According to statistics, 45% of human disease-related deaths are associated with organ fibrosis, among which pulmonary fibrosis poses a severe threat to patients' lives. In recent years, the application of novel therapeutic approaches (such as tumor immunotherapy and organ transplantation) and COVID-19 infections have further expanded the clinical demand for the diagnosis and treatment of pulmonary fibrosis. Currently, the two small-molecule drugs approved for idiopathic pulmonary fibrosis (IPF) (pirotinib and nintedanib) can only slow the decline in lung function and fail to improve patient mortality . Therefore, early diagnosis and early treatment of pulmonary fibrosis have become a clinical consensus , urgently requiring the emergence of innovative technologies and methods.
Recent studies have demonstrated that collagen is not only a product of fibrosis but also a driving factor in its sustained progression . Therefore, identifying key molecular targets that promote collagen-driven fibrotic progression represents a critical direction for anti-fibrotic therapeutic research. Human collagen receptors identified include the discoidin domain receptor (DDR) family (including DDR1 and DDR2) and the integrin family (including α1β1, α2β1, α10β1, and α11β1). Extensive literature and preliminary research by various groups have established that DDR2 is the collagen receptor with the most significantly elevated expression level in the lung tissue of IPF patients. Unlike the "fast-on, fast-off" activation pattern of cytokine receptor tyrosine kinases (RTKs), the tyrosine phosphorylation of DDR1 and DDR2 requires the binding of large ligand molecules such as collagen for several hours before induction and can persist for dozens of hours, exhibiting a unique "slow-on, slow-off" pattern. This activation characteristic suggests that such molecular mechanisms may underlie the enduring biological effects mediated by DDRs in the progression of chronic fibrotic diseases.
No gender restriction, age ≥18 years (inclusive);
Patients with interstitial lung disease who meet one of the following diagnoses: connective tissue disease-associated interstitial lung disease (CTD-ILD), idiopathic nonspecific interstitial pneumonia (iNSIP), chronic allergic pneumonia, sarcoidosis, environmental/occupational lung disease, or unclassifiable idiopathic interstitial disease (IIP);
Screening subjects who were definitively diagnosed with interstitial lung disease (ILD) by high-resolution computed tomography (HRCT) within the preceding 6 months;
In the first 3 months prior to screening, the carbon monoxide diffusion capacity (DLCO) (Hb-corrected) was within 30% to 80% (inclusive) of the predicted value; the forced vital capacity (FVC) was within 40% to 70% (inclusive) of the predicted value;
patients in critical condition requiring emergency care;
Individuals with drug and/or alcohol abuse, or those with allergic predisposition;
women of childbearing potential, pregnant and lactating women;
bacterial, viral or fungal infections that require systemic treatment;