Our Science


Our most advanced program, neihulizumab, is a first-in-class antibody targeting a variety of autoimmune and immune-mediated inflammatory diseases.

Therapeutic Platform

Our Product


A growing pipeline of innovative drug candidates for immunemediated diseases.
AltruBio has built a differentiated pipeline of biologic therapies targeting diseases of inflammation with products at various stages of development.

Mar, 2020



Neihulizumab/AbGn-168H is a humanized therapeutic antibody with a unique mechanism of action, which preferentially induces apoptosis of late-stage activated T cells. This novel activated-T cell apoptosis-inducing antibody effectively eliminates chronic pathogenic T cells while fully maintaining host defense. A long lasting drug-free remission and less concern of increasing infection/cancer risks are its substantial clinical benefits. These two characteristics, which have been well demonstrated in our proof of concept clinical studies, offer a sustainable competitive advantage over existing therapies.

Our lead candidate AbGn-168H/Neihulizumab has demonstrated the proof of clinical efficacy in Phase II clinical trials for T-cell mediated diseases such as psoriasis, psoriatic arthritis and ulcerative colitis. This innovative drug candidate has the potential to bring game-changing benefits to the patients with many other T-cell mediated diseases. There are currently two ongoing clinical studies with it: A phase I study in patients who develops steroid-refractory acute graft versus host disease (GVHD) after allogeneic hematopoietic cell transplantation (HCT), and also in the front-line setting of acute GVHD.


Inheriting the unique mechanism of action from AbGn-168H, AbGn-268 is subtly designed as a multiple-valence molecule to achieve a better efficacy. From preliminary experimental results, AbGn-268 exhibits not only comparable safety profiles, but also improved potency in eliminating chronic pathogenic T cells. Therefore, a lower dosage to obtain an equal efficacy in clinical is expected.