Coherus Oncology Publishes Preclinical And Clinical Biomarker Research In Molecular Cancer Therapeutics Describing The High Selectivity, Picomolar Binding Affinity And Significant Effector Mediated Killing Of CCR8+ Cells Of Its Investigational Anti-CCR8 Monoclonal Antibody;

Coherus Oncology, Inc. (NASDAQ:CHRS) today announced the publication of preclinical and clinical biomarker research in Molecular Cancer Therapeutics describing the high selectivity, picomolar binding affinity and significant effector mediated killing of CCR8+ cells of its investigational anti-CCR8 monoclonal antibody. The findings show that the antibody, now named tagmokitug, demonstrated no off-target binding, and selectively eliminates CCR8+ T regulatory cells and not other T cells, supporting its potential as an anticancer treatment. The full article may be accessed in the December 2025 issue of Molecular Cancer Therapeutics.

The publication provides important scientific evidence for the program and supports the ongoing advancement of tagmokitug in clinical studies evaluating its antitumor activity across multiple solid tumor settings in combination with toripalimab.

"This publication presents the robust pharmacology of tagmokitug in preclinical and clinical studies, and with a selectivity profile and potent binding and killing of CCR8+ T regulatory cells and not other immune cells. These data provide evidence that tagmokitug has the potential for a differentiated profile," said Theresa LaVallee, PhD, Chief Scientific and Development Officer at Coherus. "The data show a high abundance of CCR8 target expression in a broad range of solid tumors suggesting the promise of the tagmokitug program. We look forward to advancing the development as we continue to explore tagmokitug in patients with solid tumors."

Key highlights from this publication include:

CCR8 is highly abundant and preferentially over expressed in Treg cells in solid tumors and that most solid tumors have a high level of CCR8.

Anti-tumor and tumor immune remodeling activity of anti-CCR8 antibody treatment was observed in mouse tumor models and activity was enhanced with anti-PD-1 antibody combination treatment.

Tagmokitug has robust characteristics with picomolar binding affinity, exquisite selectivity for CCR8 with no off target binding and potent target cell killing by a bind and kill mechanism that induces tumor regression in mice.

In the first-in-human clinical study, proof of mechanism is established with translational data showing tagmokitug administration leads to selective reductions in CCR8+ Tregs and not other T cell subsets in cancer patients.