Novel medicines to treat fibrosis no matter the cause
Inspired by nature. Fueled by insight.
Our mission is to treat fibrosis,
regardless of the cause, tissue or diagnosis.
Wherever fibrosis occurs in the body, or whatever causes it, certain underlying mechanisms are the same. Whether driven by injury, toxins, immune dysfunction or unidentifiable factors, fibrotic cells produce a cascade of signaling proteins that ultimately lead to the replacement of healthy, functional tissue with collagen and other connective material. The resulting scarring and loss of tissue architecture can lead to failure of crucial organs such as the heart, kidneys, lungs or liver.
At Tribune Therapeutics, we are developing novel medicines that efficiently target multiple drivers of fibrosis to stop this cycle of scar formation. Our strategy co-opts natural mechanisms, interrupting signaling by key CCN protein family members (such as CCN2, also known as CTGF) that play a central role in the pro-fibrotic pathway. By leveraging new observations about the structure-function relationships of these proteins, we are able to produce strong anti-fibrotic effects in animal models of both lung and kidney fibrosis. Our most advanced candidate, TRX-44, interferes with activated pro-fibrotic CCN domains to block fibrotic signaling without the pharmacokinetic challenges faced by more limited approaches.
Tribune Therapeutics is a preclinical biopharmaceutical company building a promising pipeline of novel medicines to treat patients with a wide range of fibrotic diseases. It was founded in 2020 with funding from HealthCap and Novo Seeds. The company’s pipeline is based on research by co-founder Dr. Ole Kaasbøll, who built upon decades of research on CCN signaling in the lab of Dr. Håvard Attramadal.
We are a science-driven biotech company committed to improving patients’ lives. We are always looking to connect with people who have pharmaceutical development experience and share our goals.
Contact us using the link below to learn more about opportunities at Tribune.