Building the future of fibrosis therapeutics.

PDAC is among the deadliest solid tumors, with a 5-year survival barely reaching 12%. Its dense desmoplastic stroma blocks chemotherapy, T-cell infiltration, and immune access — and recent immunotherapy advances have shown no impact.

ITGA5 (integrin α5) is overexpressed on cancer-associated fibroblasts in PDAC stroma but expressed at low-to-negligible levels in healthy tissues. Disrupting ITGA5 collapses the stromal shield and re-exposes tumor cells to standard-of-care therapy.

ST-102 is a 7-amino-acid non-RGD cyclic peptide (L/D isomer mix) that simultaneously blocks ITGA5 on myCAFs (reducing ECM production and FAK signaling) and iCAFs (suppressing IL-6 secretion and STAT3-driven resistance). In vivo, ST-102 boosts intra-tumoral drug accumulation and shifts the immune microenvironment toward CD8⁺ T-cell infiltration and M1 macrophage polarization.

IND-enabling studies. GLP toxicology with Charles River, CMC with PolyPeptide, and clinical development planning with SGS underway. ST-102 is a short and stable peptide with long shelf life, easily manufactured and scaled up and is administered systematically.

IPF is a progressive, fatal interstitial lung disease with a median survival of 3–5 years. Current antifibrotics slow decline but do not halt or reverse disease.

Sustained ITGA5-driven myofibroblast activation drives the scarring cascade in IPF. Targeted ITGA5 inhibition aims to stop progression and enable parenchymal repair.

Peptide-based ITGA5 antagonism reduces TGF-β–mediated fibroblast-to-myofibroblast transition and lowers collagen I/III deposition in the alveolar interstitium.

Preclinical — efficacy and PK/PD established in established lung fibrosis models.

Stromal fibroblasts shield and support tumor cells in lung metastasis, limiting the reach of systemic chemotherapy and shortening survival.

Conjugating an ITGA5-binding peptide to polymeric nanoparticles enables fibroblast-selective delivery of cytotoxic payloads directly to the metastatic niche.

AV3 peptide conjugated to polymeric nanoparticles (AV3-PNP) delivers docetaxel to ITGA5-positive fibroblasts in lung metastasis, significantly reducing established lung metastases in vivo versus free drug.

Preclinical — in vivo proof-of-concept in PDAC-induced lung metastasis models.