Abzena’s customer Tasrif Pharmaceutical, LLC announced the grant of its second U.S. patent, expanding its intellectual property targeting the Poliovirus Receptor (CD155/PVR). Together with Tasrif’s foundational issued U.S. patent, this expanded portfolio covers a proprietary panel of humanised monoclonal antibodies and antigen-binding fragments, including the lead candidate, TSRF-786C IgG4 (S241P), humanised using Abzena’s Composite Human Antibody™ (CHAb) platform. Tasrif is also leveraging its patented CD155-binding platform to engineer next-generation modalities, including Antibody-Drug Conjugates (ADCs), Bispecifics, T-cell engagers, CAR-T, and CAR-NK cell therapies. National Phase patent applications originating from Tasrif’s PCT international application are currently pending in Japan, Europe, Canada, Australia, and China.
To address central nervous system (CNS) malignancies, Tasrif evaluated its CD155-targeting platform in a syngeneic GL261 glioblastoma mouse model using a surrogate anti-mouse CD155 antibody. The study confirmed in vivo target engagement and tumour-specific accumulation within GL261 brain tumours. Building on this proof-of-concept, Tasrif is advancing brain-penetrating bispecific antibodies — comprising humanised Anti-CD155 × Anti-Transferrin Receptor (Anti-CD155 × Anti-TfR) — specifically engineered to cross the blood-brain barrier for CNS indications.
For systemic cancer indications, lead candidate TSRF-786C exhibits sub-nanomolar binding affinity for CD155, as confirmed by Surface Plasmon Resonance (SPR). Selection of TSRF-786C was validated through extensive preclinical profiling, demonstrating precise target specificity via the Retrogenix® Cell Microarray Platform Assay, low immunogenicity via Abzena’s EpiScreen® DC T-cell assay, a favourable profile on Cytokine Release Assay (CRA), and excellent thermostability and freeze-thaw resilience. Crucially, TSRF-786C demonstrates robust cross-reactivity with non-human primate (NHP) CD155, enabling planned IND-enabling safety and toxicology studies.
In pilot studies using humanised mouse models of pancreatic and lung cancer, TSRF-786C successfully modulated the key PVR (CD155)–DNAM-1 (CD226) immune axis. Treatment with TSRF-786C yielded a statistically significant increase in the percentage of CD226 (DNAM-1)-positive T cells (both CD4 and CD8) within the lung tumour microenvironment, as well as a statistically significant increase in the percentage of CD226 (DNAM-1)-positive tumour-infiltrating Natural Killer (NK) cells in the pancreatic tumour microenvironment. Notably, TSRF-786C did not alter local PD-1 expression, thus providing a strong rationale for combination strategies with anti-PD-1 therapies. These data support the ongoing preclinical development of TSRF-786C, with IND-enabling safety and toxicology evaluations for systemic cancers.
