Researchers at the University of Aberdeen in the United Kingdom have announced a breakthrough drug designed to reduce fatty deposits inside arteries. The findings were published in the Journal of Translational Medicine, signaling a potential new approach to cardiovascular protection.
The drug is based on a compound called trodusquemin and works by dampening the activity of the enzyme PTP1B. Elevated PTP1B levels are commonly seen in individuals with obesity and diabetes and are also linked to chronic inflammatory states, including sepsis, diabetic foot complications, and allergic pneumonia. When PTP1B rises, a cascade of events can unfold that causes white blood cells, or leukocytes, to take up oxidized cholesterol. Those leukocytes can then transform into foam cells that are loaded with low-density lipoproteins, or LDL. The accumulation of such altered cells in arterial walls contributes to stiffness and plaque formation, a hallmark of atherosclerosis.
In laboratory experiments with mice, the new trodusquemin-based drug prevented leukocytes from becoming foam cells by inhibiting PTP1B activity. This suggests a direct intervention point to halt early plaque development and preserve arterial elasticity, a key factor in maintaining vascular health.
Additional studies showed that genetically removing PTP1B from the genome in mice led to lower circulating LDL levels. Since LDL is a major driver of plaque formation, these results reinforce the idea that suppressing PTP1B can influence lipid balance and vascular risk in a meaningful way.
Researchers noted that the drug’s effects observed in animal models are expected to translate to humans, though clinical trials will be necessary to confirm safety and efficacy in people. The team described their discovery as opening a new therapeutic channel for protecting against atherosclerosis, the primary cause of many heart attacks and strokes. This line of work aligns with broader efforts to identify molecular targets that can halt the progression of cardiovascular disease at the cellular level.
Beyond the laboratory findings, the researchers emphasized the potential for the trodusquemin-based therapy to complement existing strategies for heart health. While lifestyle choices such as diet and physical activity remain foundational, pharmacological interventions targeting PTP1B could offer additional protection for patients at elevated cardiovascular risk. The ongoing work also highlights the value of translating molecular insights into practical treatments that can reduce the burden of atherosclerosis on patients and healthcare systems alike.
As the science advances, experts caution that results from animal models require careful validation in human trials. They also stress the importance of comprehensive risk assessment, long-term safety data, and exploration of how this therapy might interact with current lipid-lowering medications and anti-inflammatory regimens. If successful, this approach could reshape preventive cardiology and provide a new tool in the fight against heart disease and stroke.
In the broader context, this development fits with a growing interest in how metabolic and inflammatory pathways intersect with vascular health. Researchers continue to map the precise mechanisms by which PTP1B influences lipid processing, immune cell behavior, and arterial remodeling. The goal is to produce safe, effective treatments that can be integrated into standard care, ultimately reducing the prevalence of atherosclerotic complications worldwide.