Keyora Antarctic Krill Oil EP-6: The DPA Repair-to-Resolution Biology Map: Endothelial Recovery, Platelet Membranes, Pro-Resolving Mediators, Macrophage Clearance, and Evidence-Matched Tissue Recovery

Background Long-chain omega-3 fatty-acid science has historically been dominated by eicosapentaenoic acid (EPA, 20:5n-3) and docosahexaenoic acid (DHA, 22:6n-3). Their extensive analytical, nutritional, mechanistic, and clinical evidence bases established EPA and DHA as the principal reference objects through which marine omega-3 exposure was measured, compared, and communicated. This scientific success also produced an interpretive narrowing. Docosapentaenoic acid (DPA, 22:5n-3) remained present within marine lipid sources and long-chain n-3 metabolism while receiving substantially less molecule-specific attention. Lower natural abundance in many marine lipid sources, co-occurrence with EPA and DHA, historical limitations in purified-DPA availability, and repeated EPA-DHA-centered analytical and clinical reporting contributed to a situation in which DPA could be biologically present but scientifically under-recognized. DPA consequently became the “missing third Omega-3” primarily through under-measurement, under-disclosure, and limited independent experimental attribution rather than through biological absence. Keyora Antarctic Krill Oil EP-6 develops Keyora [The DPA Transparency and Repair Biology Standard] to integrate two questions that must remain connected but distinct. The first is a transparency question: Is DPA independently identified, measured, quantified, and disclosed as 22:5n-3? The second is an evidence question: What biological or clinical conclusions can legitimately be attached to that measured DPA exposure? EP-6 integrates DPA molecular identity, human metabolic observability, vascular endothelial biology, DPA-derived lipid mediators, active inflammatory resolution, platelet membrane responses, preclinical tissue-protective biology, exact-product DPA exposure, and evidence-transfer boundaries into one molecule-to-product interpretation standard. The framework is deliberately evidence-bounded. Repair-oriented molecular and cellular biology does not automatically establish therapeutic tissue regeneration, functional revascularization, thrombosis prevention, or finished-product clinical efficacy. Objective The objectives of EP-6 are to: explain why DPA became comparatively invisible within an EPA-DHA-centered Omega-3 research and reporting system; establish n-3 DPA as a chemically distinct 22:5n-3 long-chain Omega-3 fatty acid rather than an unnamed remainder or biologically disposable intermediate; distinguish DPA metabolic position from DPA molecular identity; examine human evidence demonstrating that purified DPA can be administered and independently observed across circulating and cellular lipid compartments; define vascular repair as a multi-stage biological process before interpreting DPA-specific endothelial findings; evaluate direct evidence linking DPA with context-dependent endothelial migration, VEGF-responsive behavior, tube formation, and VEGFR-2/KDR expression; separate endothelial migration, angiogenesis, functional vessel formation, revascularization, and human clinical regeneration as different biological and evidentiary levels; examine DPA as both a membrane substrate and a precursor for structurally distinct specialized pro-resolving lipid mediators; integrate DPA-derived resolvin, protectin, maresin-related, and 13-series mediator pathways with phagocyte clearance and inflammatory-resolution biology; evaluate DPA incorporation into platelet phospholipids and experimental platelet-response pathways without converting platelet modulation into claims of human thrombosis prevention; distinguish parent-DPA biology from the biological effects of isolated DPA-derived lipid mediators; distinguish human metabolic evidence, cellular mechanistic evidence, mediator-specific evidence, preclinical tissue evidence, and finished-product clinical evidence; reconstruct the current Keyora Antarctic Krill Oil exposure of 23 mg DPA per softgel as an exact-product dose object; establish why this 23 mg exposure cannot automatically be treated as equivalent to gram-scale purified-DPA research doses, isolated mediator exposures, cell-culture concentrations, or clinical therapeutic thresholds; convert the complete evidence architecture into a four-stage public interpretation standard: Measurement → Disclosure → Interpretation → Evidence Matching. DPA as the Missing Third Omega-3 The historical prominence of EPA and DHA reflects accumulated evidence rather than a complete chemical definition of long-chain Omega-3 biology. EPA and DHA became dominant research objects because they accumulated: larger experimental literatures; established analytical methods; repeated clinical investigation; familiar nutritional dose conventions; extensive biomarker use; strong public and professional recognition. DPA generally occurred at lower abundance