Landos’ AI-based discovery platform 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 Chronic Obstructive Pulmonary Disease (COPD).

Asthma encompasses a wide range of allergic and inflammatory diseases. NLRX1 activation may lessen the severity of disease through the innate immune system.

COPD is an inflammatory disease of the lung characterized by chronic bronchitis and emphysema and caused primarily by environmental exposures and cigarette smoke. NLRX1 activation may ameliorate alveolar destruction in patients with COPD.

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.

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

Multiple sclerosis is a chronic inflammatory, demyelinating and neurodegenerative disorder of the central nervous system. NLRX1 is uniquely positioned as the natural counterbalance to inflammatory NLRs that are overactive in MS, as well as contributing to the prevention of neurodegeneration.

Alzheimer’s disease is an inflammatory and neurodegenerative disease that causes dementia. NLRX1 activation may protect neurons from oxidative stress and ameliorate CNS inflammation in patients with this disease.

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.

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.

LABP-69 is an oral, small molecule PLXDC2 pathway agonist in development for the treatment of diabetic nephropathy and rheumatoid arthritis (RA). Diabetic nephropathy is a main complication in both type 1 and type 2 diabetes and is the leading cause of End Stage Renal Disease. 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.

RA is characterized by a swelling and loss of mobility in joints caused by excessive inflammation and infiltration into the joint synovium. Activation of PLXDC2 has the potential to influence osteoclast genesis and angiogenesis in patients with RA.

In preclinical studies to date, LABP-69 decreased TNF and IL-6 production from macrophages stimulated with LPS. In rodent RA models, LABP-69 improved disease outcomes.