Comprehensive Interactive Dashboard for Senolytic Cell Removal Drug Development
Interactive Control: Adjust the age slider to observe real-time changes in cellular populations, senescence burden, and tissue-specific impacts. This simulation models the natural progression of cellular aging and the accumulation of senescent cells over the human lifespan.
Senolytic drugs represent a revolutionary approach to aging intervention by selectively eliminating senescent cells - the "zombie cells" that drive age-related tissue dysfunction and chronic disease.
This interactive analysis demonstrates the therapeutic potential of senolytic interventions across multiple tissue systems, providing quantitative evidence for drug development priorities and clinical trial design.
Real-time visualization of senescent cell behavior and SASP factor release at age 93
Green: Optimal cellular health with minimal senescence burden. Yellow: Increasing senescent cell accumulation and SASP activity. Red: Significant senescence burden requiring therapeutic intervention.
How different cellular markers change with age - your current age (93) is highlighted
High senescent cell burden driving age-related diseases
Significant decline in regenerative capacity and immune function
At age 93, senescent cells comprise NaN% of the total cellular population. Senolytic intervention could potentially eliminate 85-95% of these cells, shifting the healthy cell percentage from NaN% to approximately 79.3%, representing a significant improvement in tissue function and reduced inflammatory burden.
Satellite cell senescence severely impairs muscle regeneration capacity, leading to sarcopenia and reduced physical performance. Senescent muscle stem cells lose their ability to repair damaged tissue.
At the simulated age of 93 years, comprehensive biomarker analysis reveals the following cellular aging signatures critical for senolytic drug targeting:
p16INK4a+ cells, SA-β-gal+ populations, SASP-high senescent cells
IL-6, TNF-α, MMP levels, telomere length, DNA damage markers
70-90% reduction in senescence markers within 2-4 weeks
Selective targeting with minimal impact on healthy cell populations
Senolytic drugs exploit unique vulnerabilities in senescent cells' survival pathways. Unlike healthy cells, senescent cells rely heavily on pro-survival networks including BCL-2, PI3K/AKT, and p53/p21 pathways.
The SASP (Senescence-Associated Secretory Phenotype) creates a toxic microenvironment through secretion of over 50 inflammatory factors, growth factors, and matrix-degrading enzymes.
IL-6, TNF-α, IL-1β drive systemic inflammation and tissue dysfunction
MMPs and other proteases compromise tissue architecture and function
BCL-2 family proteins and PI3K/AKT prevent senescent cell clearance
15+ compounds under investigation
Safety & dosing studies
Efficacy demonstration
Large-scale validation
Recent Phase II trials demonstrate 36% improvement in 6-minute walk test, 40% reduction in inflammatory markers (IL-6, TNF-α), and significant improvements in quality of life scores within 5-11 weeks of treatment.
Source: Mayo Clinic Proceedings, 2019; Nature Medicine, 2021
Our Next-Generation Senolytic Solution
Advanced senescent cell identification and selective elimination technology
Minimal impact on healthy cells with optimized therapeutic window
Clinical validation with measurable improvements in healthspan markers
Transforming senescence research into therapeutic reality