GB0139 (formerly TD139) is an experimental treatment for idiopathic pulmonary fibrosis (IPF) that is being developed by Galecto

How does GB0139 work?

Pulmonary fibrosis is thickening of the lungs’ tissue making it harder for the lungs to expand. The fibrosis — scar tissue — also makes it more difficult for the lungs to exchange oxygen and carbon dioxide with the blood. This makes it harder for patients to get enough oxygen when they breathe.

Idiopathic means without a known cause. While pulmonary fibrosis can occur within families (familial pulmonary fibrosis), most cases are idiopathic.

GB0139 is taken with an inhaler (similar to many asthma medications). The medication contains a small molecule that inhibits a protein called galectin-3. This protein promotes tissue scarring and inflammation.

By blocking galectin-3, GB0139 may be able to reduce lung fibrosis.

Researchers have shown a considerable reduction in the amount of fibrotic tissue formation and the formation of fibrosis in preclinical studies involving the knockout of the gene that provides instructions for making galectin-3. 

GB0139 in clinical trials

A Phase 1/2 clinical trial (NCT02257177) assessed the safety and tolerability of GB0139 in healthy volunteers and patients with IPF. In the first part of the study, 36 healthy men received GB0139. The second part of the study was a randomized placebo-controlled study. It enrolled 24 men and women with IPF. Researchers assigned patients randomly to receive either GB0139 or placebo for two weeks.

The results demonstrated that the treatment was safe and that patients tolerated it well. Patients also showed improvements in several markers of inflammation.

A Phase 2b clinical trial (NCT03832946) of this treatment is now enrolling up to 450 eligible IPF patients at sites across the U.S., Canada, Europe, U.K., and Israel.

Patients will receive one of two doses of GB0139 (either 3 mg once daily or 10 mg once daily) or a placebo. The primary outcome measure will be the change in forced vital capacity (FVC, the total amount of air that a patient can expel in one forced breath) between the start of the study and the endpoint at 52 weeks.

 

Last updated: May 12, 2020

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Pulmonary Fibrosis News is strictly a news and information website about the disease. It does not provide medical advice, diagnosis, or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website.

Patrícia holds her PhD in Medical Microbiology and Infectious Diseases from the Leiden University Medical Center in Leiden, The Netherlands. She has studied Applied Biology at Universidade do Minho and was a postdoctoral research fellow at Instituto de Medicina Molecular in Lisbon, Portugal. Her work has been focused on molecular genetic traits of infectious agents such as viruses and parasites.
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Özge has a MSc. in Molecular Genetics from the University of Leicester and a PhD in Developmental Biology from Queen Mary University of London. She worked as a Post-doctoral Research Associate at the University of Leicester for six years in the field of Behavioural Neurology before moving into science communication. She worked as the Research Communication Officer at a London based charity for almost two years.
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Patrícia holds her PhD in Medical Microbiology and Infectious Diseases from the Leiden University Medical Center in Leiden, The Netherlands. She has studied Applied Biology at Universidade do Minho and was a postdoctoral research fellow at Instituto de Medicina Molecular in Lisbon, Portugal. Her work has been focused on molecular genetic traits of infectious agents such as viruses and parasites.
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