Our Science

ADDRESSING UNMET MEDICAL NEEDS

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

Therapeutic Platform

Our Products

INNOVATIVE SOLUTIONS

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

Mar, 2023

ALTB-168

Neihulizumab

Neihulizumab/ALTB-168 is a humanized therapeutic antibody with a unique mechanism of action, preferentially inducing 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, leading to durable clinical efficacy without increasing the risk of infection or cancer.These two characteristics, which have been well demonstrated in our proof of concept clinical studies, offer a sustainable competitive advantage over existing therapies.

ALTB-168/Neihulizumab has demonstrated 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 patients with many other T-cell mediated diseases. We have two ongoing clinical studies : A phase I study in patients who develop steroid-refractory acute graft versus host disease (GVHD) after allogeneic hematopoietic cell transplantation (HCT), and a second study in the front-line setting of acute GVHD.
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ALTB-268

Inheriting the unique mechanism of action from ALTB-168, ALTB-268 is subtly designed as a multiple-valence molecule to achieve better efficacy. From preliminary experimental results, ALTB-268 exhibits not only comparable preliminary 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.
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Publications

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