OUR DATA
Preclinical Evidence
Consistent antifibrotic activity across multiple organ systems and disease models
Preclinical studies show reversal or reduction of established fibrosis across pulmonary, cardiac, renal and hepatic models.
Pulmonary Fibrosis
Both VB0004 and VB4-A79 demonstrated significant reductions in pulmonary fibrosis in the bleomycin-induced lung fibrosis model. Treatment was administered after fibrosis was already established, and both compounds produced significant reductions in pulmonary fibrosis compared to vehicle control, with histology confirming near-normal lung architecture restored at the end of the treatment period.
Cardiac Fibrosis
VB0004 produced a dose-dependent reduction in myocardial fibrosis in spontaneously hypertensive rats. At the highest dose studied, fibrosis was reduced to levels significantly below those present at the start of treatment, demonstrating reversal of pre-existing cardiac fibrosis and restoration of normal tissue architecture. VB4-P5 has also shown activity in cardiac fibrosis models.
Renal Fibrosis
VB0004 reversed renal interstitial fibrosis at all doses tested, with restoration of normal tubular architecture. VB4-P5 has demonstrated significant reductions in renal fibrosis in preclinical models and is the subject of an existing licensing agreement with an international biotechnology company.
Liver Fibrosis
VB4-A32 demonstrated significant reductions in liver fibrosis in a high-fat-diet-induced rat model of fatty liver disease, supporting its potential in the treatment of metabolic-associated steatohepatitis.
Macrophage Activation
In addition to its effects through the NPR-C/cGMP pathway, VB0004 demonstrated a concentration-dependent activation of macrophages in vitro, consistent with a second mechanism of action in which activated macrophages engulf and degrade established collagen deposits. This dual mechanism of action may underpin the reversal of established fibrosis observed across multiple organ models.