Landos has produced a pipeline of potentially first-in-class, oral, small molecule therapeutic candidates that aim to address unmet needs for patients with autoimmune disease.

LABP-73 is an oral, small molecule NLRX1 pathway agonist in development for the treatment of asthma and eosinophilic disorders.

Asthma encompasses a wide range of allergic and inflammatory diseases. Severe sub-types of asthma, including both neutrophilic and mixed eosinophilic manifestations, lack effective treatment options.

In preclinical studies to date, LABP-73 decreased TNF and interferon gamma producing CD4+ T cells in vitro and reduced inflammatory responses in multiple animal models of asthma.

We believe that LABP-73, if approved, has the potential to improve on the current treatment options by addressing both epithelial and immune dysfunction to resolve neutrophilic and eosinophilic inflammation, improve pulmonary function and reverse underlying fibrosis.

LABP-66 is an oral, small molecule NLRX1 pathway agonist in development for the treatment of multiple sclerosis (MS) and neurodegenerative disorders.

Multiple sclerosis is a chronic inflammatory, demyelinating and neurodegenerative disorder of the central nervous system.

Progressive MS presents with cortical lesions comprised of activated microglia and an overall increase in microglia in the brain. These microglia, as well as IL-12- and TNF-producing dendritic cells, contribute to direct neuronal damage as well as the ongoing demyelination that disrupts axonal architecture.

In preclinical studies to date, LABP-66 protected against neuronal cell death upon stimulation with oxidative or inflammatory stress as well as deceased expression of inflammatory cytokines in the spinal cord and brain.

We believe LABP-66 may represent a novel approach to addressing an unmet clinical need in neurodegenerative disorders and progressive MS, for which no current therapy slows the progression of cognitive decline and neurological damage.

LABP-69 is an oral, small molecule PLXDC2 pathway agonist in development for the treatment of rheumatoid arthritis (RA), ulcerative colitis and Crohn’s disease.

RA is characterized by swelling and the loss of mobility in joints caused by excessive inflammation and immune cell infiltration into the joint synovium. Activation of PLXDC2 may result in the downregulation of TNF, MCP1 and other cytokines, thereby helping to return the tissue to homeostasis in the deficiency of the native ligand.

LABP-69 aims to increase IL-10 secretion and down-regulate pro-inflammatory signals and angiogenesis. Results in two rodent models of RA demonstrate the role of PLXDC2 and the effect of LABP-69 in abrogating disease severity. LABP-69 is designed to activate PLXDC2 in a broad array of immune and non-immune cells, shifting them towards an anti-inflammatory state and compounding its therapeutic effects.