Researchers in a collaborative study evaluate DT-109, an orally deliverable tripeptide, for its effects on advanced atherosclerosis and vascular calcification in cynomolgus monkeys. Administered daily alongside a high-cholesterol diet, DT-109 significantly reduces lesion formation, inflammatory signaling, and arterial calcification while promoting smooth muscle cell contractile marker expression. These findings suggest a multifaceted therapeutic approach to combat cardiovascular disease by targeting inflammasome pathways and plaque stability.

Key points

• Orally administered DT-109 (Gly-Gly-Leu) peptide at 150 mg/kg/day in cynomolgus monkeys.
• Five-month treatment with a cholesterol-rich diet showed significant reductions in aortic and coronary lesion size.
• DT-109 downregulates pro-inflammatory genes NLRP3, AIM2, CASP1 and oxidative stress markers NCF2, NCF4.
• Treatment reduces vascular calcification and macrophage content while increasing SMC contractile markers ACTA2, CNN1, TAGLN.
• In vitro assays confirm DT-109 inhibits NLRP3 inflammasome activation and smooth muscle cell calcification.

Why it matters: These results demonstrate a novel peptide-based strategy that combines anti-inflammatory and anti-calcific actions to address advanced atherosclerosis, a leading cause of cardiovascular mortality. By demonstrating efficacy in primate models, DT-109 bridges the gap between rodent research and human application, offering a promising route to more effective, orally available therapies that can regress plaque and restore vascular function.

Researchers publishing in Aging Cell report that senescent macrophages in old skeletal muscle release the antiangiogenic VEGF-A165B isoform, impairing endothelial function and slowing revascularization in peripheral arterial disease models.

Key points

• Senescent macrophages accumulate in ischemic skeletal muscle of aged mice.
• Transplantation experiments show these macrophages inhibit revascularization.
• Senescent cells upregulate antiangiogenic VEGF-A165B isoform secretion.
• Elevated plasma VEGF-A165B correlates with disease severity in elderly PAD patients.
• Senolytics like dasatinib plus quercetin offer a strategy to clear senescent macrophages.

Why it matters: Uncovering senescent macrophages as drivers of poor vascular regeneration identifies a novel therapeutic target. This insight paves the way for senolytic interventions to improve blood flow recovery in age-related vascular diseases, potentially enhancing healthspan.

A team led by the University of Rochester finds that bat fibroblasts require only two oncogenic alterations—RAS activation plus p53 or pRb inactivation—for malignant transformation. Despite this minimal barrier, bats sustain high basal p53 activity and apoptosis, alongside active telomerase, offering insights into their remarkable longevity and tumor resistance.

Key points

• Bat fibroblasts from three species transform with just HRasG12V plus p53 or pRb inactivation.
• All four bat species display constitutive telomerase activity in somatic cells and tissues.
• Basal TP53 and WRAP53 transcripts are elevated, driving high p53‐mediated apoptosis.
• Stress‐induced premature senescence triggers reduced SASP and enhanced apoptosis in bat cells.
• Xenograft assays confirm two‐hit transformed bat cells form tumors in nude mice.
• Genomic analyses reveal TP53 duplications in Myotis lucifugus, suggesting expanded p53 dosage.

Why it matters: This study overturns assumptions about stringent cell‐intrinsic cancer defenses in long‐lived species by showing bats transform easily yet rely on apoptosis and immune surveillance to suppress tumors. Understanding these mechanisms could inspire novel anti‐cancer and longevity‐promoting therapies.

Therini Bio reports positive Phase 1a results for THN391, a humanized monoclonal antibody that selectively neutralizes fibrin-induced neuroinflammation without affecting coagulation. Using ascending single and multiple dosing, the drug shows safety, dose-proportional pharmacokinetics, and supports monthly administration. Phase 1b studies will assess efficacy in Alzheimer’s disease and diabetic macular edema.

