immortalized EndoC-βH3® cells is 10-20 % that of native human beta cells (~1-2 μg/million cells).

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Glucose stimulated insulin secretion (GSIS)

De-immortalized EndoC-βH3® cells secrete insulin upon glucose stimulation; secretion is further potentiated by IBMX.