ALPN-101 (ICOSL vIgD Fc), a Dual Antagonist of the ICOS and CD28 Costimulatory Pathways, for Treatment of Steroid Refractory Acute GVHD ( aGVHD ): Case Report

First-in-human study of the safety, tolerability, pharmacokinetics, and pharmacodynamics of ALPN-101, a dual CD28/ICOS antagonist, in healthy adult subjects

A Double Blind, Placebo Controlled, Single Ascending Dose (SAD) and Multiple Ascending Dose (MAD) Study of ALPN-101, a First-In-Class Dual ICOS/CD28 Antagonist, in Healthy Volunteers (HV)

An Open Label Study of ALPN-101, a First in Class Dual CD28/ICOS Antagonist, in Subjects with Steroid Resistant or Steroid Refractory Acute Graft Versus Host Disease (BALANCE)

Acazicolcept (ALPN-101), a dual ICOS/CD28 antagonist, demonstrates efficacy in systemic sclerosis preclinical mouse models

ICOSL+ plasmacytoid dendritic cells as inducer of graft-versus-host disease, responsive to a dual ICOS/CD28 antagonist

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, a First-in-Class Dual ICOS/CD28 Antagonist, Suppresses Key Effector Mechanisms Associated with Sjögren’s Syndrome and Systemic Lupus Erythematosus

ALPN-101, a First-in-Class Dual ICOS/CD28 Antagonist, Suppresses Key Effector Mechanisms Underlying Rheumatoid and Psoriatic Arthritis

Protein Engineering by Directed Evolution to Derive ALPN-101, a Dual ICOS/CD28 Antagonist ICOSL Variant Ig Domain (vIgD)-Fc Fusion Protein for the Treatment of Inflammatory Diseases

ALPN-101, a Dual ICOS/CD28 Antagonist, Demonstrates Potent and Dose-Dependent Suppression of Graft vs. Host Disease (GvHD) in a Human/NSGTM Mouse Xenograft Model, with Activity Superior to CD28 or ICOS Single Pathway Antagonists

Therapeutic Candidate ALPN-101, a Dual ICOS/CD28 Antagonist, Potently Suppresses Human/NSG Mouse Xenograft Graft vs. Host Disease (GvHD) in a Dose Ranging Study and Reduces Disease Activity in a Mouse Model of Hemophagocytic Lymphohistiocytosis (HLH)

ALPN-101, a Dual ICOS/CD28 Antagonist, Potently Suppresses Disease in Multiple Mouse Models of Autoimmunity

Therapeutic Candidate ALPN-101, a Dual ICOS/CD28 Antagonist, Demonstrates In Vivo Efficacy in an Experimental Autoimmune Encephalomyelitis (EAE) Model

Novel Variant Ig Domain (vIgD) Proteins Generated Via Directed Evolution of IgSF Domains Have Therapeutic Efficacy in Animal Models of Graft Versus Host Disease

A Study of ALPN-202, a PD-L1-dependent CD28 Costimulator and Dual Checkpoint Inhibitor, in Combination with Pembrolizumab in Patients with Advanced Malignancies (NEON-2)

First in Human Dose Escalation of ALPN-202, A Conditional CD28 Costimulator and Dual Checkpoint Inhibitor, in Advanced Malignancies (NEON-1)

NEON-1: A First-in-Human Phase I Open-Label Study of ALPN-202, a Conditional CD28 Costimulatorand Dual Checkpoint Inhibitor, in Advanced Malignancies

NEON-1: A first in human phase I open label study of ALPN 202, a conditional CD28 costimulator and dual checkpoint inhibitor, in advanced malignancies

Development of a Clinical Ex Vivo Assay for the Assessment of Therapeutic CD28 Costimulatory Pathway Engagement

ALPN-202 Combines Checkpoint Inhibition with Conditional T Cell Costimulation to Overcome T Cell Suppression by M2c Macrophages and Improve the Durability of Engineered T Cell Anti-Tumor Responses

Development of Novel Monoclonal Antibodies for the Robust Detection of CD28, CD80, and CD86 by Immunohistochemistry in Human Tumors

ALPN-202, a Conditional CD28 Costimulator and Dual Checkpoint Inhibitor, Utilizes Multiple Mechanisms to Elicit Potent Anti-Tumor Immunity Superior to Checkpoint Blockade

ALPN-202, a Conditional CD28 Costimulator and Dual Checkpoint Inhibitor, Enhances the Activity of Multiple Standard of Care Modalities

ALPN-303, an Enhanced, Potent Dual BAFF/APRIL Antagonist Engineered by Directed Evolution for the Treatment of Systemic Lupus Erythematosus (SLE) and Other B Cell-Related Diseases

ALPN-303, an Enhanced, Potent Dual BAFF/APRIL Antagonist Engineered by Directed Evolution for the Treatment of Systemic Lupus Erythematosus (SLE) and Other B Cell-Related Autoimmune Diseases

B Cell Modulatory Variant TNF Receptor Domains (vTDs) Identified by Directed Evolution to Inhibit BAFF and APRIL, Alone or Combined with Variant Ig Domains (vIgD™) that Inhibit T Cell Costimulation, for the Treatment of Systemic Lupus Erythematosus and Other Severe Autoimmune Diseases

Engineered Variant Domain Fusion Proteins Provide Checkpoint Inhibition and Tumor Antigen-Dependent CD28 Costimulation Resulting in Potent Anti-Tumor Immunity

“Switch” Transmembrane Immunomodulatory Proteins (TIPs) Consisting of High-Affinity PD-1 Extracellular Domains (PD-1 vIgDs) and Costimulatory Intracellular Domains Potently Enhance the Activity of TCR-Engineered T Cells