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PLN-74809 is an oral small-molecule dual-selective inhibitor of α_vβ₆ and α_vβ₁ integrins for the treatment of IPF and PSC.

While present at very low levels in healthy tissues, these integrins are upregulated in the lungs of IPF patients and the bile ducts of PSC patients where they activate TGF-β, a key driver of the fibrotic process. Blocking these integrins is designed to stop TGF-β activation, potentially halting the growth of scar tissue.

PLN-74809 has received Fast Track Designation and Orphan Drug Designation from the U.S. Food and Drug Administration (FDA) in IPF and PSC and Orphan Drug Designation from the European Medicines Agency (EMA) in IPF and PSC. We completed enrollment in the Phase 2a clinical trial of PLN-74809 in patients with idiopathic pulmonary fibrosis (IPF) and announced positive data from the trial. We are currently recruiting participants for a Phase 2a trial of PLN-74809 in PSC.

PLN-74809 is an oral small-molecule dual-selective inhibitor of α_vβ₆ and α_vβ₁ integrins for the treatment of IPF and PSC.

While present at very low levels in healthy tissues, these integrins are upregulated in the lungs of IPF patients and the bile ducts of PSC patients where they activate TGF-β, a key driver of the fibrotic process. Blocking these integrins is designed to stop TGF-β activation, potentially halting the growth of scar tissue.

Our oncology program focuses on selective inhibition of α_vβ₈, an integrin that can activate TGF-β in the tumor microenvironment, causing an anti-inflammatory effect and potential resistance to immuno-oncology therapeutics such as checkpoint inhibitors.

Muscular dystrophy comprises a group of inherited diseases, all characterized by inborn errors in dystrophin, a protein that anchors muscle cells to the extracellular matrix and facilitates contraction.  The lack of dystrophin results in muscle cell damage upon contraction, causing a progressive loss of muscle function over time.

We have identified PLN-101325, an α₇β₁ integrin activating antibody that acts as a compensatory anchor for muscle cells in patients with Duchenne muscular dystrophy, as well as other types of muscular dystrophy. Utilizing PLN-101325 to activate α₇β₁, we have shown in animal models the ability to increase muscle strength and decrease muscle damage caused by contraction. This program is currently in preclinical development.

Our second product candidate, PLN-1474, is a small-molecule selective inhibitor of α_vβ₁ for the treatment of late stage liver fibrosis associated with nonalcoholic steatohepatitis (NASH). The integrin α_vβ₁ activates TGF-β in the liver, leading to fibrosis and, potentially, liver failure.
By blocking α_vβ₁-mediated TGF-β activation, PLN-1474 has the potential to treat liver fibrosis in NASH patients. PLN-1474 has successfully completed a Phase 1 study with favorable results.