XTuit Pharmaceuticals, Inc. is a biopharmaceutical company developing novel microenvironment-activated therapeutics targeting key mechanisms resulting in hypoxia, decreased drug uptake, drug resistance, and decreased immune response. The Company’s proprietary drug development pipeline and integrated, sophisticated clinical biomarker platform will be used for accelerated clinical development across selected cancers and fibrotic disorders. XTuit’s compounds act through pleiotropic mechanisms to inhibit extracellular matrix synthesis and stabilization, and to silence activated stromal cells, including cancer-associated fibroblasts and stellate cells. As a result, XTuit compounds alleviate hypoxia and enable enhanced drug uptake through solid stress reduction. Moreover, the drugs have been shown to down-regulate stroma-induced tumor and inflammation signaling pathways to overcome treatment resistance. XTuit’s first two lead series are being developed for early clinical proof-of-concept in liver diseases and cancer. The Company’s founders include Rakesh K. Jain, Ph.D., Andrew Werk Cook Professor of Tumor Biology (Radiation Oncology) at Harvard Medical School and Director, Edwin L. Steele Laboratory for Tumor Biology at the Massachusetts General Hospital; Robert Langer, Sc.D., David H. Koch Institute Professor at the Massachusetts Institute of Technology; Ronald Evans, Ph.D., March of Dimes Chair in Molecular and Developmental Biology and Professor and Director of the Gene Expression Laboratory at the Salk Institute as well as Howard Hughes Medical Institute Investigator; and Alan Crane of Polaris Partners. XTuit is backed by leading investors, including Polaris Partners, New Enterprise Associates, CTI Life Sciences, Arcus Ventures and Omega Funds.


The microenvironment, or stroma, is significantly altered in cancer and fibrotic disorders, contributing to and promoting the advancement of disease. The microenvironment is in a pro-inflammatory state and becomes stiff through deposition of extracellular matrix components, including collagen and hyaluronan, which are stabilized by matrix molecules. Moreover, stromal cells, including cancer-associated fibroblasts, stellate cells, and monocyte/macrophage-derived cells, expand and are reprogrammed to an active state. This activation results in up-regulation of several key signaling pathways in the stroma. As a consequence of these biological changes, there is increased solid stress in the stroma, resulting in vessel compression and ultimately hypoxia, as well as stroma-induced signaling to the tumor and inflammatory cells that can result in disease progression and treatment resistance to standard-of-care agents.