Supplements and Compounds Library
Every article, presentation, spotlight, and news item we've tagged to Supplements and Compounds.
Showing 217–240 of 328
Renue by Science wins precision recovery & performance award
Renue by Science received recognition for its Total NAD+ Restoration Protocol, a multi-pathway supplement approach designed to address age-related NAD+ decline through enhanced precursor delivery, reduced NAD+ catabolism, improved mitochondrial efficiency, and cellular repair support. NAD+ restoration represents a targeted intervention in the metabolic foundation of cellular aging.
Senescent Cell Diversity Defines Fibrotic vs Inflammatory Aging
Senescent cells—those that have stopped dividing—adopt distinct molecular profiles depending on how they became senescent. Primary senescence (triggered by direct DNA damage) activates fibrosis and tissue-remodeling programs, while secondary senescence (induced by signals from other senescent cells) drives inflammatory pathways. Both share conserved stress-response mechanisms, revealing that senescence heterogeneity fundamentally shapes how these cells contribute to aging.
The ‘rising tide’ of mitochondrial therapies in longevity
Mitochondrial dysfunction is increasingly recognized as a central mechanism underlying age-related disease, not merely a feature of rare genetic conditions. The FDA approval of elamipretide (Forzinity) for Barth syndrome represents the first regulatory validation of mitochondria-targeted therapeutics, positioning this class of drugs as potential interventions for common age-related conditions including neurodegeneration and cardiac disease.
Rubedo reports early clinical signal for senotherapeutic drug
Phase 1 data for RLS-1496, a GPX4 modulator, demonstrate safety and dose-dependent target engagement alongside reductions in senescence markers and clinical improvement in inflammatory skin conditions. The drug operates through a dual mechanism: clearing senescent cells via ferroptosis while restoring redox balance in stressed neighboring cells, representing a shift toward cellular recalibration rather than indiscriminate senescent cell clearance.
Methionine Restriction Triggers Autophagy Through Epigenetic Control
Methionine restriction extends lifespan in yeast by reducing S-adenosylmethionine production, which prevents methylation of protein phosphatase 2A and triggers sustained autophagy. Early-stage methionine restriction appears sufficient to activate this longevity pathway, suggesting a potential therapeutic target for human healthspan extension without sustained dietary restriction.
FGF21 Gene Therapy Extends Lifespan 20% in Aging Mice
Late-life delivery of FGF21 gene therapy via muscle targeting extended median lifespan in mice by 20.5% while improving metabolic health, mitochondrial function, and reducing age-related pathology across multiple organs. The intervention mimics metabolic benefits of exercise and caloric restriction without requiring sustained behavioral change.
Springfield Wellness Center marks 25 years of NAD+ IV therapy
Springfield Wellness Center has operated for 25 years using intravenous NAD+ therapy as part of a multimodal protocol for addiction recovery and brain restoration. The clinic's longevity and expansion suggest sustained clinical utility, though the evidence base and mechanistic clarity for NAD+ infusions in longevity contexts remain limited.
Lifespan and Fecundity Impacts of Reduced Insulin Signalling Can Be Directed by Mito‐Nuclear Epistasis in Drosophila
Reduced insulin signaling extends lifespan in Drosophila, but the effect—beneficial or detrimental—depends on the genetic interaction between mitochondrial and nuclear DNA. This reveals that conserved aging mechanisms operate differently across individuals based on mito-nuclear epistasis, with direct implications for personalized longevity interventions.
Rejuvenation Roundup February 2026
A February 2026 research roundup covering advances in cellular reprogramming, senolytic effectiveness, immune cell restoration, and cognitive interventions demonstrates multiple convergent pathways for addressing age-related decline. The collective findings suggest that aging is modifiable across multiple biological domains, with implications for clinical translation in vision, neurological, and metabolic disease.
Senescent fibroblast subtypes drive pulmonary fibrosis progression
Senescent fibroblasts—cells that have stopped dividing but remain metabolically active—exhibit distinct subpopulations with different DNA damage responses, a finding that clarifies how these cells contribute to idiopathic pulmonary fibrosis. This heterogeneity explains why standard anti-senescence approaches may fail in IPF and points toward subtype-specific interventions to halt progressive lung scarring.
Fasting mimetic shows metabolic effects in trial
A randomized controlled trial of a fasting mimetic formulation in overweight older adults with elevated HbA1c showed reductions in LDL particle number, oxidized LDL, and fasting glucose over eight weeks. The compound—a blend of spermidine, nicotinamide, palmitoylethanolamide, and oleoylethanolamide—reproduced several cardiometabolic signatures associated with fasting without dietary restriction, though durability beyond the study period remains undemonstrated.
