The science adding years to human lives can now do the same for your best friend.

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For decades, the most rigorous longevity research in the world has been focused on humans. The molecular pathways that govern aging—NAD+ depletion, mitochondrial decline, chronic inflammation—have been well mapped. We’re applying and extending proven science from humans to the animals who age alongside us.

The science adding years to human lives can now do the same for your best friend.

For decades, the most rigorous longevity research in the world has been focused on humans. The molecular pathways that govern aging—NAD+ depletion, mitochondrial decline, chronic inflammation—have been well mapped. We’re applying and extending proven science from humans to the animals who age alongside us.
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Mechanisms first, formula second

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Mechanisms first, formula second

Decades of research. Finally for them.

Most pet supplement brands start with an ingredient. We start with a mechanism. The pet industry standard is to pick an ingredient, and then find studies that support it. We do the opposite. We start with the science of how aging actually works - what breaks down, what depletes, what stops functioning - and let that determine what goes into the blend. 

From mechanism to molecule.

Our process begins with primary literature on mammalian aging: human and animal longevity data, reviewed for the pathways with the strongest interventional evidence. This is because much of the molecular science is conserved across mammalian species at a level that makes the human data directly relevant. This body of evidence is the substate from which every formulation decision is derived. 

“Truth be told, there were no good options available. So, we created our own.”

Decades of research. Finally, for them.

Most pet supplement brands start with an ingredient. We start with a mechanism. The pet industry standard is to pick an ingredient, and then find studies that support it. We do the opposite. We start with the science of how aging actually works - what breaks down, what depletes, what stops functioning - and let that determine what goes into the blend. 

From mechanism to molecule.

Our process begins with primary literature on mammalian aging: human and animal longevity data, reviewed for the pathways with the strongest interventional evidence. This is because much of the molecular science is conserved across mammalian species at a level that makes the human data directly relevant. This body of evidence is the substate from which every formulation decision is derived. 

“Truth be told, there were no good options available. So, we created our own.” 

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The Hallmarks of Aging

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The Hallmarks of Aging

In 2013, López-Otín et al. published a landmark framework in Cell identifying biological processes that drive aging across mammalian species.[1] The 2023 update remains the foundational taxonomy for longevity science globally. We mapped each hallmark against the canine aging literature, cross-referencing human longevity data, veterinary research, and interventional studies across mammalian models, to identify where the evidence for meaningful action is strongest. 


Three hallmarks emerged as both upstream and addressable. These hallmarks are the most mechanistically tractable, and the most directly supported by interventional evidence in the current scientific literature. These are the targets of ESB-01.

In 2013, López-Otín et al. published a landmark framework in Cell identifying biological processes that drive aging across mammalian species.[1] The 2023 update remains the foundational taxonomy for longevity science globally. We mapped each hallmark against the canine aging literature, cross-referencing human longevity data, veterinary research, and interventional studies across mammalian models, to identify where the evidence for meaningful action is strongest. 

 

Three hallmarks emerged as both upstream and addressable. These hallmarks are the most mechanistically tractable, and the most directly supported by interventional evidence in the current scientific literature. These are the targets of ESB-01.

 


 




 

H1 · Targeted
Epigenetic alterations

NAD+ levels drop by up to 50% as we age, causing our gene regulation to drift and the wrong genes to switch on or off — accelerating biological aging.

H2 · Targeted
Mitochondrial Dysfunction

Aging mitochondria generate less ATP and more reactive oxygen species, degrading cellular energy output and driving oxidative damage.

H3 · Targeted
Chronic Inflammation

Senescent cells accumulate with age and release a sustained cocktail of pro-inflammatory signals that degrades surrounding tissue and accelerates systemic aging. 

NOT DIRECTLY TARGETED IN ESB-01

H4
Telomere Attrition

Progressive shortening of chromosomal caps with each cell division, ultimately triggering cellular senescence or apoptosis

H5
Epigenetic Alterations 

Age-related disruption of gene expression patterns, including aberrant DNA methylation — now measurable in dogs via canine epigenetic clocks.

H6
Loss of Proteostasis 

Accumulation of misfolded proteins as autophagy and proteasomal clearance mechanisms decline with age.

[1] López-Otín C, Blasco MA, Partridge L, Serrano M, Kroemer G. Hallmarks of aging: An expanding universe. Cell. 2023 Jan 19;186(2):243-278. doi: 10.1016/j.cell.2022.11.001. Epub 2023 Jan 3. PMID: 36599349.
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Three compounds. One formulation.

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Three compounds. One formulation.

