Clinical Trials on Record
All controlled studies to date — chronological order
| Trial | Design | N | Dose / Duration | Key Finding |
|---|---|---|---|---|
| Stallings et al. — Pharmacokinetics | Controlled, human | — | Single oral dose C15:0 | Every 100 mg C15:0 raises circulating levels by ~1 µg/mL; confirmed predictable dose-response bioavailability |
| Venn-Watson et al. — Navy dolphin longevity study | Longitudinal, controlled | ~50 dolphins | Dietary C15:0 supplementation | Higher C15:0 correlated with slower aging rate biomarkers, higher hemoglobin, improved metabolic indices in long-lived mammals |
| TANGO RCT — Am J Clin Nutr, 2024 Mar;119(3):788–799 | Randomized, controlled, 3-arm | ~90 females with NAFLD | C15:0 + Med diet vs. Med diet alone vs. control · 12 weeks | C15:0 arm: −33% liver fat, lower LDL-C, favorable gut microbiome shift (Bifidobacterium adolescentis ↑) — above and beyond diet alone |
| Vascular health pilot — Human, controlled | Controlled | Small cohort | Daily C15:0 · 12 weeks | Improvements in vascular health markers and mood indices observed |
| Robinson / Schwimmer RCT — J Nutrition, 2024 (NCT04947176) | Double-blind, randomized, placebo-controlled | 30 (20 treatment, 10 placebo) | 200 mg/day fatty15 vs. rice flour · 12 weeks | Threshold group (C15:0 >5 µg/mL): ALT −29 U/L, AST −6 U/L, hemoglobin +0.6 g/dL. No adverse events. 2/3 of participants at baseline met criteria for C15:0 deficiency. |
| LDL RCT — Adult women with high BMI | Randomized, controlled | — | Pure C15:0 · 12 weeks | Significant LDL-cholesterol reduction in women with elevated BMI who reached sufficient C15:0 levels |
Mechanism — Why C15:0 Is Structurally Different
Odd-chain saturated fatty acids behave fundamentally differently from even-chain and unsaturated fats
C15:0 integrates into cell membranes as a structurally stable, odd-chain saturated fatty acid. Unlike even-chain saturated fats (which pack too rigidly) or unsaturated fats (which are peroxidation-prone), C15:0 occupies a mechanical sweet spot — reducing membrane fragility and ferroptosis risk. Studies demonstrate 80% improvement in cellular stability with C15:0 supplementation.
C15:0 activates AMPK — the cellular energy sensor and metabolic master switch — and inhibits mTOR, the primary driver of cellular aging and senescence. These are the same two pathways targeted by metformin (AMPK) and rapamycin (mTOR) respectively. C15:0 achieves both simultaneously at physiologically relevant concentrations.
C15:0 directly rescues mitochondrial function at Complex II of the electron transport chain by increasing succinate production. Mitochondrial dysfunction is a primary hallmark of aging — and Complex II is rarely targeted by other longevity compounds. This is a mechanistically distinct contribution to the longevity stack.
As a dual partial PPAR alpha/delta agonist, C15:0 activates metabolic regulators that govern fat burning, inflammation, liver function, and cardiovascular homeostasis. This mechanism underpins its demonstrated activity in NAFLD (TANGO trial) and cardiometabolic endpoints seen across cohort and clinical studies.
Ferroptosis is iron-dependent lipid peroxidation cell death — a key driver of accelerated cellular aging. C15:0, as a stable saturated fatty acid incorporated into membranes, reduces the substrate available for lipid peroxidation. The 2024 Cellular Stability Hypothesis paper formally proposes C15:0 deficiency as "Cellular Fragility Syndrome" — the first new nutritional deficiency syndrome in 75 years.
C15:0 produces a novel endocannabinoid metabolite, pentadecanoylcarnitine (C15:0-carnitine), with pleiotropic activity relevant to mood, inflammation, sleep, and physical health. This metabolite acts on CB1/CB2 receptors and has anti-inflammatory properties measured across multiple cell systems. Identified in a 2022 paper in Scientific Reports.
C15:0 vs. Rapamycin, Metformin & Acarbose
BioMAP Diversity PLUS system — 148 biomarkers across 12 primary human cell systems (Nutrients, PMC10649853, Oct 2023)
Using the gold-standard pharmaceutical phenotyping platform (BioMAP, used by pharma companies to screen drug candidates), researchers measured dose-dependent activities of C15:0 against three leading longevity-enhancing compounds. Results are the number of clinically relevant biomarker hits at each compound's optimal dose.
Note: These are cell-based (in vitro) assays, not human clinical outcome data. They indicate mechanistic breadth and potency, not proven clinical equivalence. Rapamycin and metformin both have decades of clinical trial data that C15:0 does not yet match. Interpret accordingly.
100+ Publications — Research Categories
Breadth of peer-reviewed evidence across health domains
Dosing Protocol
Based on clinical trial data and pharmacokinetic studies
Evidence-Based Dosing — C15:0 (Fatty15)
Safety Profile
Excellent safety record across all clinical trials — no significant adverse events reported in any study to date. No drug interactions identified. Side effects were statistically equivalent between fatty15 and placebo groups in the Schwimmer RCT. C15:0 is a naturally occurring dietary fatty acid present in whole-fat dairy — the supplement delivers a concentrated pure form. Long-term safety data beyond 12 weeks is limited; trials of 6+ months are needed.
Product — Only One Option
Fatty15 is the only commercially available pure C15:0 supplement; no generic competitors with equivalent purity currently exist
The only form of C15:0 tested in human RCTs. No generic equivalent with equivalent purity and clinical validation currently exists. Developed in collaboration with US Navy research. Subscription available — price per capsule drops significantly with 90-day subscription. Available via Amazon or direct.
Shop Fatty15 Direct ↗ Fatty15 on Amazon ↗As C15:0 awareness has grown, generic versions have appeared on Amazon and iHerb. EBL does not endorse these: purity is unverified, concentration is often lower, and none have been tested in clinical trials. If cost is a barrier, a 90-day Fatty15 subscription reduces per-dose cost significantly.