Key points

• THN391 is a humanized monoclonal antibody targeting the inflammatory epitope on fibrin.
• Phase 1a trial was randomized, double-blind, placebo-controlled with single and multiple ascending doses.
• The treatment showed no serious adverse events, preserved coagulation, and avoided anti-drug antibody responses.
• Pharmacokinetic analysis revealed dose-proportional exposure and a half-life supportive of once-monthly dosing.
• Phase 1b trials will evaluate clinical efficacy in Alzheimer’s disease and diabetic macular edema cohorts.

Why it matters: By demonstrating safety and monthly dosing feasibility of THN391, this study substantiates targeting fibrin-mediated neuroinflammation as a novel approach to treating Alzheimer’s and retinal degenerative diseases. This upstream intervention could shift paradigms from symptomatic relief to disease modification in neurodegeneration and vascular dysfunction.

Wonderfeel, led by biomedical researcher Dr. Andrew Salzman, unveils Youngr™ and Capsuls™, two high-dose NMN supplements designed to elevate NAD+ levels. By delivering stable NMN precursors in clean-label capsules, these products enhance mitochondrial function, DNA repair, and sirtuin activity to support cellular energy, metabolic health, and healthy aging. Formulated in cGMP facilities and third-party tested, they cater to biohackers and wellness seekers seeking evidence-based longevity solutions.

Key points

• 900 mg NMN plus resveratrol, hydroxytyrosol, ergothioneine, and vitamin D3 in Youngr™ formula
• 1000 mg pure NMN per serving in Capsuls™ for high-dose NAD+ support
• Manufactured in cGMP-certified US facilities and third-party tested for purity
• Clean-label vegan capsules engineered for NMN stability and optimal absorption
• Synergistic multi-ingredient approach targets sirtuin activation, mitochondrial ATP production, and DNA repair
• Formulations designed to counteract age-related NAD+ decline and support metabolic resilience

GenuinePurity’s new Longevity+ formula integrates five researched compounds—NMN, cycloastragenol, CoQ10, resveratrol, and selenium—in clinically aligned doses. Delivered via enteric-coated capsules for optimal absorption, it targets NAD+ restoration, telomere integrity, mitochondrial performance, and antioxidant defense to support cellular renewal and healthy aging.

Key points

• 250 mg NMN per serving for NAD+ biosynthesis enhancement
• 2 mg cycloastragenol to activate telomerase and support telomere integrity
• 200 mg CoQ10 optimized for mitochondrial ATP production
• 100 mg resveratrol to modulate sirtuin activity and epigenetic regulation
• 100 µg selenium for glutathione-peroxidase antioxidant defense

Why it matters: By combining NAD+ precursors, telomere stabilizers, mitochondrial enhancers, and antioxidants into one formula with improved bioavailability, Longevity+ addresses multiple aging pathways simultaneously. This integrated strategy may offer a more balanced and convenient alternative to piecemeal supplement stacks, potentially improving cell function and healthspan.

Scientists at the National Institute on Aging investigate telomere attrition, the progressive shortening of protective DNA caps on chromosomes, and its role in cellular senescence. They review strategies such as telomerase activation, NAD⁺ supplementation, and lifestyle interventions to maintain telomere integrity and propose approaches to mitigate age-related disease by extending healthspan.

Key points

• Progressive telomere shortening drives replicative senescence and age-related decline
• Telomerase activation via TERT gene delivery can restore telomere length in preclinical models
• Senolytics such as dasatinib and quercetin clear senescent cells to reduce inflammation
• NAD⁺ boosters (nicotinamide riboside) enhance sirtuin activity and DNA repair
• Caloric restriction and intermittent fasting activate longevity pathways and slow aging
• Stem cell therapy offers potential tissue regeneration by rejuvenating aged cells

Why it matters: Targeting telomere maintenance shifts aging research toward fundamental mechanisms rather than symptoms. Preserving chromosomal integrity promises to extend healthspan and tackle multiple age-associated diseases simultaneously, offering advantages over traditional, single-disease therapies.