The human organism is an intricate system. It is a finely tuned clockwork of cells in which a single malfunctioning protein can wreak havoc. On the other hand, a single protein or the blocking of a protein can alleviate or cure.
Swedish startup Galecto Biotech develops drugs based on the galectin 3 protein. This protein has such roles as forming fibrosis in vital organs such as the lungs, kidneys and liver.
“At Galecto Biotech we have developed novel drugs that we call galectin modulators. They bind to proteins from the galectin family and we develop these for the treatment of important human diseases like fibrosis and cancer,” says Hans T. Schambye, CEO of the company.
One disease Galecto Biotech is targeting is idiopathic pulmonary fibrosis. This is a progressive and ultimately fatal lung disease in which lung capacity is restricted because the lung tissue is scarred. Only partial treatment options are available, so treating idiopathic pulmonary fibrosis remains a very substantial unmet need.
Penetrating deep into the lung
“In a clinical phase 1b/2a study in patients with idiopathic pulmonary fibrosis, our inhaled galectin modulator has been shown to penetrate deep into the lung and target the macrophages. And the macrophages respond by changing, and that results in biomarker changes in the plasma of the patients. This is a very promising sign that we will be able to change the fibrosis in these patients,” says Hans T. Schambye.
The next step is a phase 2B study in 300 patients where the target is to show that the drug preserves the lung function of the patients Hans T. Schambye, CEO, Galecto Biotech
Galecto Biotech was incubated by Novo Seeds until the xxx MEUR seed round in 201xx. Galecto was first funded through the pre-seed grant programme of the Novo Nordisk Foundation, and Novo Seeds led the subsequent financing rounds.
“Novo Seeds has been very important for Galecto. They helped shape the company right from the start, and they have made several investments that has brought us to where we are today,” says Hans T. Schambye.