CureC9 and BrainXell have partnered to expand access to patient-derived iPSC models for C9orf72-associated ALS and FTD, aiming to accelerate research and treatment development.

The collaboration connects patients, researchers, nonprofits, and industry to remove barriers and speed up discoveries for neurodegenerative diseases.

The initiative seeks to create a resource that benefits both academic researchers and industry by enabling exploration of disease biology and therapeutic strategies for ALS and FTD.

A framework for patient engagement in research will accompany the model, enabling broader participation across academia and industry.

A portion of program proceeds will support CureC9’s mission to accelerate research, with patients and families invited to contribute biological samples to expand the repository.

The program includes ongoing patient engagement, allowing individuals affected by C9orf72-related disease to contribute samples to grow the repository.

The initiative features patient engagement with contributions of biological samples from affected families, supporting CureC9’s mission through a portion of proceeds.

The model aims to standardize and commercially provide iPSC models to researchers worldwide, reducing barriers and enabling better understanding of disease biology and therapy evaluation.

Researchers will have access to standardized, commercially available models to accelerate discovery and evaluation of potential therapies.

The standardized, commercially available models are designed to help study disease biology and assess new therapeutic approaches.

Yentli Soto Albrecht, PhD, CureC9 co-founder, and her late father donated skin cells to BrainXell to establish the first patient-derived lines in a growing C9orf72 biorepository, to be reprogrammed into iPSCs and differentiated into motor neurons, astrocytes, and microglia.

The partnership will create and expand a biorepository of patient-derived cell lines by reprogramming donated skin cells into iPSCs and differentiating them into motor neurons, astrocytes, and microglia to model CNS cell types relevant to the disease.