Elevated Gal3 levels are linked to chronic inflammation, fibrosis, neurodegeneration, and metabolic dysfunction, all of which accelerate aging.
Gal3 acts as an immune regulator of inflammatory pathways, contributing to conditions like Alzheimer’s, Parkinson’s, cardiovascular disease, and diabetes.
Chronic inflammation is a major factor in age-related disease progression and reduced longevity.

Neutralizing Gal3 with TB006 may reduce chronic inflammation and prevent toxic protein accumulation.
TB006 has demonstrated the ability to prevent formation of amyloid-beta (Aβ) and alpha-synuclein aggregates, the pathological proteins linked to Alzheimer’s and Parkinson’s disease, respectively.

The key to longevity is not just living longer but staying healthier longer (healthspan extension).
Studies suggest that delaying neurodegeneration by even 5 years could dramatically reduce disease burden and healthcare costs, while significantly improving quality of life.

Cardiovascular Health: Gal3 is linked to heart failure and arterial stiffness—neutralizing it may reduce cardiovascular risks.
Fibrosis Prevention: TB006 could help prevent organ fibrosis (e.g., liver, kidney, and lung fibrosis), which contributes to multi-organ aging.
Metabolic Health: Lowering Gal3 may improve insulin sensitivity and reduce obesity-related inflammation, helping to prevent diabetes and metabolic syndrome.

By integrating TB006 into longevity medicine, we may be able to proactively slow aging at its core biological processes, rather than just treating age-related diseases reactively.
The long-term vision: Using TB006 as part of a longevity strategy to maintain cognitive function, metabolic health, and tissue integrity well into advanced age.

✅ Reduces chronic inflammation – a major driver of aging.

✅ Prevents neurodegeneration – delaying Alzheimer’s and Parkinson’s.

✅ Protects cardiovascular and metabolic health – reducing the risk of heart disease and diabetes.

✅ Combats fibrosis – preventing tissue and organ aging.