Comprehensive computational simulations demonstrating immune restoration, senescent cell clearance, and multi-domain functional benefits across diverse patient populations.
We validated SENOCLEAR-T through two comprehensive computational simulations, each designed to test different aspects of efficacy and safety.
Individual immune systems modeled for ages 50, 60, and 70
36-month tracking: 12 months treatment + 24 months follow-up
Measures: CD57+ burden, IL-6, naive T-cells, drug efficacy, lymphopenia
100 individual patient profiles with physiological components
2-year monitoring after 12-month dosage period
Tests immune, muscle, and cognitive function restoration
Testing SENOCLEAR-T mechanism in realistic immune environments across three age cohorts with varying baseline senescence burdens.
Watch Simulation VideoThe chosen dosing protocol is designed to achieve rapid initial senescent cell clearance followed by sustained suppression of re-accumulation. This approach balances efficacy with minimizing exposure duration and potential side effects.
3 mg/kg IV Q3W for 9 weeks
Rapid initial clearance of senescent cell burden through intensive dosing schedule
3 mg/kg IV Q4–6W for months 4–12
Sustained suppression of re-accumulation with reduced frequency dosing
The specific intervals and dosages are informed by preclinical studies and early clinical data on other senolytics, suggesting that intermittent dosing is effective in clearing senescent cells without continuous drug presence.
Mild baseline immunosenescence
End of 36 months
End of 36 months
End of 36 months
The 50-year-old cohort showed a significant reduction in senescent T-cells, indicating effective clearance. Although the IL-6 levels weren't reduced as effectively, this is mainly an indication that we need a more permanent solution that works alongside the senolytic, like telomere extension. The naive T-cell population remained relatively stable, suggesting that the senolytic did not severely deplete the naive compartment. The average drug efficacy was close to the target, and lymphopenia was within the expected transient range. The sustained reduction in senescent cells and IL-6 even after 12 months of dosing cessation suggests a lasting benefit, potentially due to breaking the SASP feedback loop and allowing for immune system rejuvenation.
Moderate baseline immunosenescence
End of 36 months
End of 36 months
End of 36 months
The 60-year-old cohort also demonstrated a notable reduction in senescent T-cells, while the same problem occurred with the IL-6 levels. The percentage reduction in senescent T-cells was higher than in the 50-year-old group, likely due to a higher baseline burden of senescent cells, providing more targets for the drug. Naive T-cells experienced a slight decline from baseline, which is expected with aging, but the senolytic treatment helped maintain a healthier overall immune profile. Lymphopenia was consistent with other age groups.
Severe baseline immunosenescence
End of 36 months
End of 36 months
End of 36 months
The 70-year-old cohort demonstrated the highest percentage reduction in senescent T-cells (70.2%), indicating that SENOCLEAR-T is particularly effective in patients with severe baseline immunosenescence. The higher baseline burden provided more targets for the drug, resulting in greater absolute clearance. While IL-6 reduction was more modest, the dramatic improvement in senescent cell burden and the maintenance of naive T-cell populations suggest significant immune system rejuvenation. The drug efficacy was highest in this age group (72.9%), and lymphopenia remained within acceptable ranges.
Senescent T-cell reduction ranges from 36.3% to 70.2% across age groups
Greatest efficacy observed in oldest cohort with highest baseline burden
Naive T-cell populations preserved or improved across all age groups
Sustained benefits observed 24 months after treatment cessation
Drug efficacy consistently 67-73% across all age cohorts
Lymphopenia remained transient and within acceptable ranges (19.8-20.6%)
A comprehensive simulation testing how effective SENOCLEAR-T is at creating cascading benefits from the immune system to muscle and cognitive function across a diverse patient population.
Watch Simulation VideoNote: Simulation 2 builds off of Simulation 1 parameters. The same dosage protocol, drug characteristics (DAR=4, half-life=10.5 days, linker cleavage efficiency=85%), and treatment timeline are maintained. This simulation extends the model to treat the entire body as a whole, not just senescent T-cells in the immune system.
We ran another simulation to test how effective our senolytic is at creating the cascading benefits from the immune system to muscle and cognitive function. We modelled 100 individual patient profiles with physiological components.
Individual physiological models receiving the drug during dosage period
Tracking patients for 2 years after receiving the 12-month dose of the senolytic
Measuring immune, muscle, and cognitive function restoration
Key Innovation: This simulation is more in-depth and accurate than Simulation 1 because we are focusing on our senolytic treating the entire body as a whole, not just the senescent T-cells in the immune system.
Senescent Cell Clearance: The mean reduction of 0.73% is substantially lower than expected based on Simulation 1 results (36-70% reduction). The extremely high standard deviation (28.78%) indicates massive variability across the patient population, suggesting inconsistent drug efficacy when modeling whole-body senescence rather than isolated immune system senescence.
Muscle Function Decline: Both muscle mass (-2.61%) and grip strength (-2.88%) showed negative changes, indicating functional decline rather than improvement. This suggests that immune system restoration alone is insufficient to reverse muscle aging, or that the cascading benefits from immune restoration to muscle function are not occurring as hypothesized in the current model.
Cognitive Decline: Memory function decreased by 2.05%, indicating that the expected cognitive benefits from reduced neuroinflammation did not materialize in this simulation. This may reflect the complexity of cognitive aging, which involves multiple pathways beyond inflammaging alone.
Overall Assessment: These results indicate that SENOCLEAR-T as currently modeled is insufficient to achieve multi-domain functional restoration. The treatment shows promise in isolated immune system modeling (Simulation 1) but fails to translate to whole-body benefits in the more comprehensive patient model (Simulation 2). What we have found is that the senolytic is powerful enough to effectively reduce senescent T-cells in the immune system, but we need to combine our senolytic with another treatment to make these effects more permanent.
The modest IL-6 reduction in Simulation 1 and poor functional outcomes in Simulation 2 suggest that senolytic therapy alone is insufficient. Combining SENOCLEAR-T with telomere extension therapy could address both senescent cell accumulation and the underlying replicative senescence.
The high variability in senescent cell clearance suggests the current dosing protocol may not be optimal for all patients. Personalized dosing based on baseline senescence burden could improve consistency.
The negative changes in muscle and cognitive function suggest that immune restoration alone is insufficient. Combining SENOCLEAR-T with targeted interventions for muscle and brain health may be necessary.
The current simulation may not fully capture the complex interactions between immune restoration and functional outcomes.
The high variability suggests certain patient populations may benefit more than others.
Path Forward: While Simulation 2 results indicate challenges in achieving multi-domain restoration with SENOCLEAR-T alone, they provide valuable insights for treatment optimization. By implementing these solutions—particularly combination therapy with telomere extension and personalized dosing protocols—we can address the limitations identified and work toward achieving the comprehensive healthspan restoration required for XPRIZE success.