ALTB-268 demonstrated its anti-inflammatory effect in an acute colitis hPSGL-1 mouse model.
The data confirmed that ALTB-268 acts as an immune checkpoint enhancer, downregulating T cell effector function and restoring immune system balance.
SAN FRANCISCO, Oct. 28, 2024 (GLOBE NEWSWIRE) -- AltruBio Inc. (“AltruBio” or “the Company”), a clinical-stage biotech company developing novel immune checkpoint enhancers to address the unmet need in immunological and inflammatory diseases, with a current focus on ulcerative colitis (UC), today announced new in-vivo proof-of-concept data for their lead candidate ALTB-268 at the 9th Federation of Immunological Societies of Asia-Oceania (FIMSA) 2024 Congress, taking place in Taipei from October 23-27, 2024.
The data demonstrates ALTB-268’s in vivo efficacy and confirms its mechanism of action as an immune checkpoint enhancer in a non-clinical disease model, further supporting its clinical development for ulcerative colitis (UC).
“We are pleased to continue building evidence of ALTB-268’s potential to treat T-cell-mediated inflammatory diseases, through its unique mechanism of action as an immune checkpoint enhancer targeting the PSGL-1 pathway,” said Dr. Judy Chou, President and Chief Executive Officer of AltruBio. “The anti-inflammatory effects observed in a mouse model of acute colitis further support ALTB-268’s clinical advancement for UC. We look forward to sharing data from the ongoing Phase 2a trial in UC in the second half of 2025 and demonstrating how its distinct mechanism of action may translate into clinical potential. With its novel immune checkpoint enhancement and subcutaneous administration, ALTB-268 could transform the treatment landscape for UC and other immunological and inflammatory diseases with unmet needs.”
Poster Session: 2
Title: ALTB-268, A PSGL-1 Agonistic Antibody, Demonstrates Anti-Inflammatory Effect in an Acute Colitis Model Established in Human PSGL-1 Knock-in Mice.
Presenter: Evelyn Chiang, Ph.D.
Date and Time: Saturday October 26, 2024, 10:20 a.m. TST-10:50 a.m. TST.
Poster Number: SAT-4-013
Key data highlights include:
- Treatment with ALTB-268 inhibited human T cell activation in-vitro and in-vivo, confirming its mechanism of action.
- In a dextran sodium sulphate (DSS)-induced colitis hPSGL-1 mice model, ALTB-268 ameliorated disease severity; it reduced the disease activity index (DAI) score, the colon weight/length ratio and histological damage of colitis, in addition to reducing inflammatory cytokines and leukocyte infiltration in the colon.
- An intact leukocyte migration observed in hPSGL-1 KI mice suggests that these newly generated mice provide a valuable animal model for MOA and translational studies for anti-hPSGL-1 monoclonal antibodies and Fc-fusion proteins.
About ALTB-268
ALTB-268 is a subcutaneously administered, tetravalent agonist antibody targeting PSGL-1, a key immune checkpoint regulator. It acts as an immune checkpoint enhancer (ICE), preferentially downregulating chronically activated late-stage T effector cells, leading to their exhaustion and/or apoptosis. Its unique mechanism of action is the same as AltruBio’s bivalent, intravenously administered ICE, ALTB-168, which previously demonstrated promising Phase 2 results in ulcerative colitis, psoriasis, psoriatic arthritis, and steroid-refractory/ treatment-refractory acute graft-versus-host disease (SR/TR-aGvHD), including improved patient outcomes and clinically meaningful efficacy. A Phase 2a exploratory biomarker study for ALTB-268 in biologics-refractory ulcerative colitis patients is currently enrolling patients. A randomized global Phase 2b study open to both advanced therapy experienced and naïve patients is planned to be initiated in first half of 2025. Both studies have the same primary and secondary end points in clinical remission and endoscope improvement. Given that T-cell modulation is key in the management of multiple immunological diseases, ALTB-268 has broad indication expansion potential, making it a promising “pipeline-in-a-product.”
About AltruBio Inc.
AltruBio is a clinical-stage biotechnology company developing novel therapies leveraging immune checkpoint agonism to address unmet medical needs in immunological and inflammatory diseases. The Company’s lead candidate, ALTB-268, acts as an immune checkpoint enhancer (ICE), designed to activate natural pathways that downregulate a chronically overactivated immune system to restore balance. ALTB-268 operates through a unique mechanism of action, targeting PSGL-1, a key immune checkpoint regulator. It preferentially targets and downregulates chronically activated late-stage effector T cells, leading to their exhaustion and/or apoptosis. Currently being evaluated in a Phase 2 trial in ulcerative colitis, ALTB-268 holds the potential to be a pipeline in a product to address a range of inflammatory diseases, which AltruBio plans to explore in upcoming Phase 2 trials. Led by an expert team with successful track records in drug development and commercialization in immunology, AltruBio is dedicated to delivering safer, more effective, and durable biologic treatments to improve the lives of patients.
Note on Forward-Looking Statements
Statements made in this news release that are not historical facts are forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Words such as expects, believes, intends, and similar expressions are intended to identify forward-looking statements. Actual results may differ materially from those projected in any forward-looking statement. Specifically, there are a number of important factors that could cause actual results to differ materially from those anticipated, such as the Company’s ability to raise additional capital, and risks related to the Company’s ability to initiate, and enroll patients in, planned clinical trials. You should not place undue reliance on any forward-looking statements. The Company assumes no obligation to update any forward-looking statements as a result of new information, future events or developments, except as required by law.
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