Science

Pipeline

Stage-adapted therapies for immune-driven and fibrotic ILDs

Some ILDs, such as connective tissue disease-associated ILDs (CTD-ILDs), are driven primarily by immune dysregulation, while others, including idiopathic pulmonary fibrosis (IPF), are dominated by fibrotic processes. A.D.A. develops stage-specific therapies designed to intervene at the most biologically relevant point of disease progression.

4

Myofibroblasts deposit excess ECM, which increases tissue stiffness and impairs gas exchange. This, in turn, results in further lung injury and fibroblast activation, perpetuating a self-sustaining activation loop that ultimately drives PPF and remodeling of the lung structure

2

Fibroblasts proliferate and migrate to the site of injury, where they are activated

1

White blood cells infiltrate the site of injury and release pro-inflammatory cytokines to support tissue repair, as well as profibrotic mediators that promote the activation of fibroblasts

3

The profibrotic microenvironment promotes the differentiation of fibroblasts to myofibroblasts, which play a major role in excess fibrosis

+
White blood cells infiltrate the site of injury and release pro-inflammatory cytokines to support tissue repair, as well as profibrotic mediators that promote the activation of fibroblasts
+
Fibroblasts proliferate and migrate to the site of injury, where they are activated
+
The profibrotic microenvironment promotes the differentiation of fibroblasts to myofibroblasts, which play a major role in excess fibrosis
+
Myofibroblasts deposit excess ECM, which increases tissue stiffness and impairs gas exchange. This, in turn, results in further lung injury and fibroblast activation, perpetuating a self-sustaining activation loop that ultimately drives PPF and remodeling of the lung structure

Product

Pre-clinical

Ph. I

Ph. II - III

ADA001
IPF
Mono-therapy
ADA002
(CTD-ILD*)
Mono-therapy
ADA003
(CTD-ILD* & IPF)
Combination therapy

* currently focus on SSc-ILD model

ADA001

ADA001 is an antifibrotic formulation targeting the TGF-β pathway, a central driver of fibrosis. ADA001 is indicated for idiopathic pulmonary fibrosis (IPF), where fibrosis is the predominant process, with the aim of slowing disease progression, preserving lung function, and improving patient outcomes.

ADA002

ADA002 is a self-assembling, immunosuppressant-based nanoparticle therapy targeting autoimmune-driven interstitial lung diseases (ILDs), particularly connective tissue disease–associated ILDs (CTD-ILDs). ADA002 acts in early-stage ILDs by modulating immune responses at disease onset, with the aim of preventing fibrotic progression

ADA003

ADA003 is a combination therapy based on ADA002, incorporating an antifibrotic molecule. It is indicated for ILDs where an additional antifibrotic effect is required. This dual-action approach addresses both the immune trigger and early fibrotic signals simultaneously

4

Myofibroblasts deposit excess ECM, which increases tissue stiffness and impairs gas exchange. This, in turn, results in further lung injury and fibroblast activation, perpetuating a self-sustaining activation loop that ultimately drives PPF and remodeling of the lung structure

2

Fibroblasts proliferate and migrate to the site of injury, where they are activated

1

White blood cells infiltrate the site of injury and release pro-inflammatory cytokines to support tissue repair, as well as profibrotic mediators that promote the activation of fibroblasts

3

The profibrotic microenvironment promotes the differentiation of fibroblasts to myofibroblasts, which play a major role in excess fibrosis