The data build upon the results in models of lung fibrosis recently presented at the American Thoracic Society conference in May.
Potent IL-11 receptor blocking antibodies developed by Lassen were shown to be selective for both mouse and human IL-11R and block IL-11 signaling through both the STAT3 (canonical) and ERK (non-canonical) pathways with similar potency and abrogate both cis- and trans- IL-11 signaling.
Following TGFβ stimulation, anti-IL11R antibodies reduced collagen expression in primary IPF patient fibroblasts and decreased expression of procollagen I and metallopeptidase 1 (TIMP1) by precision cut lung slices from healthy donors.
Similar reductions in the procollagen neo-epitope release are observed in response to anti-huIL-11Rα in preliminary PCLS studies from IPF patients.
In repeat mouse bleomycin lung and skin fibrosis studies, blockade of IL-11R signaling reduced skin and lung fibrosis and decreased bronchoalveolar lavage inflammatory cells when administered prophylactically or therapeutically after tissue insult.
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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