Products04

Our multi-specific immuno-oncology drug ND021 holds the promise to outperform first generation checkpoint modulators in terms of safety and efficacy.

Pipeline

Hit discovery
Lead optimization
Preclincal PoC
IND-enabling studies
Phase I
ND021 (multispecific) Immuno-oncology
ND007 (anti-IL23RxCD3) Chronic inflammation
ND009 (anti-TNF) IBD Partner: Tillotts
ND016 (multispecific) Chronic inflammation Partner: Intarcia
ND017 Metabolic disease Partner: Intarcia
ND023 (multispecific) Immuno-oncology Partner: Ono
ND026 (multispecific) Chronic inflammation Co-development with Kaken
Multiple programs (multispecific) Immuno-oncology

ND021 – Immuno-oncology

ND007 – autoimmunity

ND009 – IBD

ND016 – autoimmunity

ND017 – metabolic disease

ND023 – Immuno-oncology

ND026 – inflammation

ND021 – Immuno-oncology

ND021 is a next generation multi-specific immuno-oncology program targeting the tumor-immunity suppressive pathway PD-1/PDL1 as well as a tumor-immunity activating pathway specifically in the tumor microenvironment. Targeting these two pathways in a combinatorial approach is expected to provide patients suffering from a broad range of cancer types with a unique novel treatment opportunity characterized by an improved benefit-to-risk profile as compared to current standard of care as well as other combinatorial immunotherapy approaches currently in clinical development. The differentiating profile of ND021 is based on its molecular design aimed at highly effective, while only local activation of a tumor-directed immune response.

Download Poster presentation at AACR Annual Meeting 2018

 

ND007 – autoimmunity

We believe that our lead program ND007, a bispecific antibody fragment, holds tremendous promise in the treatment of autoimmune diseases.

It has become clear that a class of lymphocytes called autoreactive pathogenic T cells (Tpaths) that express IL-23 receptor (IL23R) is among the main culprits in many autoimmune diseases, such as multiple sclerosis, rheumatoid arthritis, inflammatory bowel disease, and psoriasis.

In autoimmune disorders, Tpaths, once activated, produce pro-inflammatory cytokines that in their turn set in motion a cascade leading to local or systemic inflammation. To date, most novel therapeutic strategies have focused on these cytokines, one at a time. A number of these strategies have commercially been quite successful, despite a significant number of non-responders. In addition, it has been unexpectedly difficult to translate the relative success of one cytokine in one disease to another disease.

Clearly, the intricate interplay between cytokines in different diseases and stages of a disease has a high variability and sets a natural limit to the impact of engaging a single cytokine. By moving upstream, ND007 aims to directly engage the very Tpath cells that are the prime source of the various cytokines (e.g. TNF, IL-17, IL-22 or GM-CSF) that induce chronic and/or relapsing inflammation. These particular Tpath cells have a recognizable signature: they express IL23R. This prompted us to design a mechanism to specifically eliminate IL23R-expressing cells. Our anti IL23RxCD3 bispecific antibody fragment ND007 is engineered to bind on one hand to IL23R and on the other to CD3, which recruits T-killer cells to lyse the IL23R-expressing Tpath cells. We expect that this approach has the potential to demonstrate superior efficacy.

What is more, there is evidence that ND007 also depletes pathogenic memory T cells, potentially leading to long-lasting disease modification or even to cure. In multiple sclerosis there are currently three approved mechanisms for immune-cell depletion, respectively eliminating CD52-, CD20- and IL2R-positive cells. Compared to ND007 these are much less specific, and therefore we expect ND007 in addition to superior efficacy to display a superior safety profile as well.

ND009 – IBD

ND009 is an anti-TNF antibody fragment that is being developed for inflammatory bowel disease (IBD), a chronic inflammation of the digestive tract that primarily includes ulcerative colitis and Crohn’s disease. Anti-TNF therapy has been shown to reduce the need for hospitalization and surgical interventions in IBD and improve quality of life. Numab’s highly stable antibody fragment ND009 has best-in-class potency, and is licensed to Tillotts Pharma AG for the development and commercialization of innovative formulations.

ND016 – autoimmunity

ND016 is a novel multispecific antibody fragment-based molecule for the treatment of severe autoimmune disorders. In close collaboration with Intarcia Numab is developing a highly potent and stable lead molecule suitable for long-term sustained release from Intarcia’s miniaturized implantable Duros device, aiming at a once- or twice-yearly therapy. Intarcia retains the rights to commercialize this asset under license from Numab.

ND017 – metabolic disease

ND017 is a novel antibody fragment-based molecule for the treatment of metabolic disorders. Numab is developing a highly potent and stable lead molecule suitable for long-term sustained release from Intarcia’s miniaturized implantable Duros device, aiming at a once- or twice-yearly therapy. Intarcia retains the rights to commercialize this asset under license from Numab.

ND023 – Immuno-oncology

ND023 is a collaboration project partnered with Ono Pharmaceutical Co., Ltd., (the originator of the anti-PD1 antibody Nivolumab/Opdivo®) aimed at the discovery of a multi-specific antibody fragment-based molecule for immuno-oncology.

ND026 – inflammation

In ND026, Numab, together with its partner Kaken Pharmaceutical Co., Ltd., is developing a multi-specific immunomodulatory therapy for inflammatory disorders.