The data demonstrate that LASN01 is a potent inhibitor of IL-11 signaling and shows anti-fibrotic effects in multiple preclinical models.
Highlights of the translational data presented on LASN01 are as follows:
In vitro assays demonstrated potent blockade of IL-11-stimulated signaling by LASN01 and inhibition of TGF-β-stimulated collagen expression by patient-derived IPF fibroblasts.
In ex vivo assays using normal human lung tissue, LASN01 inhibited TGF-β-stimulated production of the fibrotic markers procollagen type I and tissue inhibitor of metallopeptidase 1 (TIMP1), and reduced collagen neo-epitope release from slices of diseased IPF lung tissue.
Inhibition of IL-11R signaling also showed an anti-fibrotic effect in animal models of IPF.
Studies showed a statistically significant reduction in lung fibrosis in both prophylactic and therapeutic models, concomitant with decreases in macrophage populations.
In addition, LASN01 was shown to be well-tolerated with no obvious toxicity in a multiple dose study of non-human primates and is rapidly advancing toward clinical evaluation.
Lassen Therapeutics develops breakthrough antibodies as potential treatments for fibrosis, rare diseases, and oncology.
The company's lead candidate is LASN01, a best-in-class monoclonal antibody targeting IL-11 receptor (IL-11R). IL-11, a member of the IL-6 family of cytokines, is a central mediator of fibrosis and blocking its activity has the potential to be safer than and additive to other anti-fibrotic therapeutic approaches.
IL-11 is also an important effector of tumor microenvironment organization, playing a key role as a mediator between cancer and stromal cells.
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