and frequently coexisted with EPA and DHA in mixed marine-lipid matrices. This created an experimental attribution problem. A mixed marine-oil study could establish exposure to DPA without establishing that a measured endpoint was caused by DPA independently of EPA, DHA, or the broader lipid matrix. Historical limitations in purified DPA availability further constrained molecule-specific dosing and controlled comparisons. Accordingly, the smaller DPA evidence base should not automatically be interpreted as evidence of biological irrelevance. EP-6 distinguishes: research visibility from: molecular existence and: evidence density from: molecular identity. The “missing third Omega-3” was therefore not missing from long-chain fatty-acid biology. It was comparatively missing from the dominant scientific language through which that biology was measured and interpreted. Measurement Creates Scientific Visibility A molecule can be present without being independently measurable to a consumer or investigator. Total Omega-3 does not identify how much of that total consists of DPA. Likewise, the difference between total Omega-3 and separately disclosed EPA plus DHA cannot automatically be reconstructed as exact DPA because other n-3 fatty acids may contribute to total Omega-3 depending on the composition being analyzed. EP-6 therefore establishes a fundamental sequence: possible presence→ molecular identification→ independent 22:5n-3 quantification→ quantified DPA exposure→ public disclosure→ evidence matching. Presence is the weakest of these states. Measurement converts potential composition into traceable molecular knowledge. Disclosure converts analytical knowledge into publicly interpretable product information. Neither measurement nor disclosure independently establishes efficacy. DPA Molecular Identity: 22:5n-3 DPA is chemically defined as docosapentaenoic acid, 22:5n-3. Its molecular identity can be contrasted directly with adjacent long-chain n-3 fatty acids: EPA = 20:5n-3 DPA = 22:5n-3 DHA = 22:6n-3 DPA shares five double bonds with EPA but contains a 22-carbon rather than a 20-carbon chain. DPA shares a 22-carbon chain with DHA but contains five rather than six double bonds. It is therefore structurally adjacent to both molecules while being identical to neither. The n-3 designation is equally important because it identifies the relevant Omega-3 docosapentaenoic-acid species rather than treating all 22:5 fatty-acid structures as interchangeable. The first molecular principle of EP-6 is therefore: structural similarity does not establish molecular interchangeability. The Metabolic Intermediate Trap DPA occupies an important position in EPA-DPA-DHA metabolism. EPA can undergo elongation to form DPA. DPA occupies a pathway position relevant to subsequent DHA biosynthesis, although movement toward DHA involves additional elongation, desaturation, and peroxisomal processing rather than a single unrestricted DPA-to-DHA step. DPA can also participate in metabolic movement toward EPA under defined contexts. This network created an historical interpretive shortcut. Because DPA sits between two highly recognized molecules, it could be described primarily as an “intermediate.” The term is chemically useful when describing pathway position. It becomes scientifically incomplete when it implies that DPA is merely temporary, passive, or biologically secondary. EP-6 therefore distinguishes: metabolic position from: molecular identity and: conversion possibility from: actual metabolic flux. A fatty acid can participate in a conversion pathway while remaining independently measurable in circulating and cellular lipid pools. Human DPA Metabolic Observability The availability of purified DPA enabled an important methodological transition. Rather than inferring DPA behavior from mixed marine-oil exposure or from EPA-associated changes, human studies could administer DPA directly and observe its metabolic fate. Purified-DPA studies demonstrated that DPA can be: administered as a defined exposure; detected independently; incorporated into lipid compartments; followed across postprandial metabolism; compared directly with EPA and DHA. Human crossover work comparing purified long-chain Omega-3 fatty acids identified both shared and differentiated metabolic responses across DPA, EPA, and DHA. These findings establish independent observability. They do not establish clinical superiority. Short-duration metabolic experiments primarily answer questions concerning: fatty-acid exposure; incorporation; lipid-compartment distribution; interconversion; metabolomic or lipidomic responses. They do not automatically establish disease treatment or long-term clinical outcome. DPA and Vascular Repair Biology Chapter 3 moves from metabolic identity into repair-relevant endothelial biology. Vascular repair must first be defined as a multi-stage process. Following endothelial injury, restoration can involve: loss of endothelial continuity→ resident endothelial migration→ proliferation→ ju