Our strategy is targeting the critical mechanisms shared by CNS diseases to develop therapies with broad utility. 

Our Strategy

Our strategy: targeting shared critical mechanisms and unmet needs

Currently, there is no "reparative" therapy that slows down disability progression or repairs function in multiple sclerosis (MS). For Alzheimer's disease (AD) and Amyotrophic lateral sclerosis (ALS), approved therapies moderately slow progression in early disease only. There is no effective therapy for negative symptoms or cognitive symptoms of schizophrenia. Our strategy is targeting the critical mechanisms shared by these CNS diseases to develop therapies with broad utilities.

Critical Mechanisms


Repair/protect ‘data cables’

When the myelin sheath is damaged, nerve impulses slow down or even stop, causing neurological problems. We devise strategies to promote the formation of the myelin sheath after damage to protect the axons and restore function.


Ameliorate brain environment

Neuroinflammation is a key pathological driver in many neurological diseases. We devise strategies to modulate the activities of two key immune cell types: microglia and CNS-infiltrating T cells, to alleviate neuroinflammation.

Synaptic Modulation

Boost neuronal communication

Synaptic dysfunction is associated with sensory, motor, and cognitive impairments. We harness human genetics data to devise strategies to correct synaptic dysfunction for the treatment of neuropsychiatric disorders.

Important Targets of Critical Mechanisms

Important targets of critical mechanisms

GPR17 antagonist

GPR17 acts as an intrinsic brake to the differentiation and maturation of oligodendrocytes - the myelinating cells. GPR17 antagonist promotes remyelination in diseased or injured CNS to restore neuronal health.

CSF1R inhibitor

CSF1R-mediated signaling is critical for microglia. Maladaptive microglia in disease cause neuroinflammation, remyelination blockade and axon degeneration. Intermittent treatment with CSF1R inhibitor depletes maladaptive microglia, and allows spontaneous repopulation of new microglia to restore a homeostatic CNS environment.

TYK2 inhibitor

TYK2-mediated signaling promotes naïve T cells to adapt and maintain Th1 & Th17 phenotypes. CNS infiltrating Th1 & Th17 cell activities contribute to neuroinflammation. Brain-penetrant TYK2 inhibitor blocks harmful Th1 & Th17 cell activities in the periphery and CNS to maximally protect neuronal health

Myro Pipeline

Our pipeline