SCIENCE

Our Target: The soluble Interleukin 7 Receptor (sIL7R) is a key driver of the immunopathogenesis of multiple sclerosis (MS).

sIL7R is elevated by a SNP associated with higher risk and severity of MS.

Genetically-defined: genetic variant (SNP) enhances MS risk by increasing sIL7R expression.

Gregory et al., 2007, Nature Genetics 39, 1083-1091.
Galarza-Munoz et al., 2017, Cell 169, 72-84.

Significant MS Population: sIL7R-enhancing SNP is present in 66% of MS patients.

Validated Pathway: sIL7R enhances T cell activity and autoimmunity in mouse model of Progressive MS.

Significant Unmet Need: sIL7R is associated with risk for Relapsing MS and both Primary and Secondary Progressive MS.

sIL7R is an Amplifier of Autoimmune Responses. Elevated sIL7R drives the expansion of T cells, including autoreactive T cells, and amplifies the autoreactive immune responses that drive autoimmunity.

sIL7R is a Central Autoimmune Pathway: ABS is addressing a genetically-defined subset of patients with the SNP and elevated sIL7R, which is associated with greater risk of disease, and greater disease severity in multiple autoimmune diseases.

MS

66% of MS patients have the SNP (rs6897932) and elevated sIL7R.
Strong risk factor for Primary Progressive MS – severe form of the disease and an area of great unmet need.

SLE

Elevated sIL7R is also associated with risk of systemic lupus erythematosus (SLE).
Correlates with development of Lupus Nephritis – severe form of the disease with unmet needs.

T1D

The SNP is a genetic risk factor for Type 1 Diabetes (T1D).
sIL7R is elevated in T1D, particularly during the early, islet cell destruction phase.

OTHERS

Elevated sIL7R is associated with disease activity in Sjogren’s and poor treatment response in rheumatoid arthritis.
Potentially associated with risk and severity in ulcerative colitis, Crohn’s disease, psoriatic arthritis, and ankylosing spondylitis.
Further study may reveal a subset of patients with elevated sIL7R in most or all autoimmune diseases, who could benefit from sIL7R-directed therapy.

Our Approach: Immuno-Corrective Therapy to Restore Normal Immune Function

Immuno-Suppressive vs Immuno-Corrective Treatments:

Immuno-Suppressive – Current autoimmune disease treatments, including standard of care and pipeline drugs, target components of the immune system essential for normal immune function. While this approach is effective in preventing autoimmune responses, it also hinders the capacity of the immune system to provide protection against pathogens and malignant transformation, leading to adverse effects associated with immunosuppression.

Immuno-Corrective – The ideal autoimmune disease treatment would target the root cause of the autoimmune reaction while sparing protective immunity to restore normal immune function – a corrective treatment. In line with a precision approach to autoimmunity treatment, ABS corrects a fundamental pathway that causes autoimmune disease to prevent autoimmune attacks without causing immunosuppression – in other words, to restore immune homeostasis.

ABS Selectively Targets sIL7R for Treatment of Autoimmune Diseases by Restoring Immune Homeostasis Without Causing Immunosuppression.

Akin precision treatments in oncology, ABS’ anti-sIL7R monoclonal antibodies correct the root cause of the autoimmune pathology in the genetically-defined subpopulation of autoimmune disease patients.

ABS developed the first monoclonal antibodies that specifically inhibit sIL7R while sparing the canonical membrane-bound IL7R.

By discriminating between the soluble (sIL7R) and membrane-bound (mIL7R) isoforms of IL7R, ABS’ anti-sIL7R monoclonal antibodies selectively drive the therapeutic effect of sIL7R inhibition without inducing the immunosuppressive side effects of mIL7R inhibition.