Trial Starts Dosing Lassen’s IL-11 Receptor Blocker in Healthy Adults

Inhibition of the IL-11 receptor has shown anti-fibrotic effects in preclinical models

Marisa Wexler, MS avatar

by Marisa Wexler, MS |

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Lassen Therapeutics | Pulmonary Fibrosis News | Phase 1 Clinical Trial | illustration of clinical trials medicine bottle

Dosing has begun in healthy volunteers in a Phase 1 clinical trial evaluating the safety and pharmacological properties of LASN01, an experimental therapy for pulmonary fibrosis and other diseases characterized by excessive tissue scarring, or fibrosis.

“The initiation of this trial is an important milestone for Lassen and continues our progress towards developing a new treatment option for patients with excessive fibrosis,” Puneet Arora, MD, chief medical officer of Lassen Therapeutics, which is developing the therapy, said in a press release.

The Phase 1 trial (NCT05331300) is expected to enroll 64 healthy adults, ages 18–60, who will be given one or multiple doses of LASN01. Recruitment is currently ongoing at two sites in Victoria, Australia.

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The study, expected to be completed in mid-2024, will also explore the therapy’s immunogenicity or its ability to trigger an immune response.

Interleukin-11, or IL-11, is a signaling molecule that drives inflammation and fibrosis. Last year, Lassen and Cedars Sinai Medical Center entered into an agreement to explore this signaling molecule as a potential treatment target in pulmonary fibrosis.

“IL-11 plays a critical role in the initiation and maintenance of chronic fibrotic responses and as a result, blocking this pathway represents a promising approach for multiple diseases characterized by unchecked fibrosis,” Arora said.

LASN01 is an antibody-based therapy designed to block the IL-11 receptor, or the protein receptor that IL-11 normally binds to, in order to exert its cellular effects. Blocking IL-11 has the potential to be safer than, and have additive effects over, other anti-fibrotic treatments, according to Lassen.

In experiments conducted using tissue samples from people with pulmonary fibrosis, treatment with LASN01 lowered the levels of fibrosis markers that rose in response to stimulation with TGF-beta, a signaling molecule that is a well-established driver of fibrosis. These included reductions in the production of collagen, the structural protein that is the main component of scarred tissue, as well as other fibrosis markers like tissue inhibitor of metallopeptidase 1.

In animal models of fibrosis, inhibition of IL-11 signaling was also shown to be associated with significant anti-fibrotic effects.

“We believe LASN01 has best-in-class potential to block IL-11 signaling and reduce fibrosis,” Arora said.

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