SynthesisCell biology and toxicology2025
Effects of TA-65 on telomere length, functional outcomes, and inflammation: a systematic review and meta-analysis.
Synthesis in Cell biology and toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
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Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
backgroundTA-65®, a telomerase-activating compound derived from Astragalus membranaceus, has garnered interest for its potential to modulate cellular aging. However, its mechanistic efficacy and long-term toxicological profile remain inadequately synthesized.
methodsThis PRISMA-guided meta-analysis evaluated 8 randomized controlled trials (RCTs, n = 750 participants; mean age 63.3 years) assessing TA-65's effects on telomere dynamics, functional aging indices, and safety outcomes. Primary outcomes included leukocyte telomere length (LTL) measured by Southern blot or qPCR/or flow-FISH; secondary outcomes encompassed frailty metrics (SPPB, grip strength, 6MWT), inflammatory markers (hs-CRP, IL-6), and adverse events (CTCAE v5.0). Statistical synthesis employed random-effects models (RevMan 5.3), subgroup analyses, and GRADE evidence grading.
resultsTA-65 supplementation induced moderate telomere elongation (SMD = 0.47, 95% CI: 0.31-0.62; p < 0.00001), with amplified effects in adults > 60 years (SMD = 0.63 vs. 0.36; p = 0.03). Industry-funded trials reported inflated efficacy (SMD = 0.63 vs. 0.40; p = 0.03). Critically, telomere elongation did not translate to functional improvements in frailty (SMD = 0.09, p = 0.15) or inflammation (CRP/IL-6 SMD = - 0.11, p = 0.07), revealing a telomere-function disconnect. Safety analysis (n = 487) identified mild gastrointestinal toxicity (12.4% incidence; nausea: 7.1%, abdominal discomfort: 5.3%) but no severe adverse events (e.g., oncogenesis) over 12 months. Dose-response relationships (10-50 mg/day) and measurement-method variations were non-significant (p > 0.05).
conclusionsWhile TA-65 demonstrates telomerase-activating efficacy, particularly in older adults, its failure to improve functional aging metrics underscores limitations of unimodal biomarker targeting. The absence of dose-dependent toxicity or short-term oncogenic risk is notable, yet long-term carcinogenic potential remains unaddressed. Rigorous, independent trials must evaluate TA-65's chronic toxicity, telomere-independent mechanisms, and utility within multidimensional aging frameworks. Clinical application may consider older adults with immunosenescence, incorporating safety surveillance for gastrointestinal and oncological endpoints.
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