Asperlin is an orally active marine-derived antibiotic with antifungal, anticancer, anti-inflammatory, and anti-atherosclerotic properties. It can induce apoptosis and increase reactive oxygen species (ROS) and DNA damage-related G2/M phase arrest, as well as ATM phosphorylation. Additionally, Asperlin effectively prevents HFD-induced obesity in vivo and modulates gut microbiota.

Asperlin, at concentrations of 6-25 μM for 24-48 hours, inhibits cell growth in a dose-dependent manner, induces caspase-3 and PARP cleavage, decreases Bcl-2 levels, and triggers apoptosis. This apoptotic effect in HeLa cells can be blocked by NAC [1]. At 6-25 μM for 24 hours, Asperlin increases ROS and causes DNA damage-related G2/M phase arrest and ATM phosphorylation, which can be significantly blocked by NAC or the ATM inhibitor KU-55933 [1]. Asperlin also exhibits anti-inflammatory properties in macrophages at 5-40 μM for 12 hours, reducing the expression of iNOS and COX-2 induced by LPS, and decreasing the production of TNF-α and IL-1β in mouse peritoneal macrophages and RAW264.7 macrophage cells in a dose-dependent manner [3]. At 500 μg/ml for 1 day, Asperlin effectively controls tomato late blight and wheat leaf rust disease, showing a disease control value of 95% [4].

Asperlin (40-80 mg/kg; oral administration; once daily for 12 weeks) effectively prevents obesity development in mice on a high-fat diet (HFD), enhances energy expenditure, and modulates the gut microbiota [2]. Furthermore, Asperlin (80 mg/kg; oral administration; once daily for 12 weeks) significantly inhibits atherosclerotic plaque formation in HFD-fed ApoE-/- mice, leading to reduced aortic dilation and decreased atherosclerotic lesion area [5].