Latus | Where delivery transforms treatment.

Huntington's disease is an inherited, progressive, neurodegenerative disorder that currently has no available disease-modifying therapies

At Latus, we are advancing a one-time gene therapy that aims to correct Huntington's disease at the start, promising to slow or even halt disease progression.

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HD impacts all aspects of a patient's life

Cognitive Function

Executive dysfunction, impaired judgment, planning, and concentration
Dementia
Often most impactful according to patients

Psychiatric Well-Being

Depression, anxiety, suicidality
Personality changes, mood swings, social withdrawal, irritability, aggression, perseveration, psychosis
Apathy
Substance abuse

Motor Control

Chorea and athetosis, motor impersistence, rigidity
Impaired gait
Oculomotor disturbances
Later stage: dysarthria, dysphagia, dystonia, bradykinesia, mutism

Early treatment with Latus gene therapy offers the possibility to delay or even halt HD progression

HD is caused by mutations in the huntingtin (HTT) gene leading to >39 CAG expansions. Human genetic data reveal that over time the CAG expansions grow to >150 CAGs, which causes neuronal death and leads to HD symptoms. The expansion is caused by a protein called MSH3. At Latus, we aim to reduce MSH3 expression to target HD at it's start.

~10-20 years of suffering

Huntington’s disease is fatal within ~10-20 years of symptom onset

~100K patients

Progressive onset of additional symptoms at typically 2 years after diagnosis

Our one-time gene therapy candidate is designed to fundamentally change how Huntington’s disease is treated

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Our preclinical data presentations support the potential translational impact of our Huntington's disease gene therapy

We have unveiled a novel computational model aimed at predicting the effects of knockdown of the DNA repair enzyme MSH3 on reducing somatic instability and the potential outcomes that could result for HD patients.

Our preclinical data disclosures support deep MSH3 knockdown with our investigational gene therapy, yielding reductions in somatic instability in a mouse model of HD.

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Expert Perspectives on Transforming Healthcare.

“I really hope we can find a way to slow down this disease. No parent wants to see their kid go through endless hospital visits, the pain of treatments, or spend their days in a hospital bed. We just want more happy, normal days at home, more laughter, and less tears—more time being a family without the constant stress of medical issues.”

—Caregiver

“HD remains a devastating, incurable genetic brain disease, for which we desperately need effective interventions. A breakthrough would be transformative for affected patients and families worldwide.”