Two separate articles describing preclinical data of ACE-041 published

Acceleron Pharma, Inc., a biopharmaceutical company developing novel therapeutics that modulate the growth of cells and tissues including red blood cells, bone, muscle, fat, and the vasculature, announced the publication of two separate peer-reviewed articles describing preclinical data demonstrating that treatment with ACE-041, an inhibitor of signaling through the activin receptor-like kinase 1 (ALK1) receptor, slows tumor growth and progression by inhibiting angiogenesis. The paper titled “Genetic and pharmacological targeting of activin receptor-like kinase 1 impairs tumor growth and angiogenesis” was published in the Journal of Experimental Medicine in collaboration with researchers from the Karolinska Institute in Sweden. A second paper, titled “ALK1-Fc Inhibits Multiple Mediators of Angiogenesis and Suppresses Tumor Growth,” was published in Molecular Cancer Therapeutics by researchers at Acceleron.

“The discovery that the ALK1 pathway is involved as a common, critical phase of the blood vessel development process presents numerous possibilities for ACE-041, which inhibits signaling through the ALK1 receptor.”

“We are excited by the results described in these papers, which establish an important role for ALK1 signaling in tumor angiogenesis and support the potential of ACE-041 as a promising new experimental drug for the treatment of cancer,” said Jasbir Seehra, Ph.D., Chief Scientific Officer at Acceleron Pharma. “The discovery that the ALK1 pathway is involved as a common, critical phase of the blood vessel development process presents numerous possibilities for ACE-041, which inhibits signaling through the ALK1 receptor.”

Study findings from these two publications demonstrated that treatment with an ALK1-Fc:

• Slows tumor growth and progression by inhibition of angiogenesis
• Reduces vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF)-mediated angiogenesis
• Prevents tumor angiogenesis and decreases tumor burden in several cancer models including melanoma, breast, and pancreatic islet cancer
• Conversely, ALK1 signaling is necessary for efficient tumor angiogenesis
• Tumor tissue has elevated expression of ALK-1 ligands, ALK1 receptors, and increased ALK1 signaling