PHILADELPHIA, PA — Vittoria Biotherapeutics announced a significant publication by University of Pennsylvania investigators in Science Immunology. The paper highlights the role of CD5, an immunomodulatory protein, in enhancing engineered T-cell therapies. This research is the foundation of Vittoria’s proprietary Senza5™ platform.
“We are incredibly excited about the findings shared in Science Immunology, which support the clinical translation of our Senza5™ platform and exemplify Vittoria’s commitment to pioneering potent and innovative solutions to advance the field of enabled, autologous cell therapies,” said Nicholas Siciliano, Ph.D., CEO of Vittoria Biotherapeutics.
The study, led by Marco Ruella, M.D., a physician-scientist at the University of Pennsylvania and scientific founder of Vittoria, explores how CD5 modulation boosts the efficacy of CAR T-cell therapies. Ruella stated, “This study highlights the ongoing innovation and continued commitment to advance the field of cell therapy and cancer research at the University of Pennsylvania.”
The research, titled “CD5 Deletion Enhances the Anti-Tumor Activity of Adoptive T Cell Therapies,” details how modulating the CD5 pathway can improve CAR T-cell therapy’s potency, durability, and accessibility. These enhancements may overcome challenges like CAR T exhaustion and manufacturing inefficiencies.
The publication comes as Vittoria launches its VIPER-101 clinical trial for treating T-cell lymphoma. Initial clinical data is expected in early 2025, aiming to provide insights into the Senza5™ platform’s effectiveness.
Ruchi Patel, Ph.D., the study’s lead author and a new member of Vittoria’s scientific team, expressed her excitement, “I am thrilled to see our work published in such a prestigious journal, and excited to contribute to the clinical translation of this groundbreaking technology in my new role at Vittoria.”
The Senza5™ platform promises to make CAR T-cell therapies more effective for cancer and autoimmune diseases, marking a significant advancement in the field.
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