01
LMNB1 is overexpressed
An extra copy of LMNB1 produces too much of the protein in oligodendrocytes.
Our technology
A direct approach to the genetic cause of ADLD.
ADLD is driven by too much LMNB1. OligoVale is developing a targeted gene therapy designed to lower it toward normal levels.
The biology
When LMNB1 rises, myelin breaks down.
LMNB1 helps maintain the structure of the cell nucleus. In ADLD, an extra copy of the LMNB1 gene leads to overexpression. In oligodendrocytes, the cells responsible for producing myelin, that imbalance contributes to progressive demyelination in the central nervous system.
How it works
Targeted delivery. RNA silencing. LMNB1 lowered.
Our therapeutic concept follows a direct biological sequence.
02
The payload reaches the right cells
An oligodendrocyte-targeted AAV delivers an RNA-silencing payload to the cells responsible for myelin.
03
LMNB1 moves toward normal
The payload is designed to reduce LMNB1 expression toward normal levels, with the goal of preserving myelin and halting disease progression.
OV-1
A lead program built around a defined disease mechanism.
OV-1 combines targeted AAV delivery with RNA silencing to address LMNB1 overexpression at its source. Our work is focused on generating the translational evidence required to advance the program responsibly.
Disease
Autosomal dominant leukodystrophyCell type
OligodendrocytesTherapeutic goal
Lower LMNB1 toward normalInterested in the science behind OligoVale?
We welcome scientific and partnering conversations aligned with our mission for people living with ADLD.