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Opna Bio presents promising preclinical data in multiple myeloma

Opna Bio, a clinical-stage biopharmaceutical company focused on the discovery and development of novel cancer therapeutics, presented promising preclinical data in two programs, OPN-6602, a dual EP300/CBP inhibitor in multiple myeloma, and OPN-9840, an oral, non-covalent TEAD inhibitor in malignant mesothelioma and metastatic melanoma. Data were shared at the American Association of Cancer Research (AACR) Annual Meeting, taking place April 5-10, 2024 in San Diego.

OPN-6602 Significantly Reduced Tumor Growth in Multiple Myeloma Models

OPN-6602 is an orally active, small molecule dual inhibitor of the E1A binding protein p300 (EP300) and CREB-binding protein (CBP) that demonstrated potent in vitro and in vivo anti-tumor activity in preclinical models of multiple myeloma. Multiple myeloma is an aggressive blood cancer derived from malignant plasma cells in the bone marrow.

A first-in-human Phase 1 study of OPN-6602 is planned for mid-2024 in patients with multiple myeloma.

“We are excited to begin our Phase 1 study of OPN-6602 in patients with multiple myeloma this summer. While we will study OPN-6602 initially as monotherapy, preclinical data supports testing the compound as a single agent and in combination with standard of care and next generation myeloma therapies,” said Jackie Walling, MBChB, PhD, chief medical officer.

The unique pharmacokinetic profile of the compound, with a high c-max and short half-life, is anticipated to provide a distinct advantage in the combination setting

Jackie Walling, MBChB, PhD, chief medical officer

OPN-9840 Demonstrated Single Agent Efficacy in Malignant Mesothelioma

OPN-9840 is an oral, non-covalent, pan transcriptional enhanced associate domain (TEAD) inhibitor that demonstrated dose-dependent and on-target in vitro and in vivo efficacy in preclinical models of malignant mesothelioma. Malignant mesothelioma is a rare and aggressive cancer that primarily affects the lining of the lungs or abdomen. In 40% of malignant mesotheliomas, neurofibromatosis 2 (NF2) gene mutations cause dysregulation of the Hippo pathway and increased TEAD-dependent transcription. This aberrant signaling ultimately leads to increased tumor growth and resistance to therapies.

Additional studies presented through a collaboration with Dr. Andrew Aplin’s laboratory at Thomas Jefferson University demonstrated that Opna TEAD inhibitors enhance BRAF/MEK inhibition in melanoma models by targeting drug-resistant persister cells. Dr. Aplin is a professor in cancer research and deputy director at Jefferson’s NCI-designated Sidney Kimmel Cancer Center.

OPN-9840 is set to begin IND-enabling studies and Opna is currently seeking partnerships for development.

Read the press release

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