Idiopathic pulmonary fibrosis (IPF) affects more than one million people worldwide and remains one of the most intractable respiratory diseases. Consequently, numerous drug candidates are currently undergoing clinical trials. However, most existing therapies and developmental pipelines focus on the fibrotic process itself. Recent scRNA-seq data identifies aberrant basaloid cells as the root cause, driving inflammation and fibrosis. Current therapies fail to address this underlying mechanism.

EM-001 (HBBC-EV) targets the Wnt/β-catenin pathway via specific microRNAs. It not only suppresses aberrant cell transformation but also promotes healthy lung tissue regeneration. Unlike other EVs, its unique surface profile ensures selective lung delivery, maximizing efficacy.

Chronic Obstructive Pulmonary Disease (COPD) remains a leading cause of global mortality, yet current treatments are limited to symptomatic relief and cannot restore destroyed alveolar structures.

In COPD, Lipofibroblasts (LipoFB) -essential cells that support lung stem cell (AT2) function-undergo metabolic dysfunction, which halts the lung’s natural ability to repair itself.
We developed a metabolic reprogramming strategy using Rosiglitazone to enhance the reparative potential of LipoFBs. The modified cells secrete extracellular vesicles (LipoFB-EVs) rich in the amino acid transporter LAT1.

LAT1 expressing EVs restore leucine uptake and energy metabolism, effectively suppressing inflammation and cellular senescence while regenerating the alveolar structure by restoring AT2 stemness.
Furthermore, we have successfully achieved high LAT1 expression in EVs by introducing genes into HBBC, consistent with our EM-001 platform, and have confirmed that these engineered EVs provide equivalent enhancement of cell proliferation.

Fibroblastic foci (FF) are the “leading edge” of IPF, yet their origin has long remained a mystery. Current therapies primarily target downstream inflammation or general cell activity; they fail to address the disease’s active core—the critical transition from bronchiolization to irreversible fibrosis.

Through integrated spatial and single-cell transcriptomics, our team identified WNT5A+CTHRC1+ myofibroblasts as the “executioner” cells of IPF. These cells form a pro-fibrotic niche by interacting with aberrant basaloid cells within both FF and dense fibrosis.

The team also pinpointed PAK2 as the master upstream regulator of these “executioner” cells and subsequently identified the PAK2 inhibitor FRAX486 as a promising candidate.

FRAX486 showed high therapeutic potential for IPF, its extreme poor solubility initially hindered the development of a viable dosage form. To overcome this, we successfully developed a nano-sized solid dispersion formulation, enabling its application as an effective inhalable drug for the lungs.

Cancer remains a life-threatening disease for which effective new treatments are still urgently needed. Our mission is to realize the full potential of extracellular vesicles (EVs) as next-generation drug delivery particles. By leveraging their unique ability to encapsulate multiple therapeutic molecules and achieve selective delivery to affected areas, we aim to create innovative and highly effective therapies.