Human longevity research is decades ahead — well-funded, increasingly rigorous, and producing interventional data at scale. Murine models have generated mechanistically rich findings across nearly every hallmark of aging. Yet, canine pharmacokinetics for these same compounds are almost entirely absent from the peer-reviewed literature.
 

That gap shaped how ESB-01 was built. Drawing on the human and murine evidence available, developed through extensive research processes, tested as a combined intervention, and mapped against the canine aging literature, ESB-01 was formulated as a mechanistically coherent intervention acting on three distinct nodes of the aging network.
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Testing and Validation

In collaboration with leading scientists and research partners from around the world, we conduct canine-specific bioavailability studies for outcomes across bioavailability, efficacy and absorption in dogs. Our current programme addresses two questions: how effectively do our compounds reach systemic circulation in dogs, and at what doses do we observe measurable effects on target biomarkers. 

The longevity science is moving fast. New mechanisms are being identified. Old dosing assumptions are being revised. Every significant development in this field is tracked and, where the evidence demands it, reflected in our formulation.
 

Step 01
Human-Grade Literature Review

Our research team conducts structured reviews of the primary human and murine longevity literature, with a focus on mechanistic data applicable to canine biology. Updated quarterly as new studies are published.

Step 02
Canine-Specific Bioavailability Testing

We run in-house studies measuring serum NAD+ levels and compound absorption in dogs across multiple dose points — establishing canine pharmacokinetic profiles rather than relying on extrapolated human data alone.

Step 03
Formulation Iteration

Dose rationale, bioavailability optimisation, and ingredient form selection — including our choice of quercetin dihydrate over standard quercetin for enhanced aqueous solubility — are updated as our internal data accumulates.

Step 04
Advisory Board Review

Every formulation decision is reviewed by our Scientific Advisory Board before implementation. Board members hold expertise in NAD+ metabolism, veterinary oncology, senolytic science, and comparative mammalian physiology.

Step 05
Community Longitudinal Dataset

We are building a structured outcome dataset from our customer community — tracking energy, mobility, coat condition, and veterinary biomarkers over time. The beginning of the real-world canine evidence base this field currently lacks.

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Testing and Validation

In collaboration with leading scientists and research partners from around the world, we conduct canine-specific bioavailability studies for outcomes across bioavailability, efficacy and absorption in dogs. Our current programme addresses two questions: how effectively do our compounds reach systemic circulation in dogs, and at what doses do we observe measurable effects on target biomarkers. 

The longevity science is moving fast. New mechanisms are being identified. Old dosing assumptions are being revised. Every significant development in this field is tracked and, where the evidence demands it, reflected in our formulation.

Step 01
Human-Grade Literature Review

Our research team conducts structured reviews of the primary human and murine longevity literature, with a focus on mechanistic data applicable to canine biology. Updated quarterly as new studies are published.

Step 02
Canine-Specific Bioavailability Testing

We run in-house studies measuring serum NAD+ levels and compound absorption in dogs across multiple dose points — establishing canine pharmacokinetic profiles rather than relying on extrapolated human data alone.

Step 03
Formulation Iteration

Dose rationale, bioavailability optimisation, and ingredient form selection — including our choice of quercetin dihydrate over standard quercetin for enhanced aqueous solubility — are updated as our internal data accumulates.

Step 04
Advisory Board Review

Every formulation decision is reviewed by our Scientific Advisory Board before implementation. Board members hold expertise in NAD+ metabolism, veterinary oncology, senolytic science, and comparative mammalian physiology.

Step 05
Community Longitudinal Dataset

We are building a structured outcome dataset from our customer community — tracking energy, mobility, coat condition, and veterinary biomarkers over time. The beginning of the real-world canine evidence base this field currently lacks.
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Why We Swing for the Fences

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Why We Swing for the Fences

Most dogs don't die of old age. They die of the diseases that age makes possible, after months or years of slow, visible decline that most owners are taught to accept as normal.

The goal of longevity science isn't to stretch that decline. It's to compress it: keep dogs healthier for longer, and shorten the gap between vitality and the end.

 

When we look at this graph, we see two different lives. The red line is what most dog owners experience today: a gradual erosion that starts earlier than people realise, and lasts longer than anyone wants. The blue line is what becomes possible when you stop managing symptoms and start addressing the biology underneath.

 

Over the last decade, research into longevity has shown that the mechanisms behind aging are not fixed but addressable. What was once accepted as inevitable is now understood as a process with real levers: ones that can be pulled earlier and more effectively than most owners realize. 

Finley was built around that science, and the belief that every dog deserves the full benefit of it. 

Grow with us, grow old with your dog.

Two ways to follow the science with us:

FOR THE DEEPLY INVOLVED

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