Cutting-Edge Science
Pliant is on a quest to break new ground in fibrosis treatment through innovative scientific discovery. Applying our extensive expertise in integrin and fibrosis biology, we have our sights set on creating groundbreaking new therapies for fibrosis and fibrosis-related diseases.
Our Path
Fibrosis is caused when cells that normally repair tissue through scar formation become dysregulated, or out of control. This dysregulation causes the cells to create and deposit excessive collagen in the affected organs, a process known as fibrosis. Fibrosis replaces healthy tissue with scar tissue in vital organs, causing irreparable damage and eventual organ failure.
Our Approach
The Role of Integrins in Fibrosis
The TGF-β Fibrosis Cascade
PLN-74809 – Pliant’s Tissue-Specific Approach to Treating Fibrosis
Transforming growth factor beta, or TGF-β, is a key driver of fibrosis. A number of investigational therapies for fibrotic and other diseases systemically block TGF-β, risking toxicity to a patient’s unaffected organs due to TGF-β’s many important roles in healthy tissues. At Pliant, our focus is on using tissue-specific integrin targets to block TGF-β only in affected organs, with the goal of reducing side effects.
- Dual inhibition of αvβ6 and αvβ1 reduces fibrogenesis in lung tissue explants from patients with IPF →
- TGF-β as a driver of fibrosis: physiological roles and therapeutic opportunities →
- Dual antagonists of α5β1/αvβ1 integrin for airway hyperresponsiveness →
- Insights into Protein-Ligand Interactions in Integrin Complexes: Advances in Structure Determinations →
- The integrin alpha v beta 6 binds and activates latent TGF beta 1: a mechanism for regulating pulmonary inflammation and fibrosis →