Alpine Immune Sciences Inc.

01/24/2020 | Press release | Distributed by Public on 01/24/2020 06:59

Alpine Immune Sciences Presents New Preclinical Data at 2020 Crohn’s & Colitis Congress   ALPN-101 demonstrates efficacy in treatment of chronic inflammatory bowel disease in[...]

SEATTLE--(BUSINESS WIRE)--Jan. 24, 2020-- Alpine Immune Sciences, Inc. (NASDAQ:ALPN), a leading clinical-stage immunotherapy company focused on developing innovative treatments for cancer and autoimmune/inflammatory diseases, presented new preclinical data on its lead autoimmune/inflammatory clinical program, ALPN-101, at the 2020 Crohn's & Colitis Congress in Austin, Texas.

ALPN-101 is a novel inhibitor of both the CD28 and ICOS T cell co-stimulatory pathways on both naïve and activated pathogenic T cells to provide superior efficacy to therapeutics which only interfere with a single pathway. The new data demonstrate the unique potency of ALPN-101 as measured by in vitro assays involving PBMC's (Peripheral Blood Mononuclear Cells) from patients with Crohn's Disease (CD) or Ulcerative colitis (UC) and in vivo mouse models of colitis.

In the poster titled, 'ALPN-101, A First-In-Class Dual ICOS/CD28 Antagonist, Demonstrates Efficacy in Patient-Derived PBMC In Vitro and in an In Vivo T Cell Transfer Model of Chronic Inflammatory Bowel Disease (IBD),' ALPN-101 demonstrates superior suppression of proinflammatory cytokines in vitro from human colitis patient's PBMC's more potently than single CD28 or ICOS pathway inhibitors and effector memory T cell and cytokine suppression in mouse in vivo translational models of IBD.

'The new data demonstrates the remarkable ability of ALPN-101 to suppress the progression of and completely prevent the development of colitis in preclinical models,' commented Stanford Peng, M.D., Ph.D., President and Head of Research and Development at Alpine. 'A single dose of ALPN-101 at either day 0 or day 14 resulted in milder colitis compared to study control. We are encouraged by these results and believe this data will further support the clinical advancement of ALPN-101 in the treatment of Crohn's disease and colitis.'

ALPN-101 has previously been shown to have potent immunosuppressive activity in various in vitro and in vivo models of disease, including acute graft versus host disease, inflammatory arthritis, and multiple sclerosis, Sjögren's Syndrome and Systemic Lupus Erythematosus.

The full poster presentation can be found on Alpine's website, here.

About ALPN-101

ALPN-101 is a novel Fc fusion protein of a human inducible T cell costimulator ligand (ICOSL) variant immunoglobulin domain (vIgD™), and a first-in-class therapeutic designed to inhibit simultaneously the CD28 and ICOS inflammation pathways. CD28 and ICOS are closely-related costimulatory molecules with partially overlapping roles in T cell activation likely playing a role in multiple autoimmune and inflammatory diseases. In preclinical models of graft versus host disease, Crohn's disease, colitis, inflammatory arthritis, connective tissue disease, and multiple sclerosis, ALPN-101 demonstrates efficacy superior to agents blocking the CD28 - CD80/86 or ICOS - ICOSL pathways alone.

About Alpine Immune Sciences, Inc.

Alpine Immune Sciences, Inc. is committed to leading a new wave of immune therapeutics, creating potentially powerful multifunctional immunotherapies to improve patients' lives via unique protein engineering technologies. Alpine has two lead programs. The first, ALPN-101 for autoimmune/inflammatory diseases, is a selective dual T cell costimulation blocker engineered to reduce pathogenic T and B cell immune responses by blocking ICOS and CD28. ALPN-101 has recently completed enrollment in a Phase 1 healthy volunteer trial. The second, ALPN-202 for cancer, is a conditional CD28 costimulator and dual checkpoint inhibitor. Alpine is backed by world-class research and development capabilities, a highly-productive scientific platform, and a proven management team. For more information, visit www.alpineimmunesciences.com.

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Source: Alpine Immune Sciences, Inc.

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