Our Focus

Addressing unmet needs in neurological diseases/disorders and rare diseases through the development of multiple therapeutic candidates, with proven mechanisms of action.

SLS-002

Acute Suicidal Ideation and Behavior (ASIB) in Major Depressive Disorder (MDD) and Post-Traumatic Stress Disorder (PTSD) 

  • There is no FDA-approved approved therapeutic to treat the symptoms of suicidality.
  • In 2022, there were 49,449 suicides, the highest annual number of suicides in U.S. history.
  • In 2020, suicides and non-fatal self-harm cost the U.S. over $500 billion in medical and work-loss costs, value of statistical life, and quality of life costs.
  • With a shortage of 120,000 inpatient psychiatric beds in the U.S., ASIB patients may be held for several days in the ER.
  • PTSD can develop after exposure to traumatic event stressors such as war and combat, any violence or accident, neglect, physical or sexual abuse, and/or natural disasters.

SLS-005 and SLS-009

ALS, SCA3, Huntington's and Alzheimer's Diseases

  • Mutations in the C9orf72, SOD1, FUS, and TARDBP genes can cause familial ALS and contribute to the development of sporadic ALS.
  • SCA3 (or Machado-Joseph disease) is an autosomal dominant cerebellar ataxia (ADCA I) due to CAG repeat expansions in ataxin.
  • Huntington's disease (HD) is a rare, inherited neurodegenerative disorder due to an expansion of a CAG-trinucleotide repeat in the coding region of exon 1 of the HTT gene. There is no effective therapeutic for HD.
  • Alzheimer's disease is a progressive brain disease characterized by changes in the brain—including amyloid plaques and tau proteins.

SLS-004 and SLS-007

Parkinson’s Disease (PD)

  • PD is the second most common neurodegenerative disorder in the world and currently, there is no effective treatment to prevent PD or to halt its progression.
  • Mutations in the SNCA gene, which provides the genetic code for the production of α-synuclein protein, are widely accepted as a therapeutic target to treat PD.
  • Accumulating evidence has suggested that elevated levels of α-synuclein are causative in the pathogenesis of PD.
  • Patients with impaired regulation of the SNCA gene show as high as 200% expression of α-synuclein protein.