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Lassen Therapeutics Presents New Preclinical Data on IL-11 Receptor-blocking as a Novel Therapeutic Approach for Skin Fibrosis at Keystone Symposia Conference

Excerpt from the Press Release:

SAN DIEGO–(BUSINESS WIRE)–Lassen Therapeutics, a biotech company developing breakthrough antibody therapeutics as potential treatments for fibrosis, rare diseases and oncology, today presented new preclinical data on LASN01, a monoclonal antibody targeting IL-11 receptor (IL-11R), in preclinical models of skin fibrosis at the Keystone Symposia Conference on Tissue Fibrosis and Repair: Mechanisms, Human Disease and Therapies being held in Keystone, Colorado. The data build upon the results in models of lung fibrosis recently presented at the American Thoracic Society (ATS) conference in May.

“IL-11R blockade provides a novel therapeutic approach to idiopathic pulmonary fibrosis (IPF) and potentially other grievous fibrotic diseases involving fibrosis in skin such as systemic sclerosis,” said David King, PhD, Chief Scientific Officer of Lassen. “With these promising preclinical results, we are rapidly progressing LASN01 forward for clinical evaluation.”

Highlights of the translational data presented on LASN01 at Keystone are as follows:

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 (PCLS) 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 (BAL) inflammatory cells when administered prophylactically or therapeutically after tissue insult.

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