#383 ‒ AMA #81: Biological aging tests, longevity training, emerging therapies, GLP-1 RAs, sun exposure, and more
This AMA addresses multiple longevity domains: biological aging biomarkers, exercise protocols for longevity, emerging therapeutic approaches, GLP-1 receptor agonists, and sun exposure risk-benefit profiles. The discussion emphasizes that evidence-based interpretation of these tools requires distinguishing between mechanistic plausibility and demonstrated clinical outcomes.
Senescent Cell Pathways: Primary vs Secondary Origins
Research distinguishes primary senescent cells (induced by direct damage like radiation) from secondary senescent cells (induced by signals from neighboring senescent cells). This heterogeneity in senescent cell populations has direct implications for understanding aging progression and designing interventions targeting cellular senescence.
The HIF‐1α Pathway Regulates Satellite Cell Fate During Aging Through Histone Lactylation
Pharmacological reactivation of HIF-1α signaling in aged satellite cells restores lactate-driven epigenetic remodeling and shifts cells from senescence toward a regenerative state, with treated cells demonstrating enhanced myogenic capacity and increased ATP production. This identifies a metabolic-epigenetic axis relevant to age-related muscle decline and suggests a therapeutic target for sarcopenia.
Targeting an Appetite Hormone Receptor for Stronger Muscles
Inhibiting the ghrelin receptor (GHSR-1a) improves muscle strength, exercise capacity, and mitochondrial function in aging mice, reducing sarcopenia markers without extending lifespan. Pharmacological inhibition via PF-5190457 replicates these effects and represents a translatable therapeutic approach.
SIRT6 centenarian variant activates cellular aging pathways
Genflow Biosciences is advancing SIRT6 gene therapy targeting age-related disease and metabolic dysfunction, with preclinical validation in aged dogs and planned human trials. SIRT6 activation represents a direct intervention in cellular aging pathways known to regulate energy metabolism, stress response, and tissue regeneration.
Network Medicine Maps Drugs to Aging Hallmarks
Researchers applied network medicine to map 6,442 existing drugs against the hallmarks of aging, identifying candidates that may influence longevity by targeting proteins proximal to aging-related gene modules. This approach offers a systematic method to repurpose approved medications for age-related interventions without requiring decades-long human trials.
Correction to “Spatial Reorganization of Chromatin Architecture Shapes the Expression Phenotype of Therapy‐Induced Senescent Cells”
This correction addresses a published study on how senescent cells reorganize their chromatin architecture in response to therapeutic stress. Understanding the structural changes in non-dividing cells has direct implications for improving cellular resilience and longevity through better therapeutic design.
Could PGC-1α hold the key to longevity?
PGC-1α, a transcriptional coactivator that regulates cellular energy metabolism and mitochondrial biogenesis, is emerging as a target for age-related disease intervention. Endurance Bio is advancing a small molecule (T-168) designed to upregulate PGC-1α, with Phase 2 trials underway in Parkinson's disease and potential applications across neurodegeneration, metabolic dysfunction, and frailty.
FGF21 Gene Therapy Preserves Multi-Organ Function in Aged Mice
A single injection of AAV-delivered FGF21 gene therapy extended lifespan by over 20% in aged mice while preserving function across liver, kidneys, heart, skeletal muscle, and brain. The treatment improved metabolic health markers and activated adaptive programs that countered multiple aging mechanisms simultaneously, suggesting metabolic interventions may have broader relevance to systemic resilience.
Regulatory RNA Sustains Liver Immunity and Metabolism in Aging
A regulatory RNA molecule specific to immune T cells sustains metabolic balance and immune function in the aging liver, addressing a fundamental mechanism of age-related decline. This correction validates findings on how the body maintains coordinated immune and metabolic signaling during aging.
Mitochondrial therapy restores metabolic function without appetite
MitoRx's MTRX31 targets mitochondrial dysfunction rather than appetite suppression, achieving significant fat loss while preserving muscle and metabolic function in preclinical models. This metabolic-first approach addresses a fundamental limitation of current obesity drugs: weight loss achieved through caloric restriction often comes with muscle loss and metabolic compromise.
Mirroring tissue senescence in human biofluids
Researchers have developed a non-invasive urine-based biomarker panel to monitor cellular senescence and track the efficacy of senolytic therapies. This approach enables real-time assessment of senescent cell burden without tissue biopsy, creating a practical pathway for personalized intervention monitoring in aging-related disease.
Restoring the Strength of Natural Killer Cells
Natural killer cells from older adults show reduced capacity to eliminate senescent and cancer cells due to impaired granule release and cytotoxic machinery, not recognition defects. Targeting elevated Cdc42 protein and restoring microtubular organization represents a potential intervention to restore NK cell function with age.