VetPlus Coatex Liquid for Dogs & Cats | Evening Primrose Oil GLA, Fish Oil EPA & DHA, Vitamin E, A & D3 | Skin Barrier, Coat Condition & Atopic Dermatitis Support | 65ml & 150ml

FOR ANIMAL USE ONLY — Administer as directed by a veterinarian or as per label instructions. VetPlus Coatex Liquid is a veterinary nutraceutical essential fatty acid supplement — not a veterinary medicine and not a substitute for veterinary diagnosis and treatment of dermatological conditions. Skin disease in dogs and cats requires accurate veterinary diagnosis to characterise the underlying aetiology (primary keratinisation disorder, ectoparasite hypersensitivity, food adverse reaction/food hypersensitivity enteropathy-associated skin disease, environmental atopic dermatitis [CAD/FAD], Malassezia secondary overgrowth, bacterial pyoderma, endocrinopathy-associated skin changes [hypothyroidism, hyperadrenocorticism]) before initiating supplementation. Coatex Liquid is indicated as adjunctive nutritional support for skin barrier function and coat quality in dogs and cats with confirmed or suspected essential fatty acid deficiency, atopic dermatitis, dry or scaling skin, or poor coat condition, under veterinary supervision or as a nutritional supplement in otherwise healthy animals. Store in a cool, dry place away from direct sunlight; keep the bottle tightly sealed between uses to protect PUFAs from oxidative degradation. Keep out of reach of children.

VetPlus Coatex Liquid for Dogs & Cats | Evening Primrose Oil GLA, Fish Oil EPA & DHA, Vitamin E, A & D3 | Skin Barrier, Coat Condition & Atopic Dermatitis Support | 65ml & 150ml

VetPlus Coatex Liquid is a veterinary nutraceutical essential fatty acid (EFA) supplement manufactured by VetPlus Ltd (UK), formulated to support skin barrier integrity, coat quality, and inflammatory skin conditions in dogs and cats. Coatex Liquid delivers a clinically relevant combination of essential and conditionally essential polyunsaturated fatty acids with fat-soluble antioxidant and structural vitamins: evening primrose oil (Oenothera biennis — the primary source of gamma-linolenic acid [GLA, 18:3n-6] — a conditionally essential n-6 PUFA that is specifically deficient in atopic and allergic animals due to impaired delta-6-desaturase [D6D/FADS2] enzyme activity), fish oil (providing eicosapentaenoic acid [EPA, 20:5n-3] and docosahexaenoic acid [DHA, 22:6n-3] — the long-chain n-3 PUFAs with direct anti-inflammatory eicosanoid and specialised pro-resolving mediator [SPM] signalling activity), vitamin E (d-alpha-tocopherol — both an antioxidant protecting the PUFAs in the supplement and in vivo lipid-phase antioxidant protecting skin cell membranes from PUFA lipid peroxidation), vitamin A (retinol — essential for keratinocyte differentiation and epidermal barrier gene expression), and vitamin D3 (cholecalciferol — the immunomodulatory secosteroid regulating keratinocyte proliferation and skin immune responses). Available in 65ml and 150ml bottles for easy daily addition to food.

Canine & Feline Skin Barrier Biology and the Role of Essential Fatty Acids

• The skin barrier: stratum corneum lipid lamellar body architecture and the two-compartment lipid system: the stratum corneum (SC — the outermost 10–15 cell layers of terminally differentiated, anucleate, keratin-filled corneocytes surrounded by a lipid-rich extracellular matrix) is the principal physical and chemical permeability barrier of the skin; SC barrier function depends on the extracellular lamellar lipid bilayers — secreted into the SC interstices by lamellar bodies (LB — also termed Odland bodies or membrane-coating granules) in the stratum granulosum granular layer; LBs contain: ceramides (the dominant SC lipid at approximately 50% dry weight; ceramides are sphingolipids — N-acylsphingosines — with the general structure: fatty acid (VLCFA or ULCFA) amide-linked to the amino group of sphingosine [2-amino-4-trans-octadecen-1,3-diol]; the ultra-long-chain fatty acid [ULCFA C28–C36] component of acylceramides [ceramide EOS, EODS — esterified omega-hydroxy] specifically contains linoleic acid [LA, 18:2n-6] ester-linked to the omega-OH of the fatty acid chain — and LA is therefore an essential structural component of the SC barrier ceramide pool); cholesterol (∼25% SC lipid dry weight — the SC sterol providing membrane fluidity); free fatty acids (FFAs — approximately 15% SC lipid dry weight); the molar ratio of ceramides:cholesterol:FFAs is approximately 1:1:1 in healthy canine and feline SC; disruption of this ratio (from EFA deficiency, inflammation, or genetic defects in ceramide synthesis enzymes) → increased transepidermal water loss (TEWL) → dry, scaly, flaky skin; increased percutaneous penetration of environmental allergens (house dust mite proteins Derp1/Derp2, grass pollen allergens, Malassezia allergens) → Langerhans cell sensitisation → atopic sensitisation and IgE antibody production; in canine atopic dermatitis (CAD), lamellar body secretion is deficient (reduced LB number and incompletely formed lamellar membrane structures in keratinocytes from atopic dogs confirmed by electron microscopy — Marsella et al.) → SC ceramide content is reduced in atopic dogs vs non-atopic controls (specifically: ceramide EOS and NS are the most consistently reduced ceramide fractions in CAD; Reiter et al., Vet Dermatol 2009); LA in SC ceramides (the linoleic acid esterified to acylceramide EOS) is a critical determinant of SC permeability barrier function — LA deficiency (or PUFA imbalance shifting away from LA availability for ceramide acylation) directly impairs SC barrier ceramide formation
• Delta-6-desaturase (D6D/FADS2) impairment in atopic dogs and cats — the enzymatic basis of GLA deficiency and the rationale for Coatex EPO supplementation: the endogenous n-6 PUFA metabolic pathway: dietary linoleic acid (LA, 18:2n-6) → D6D (delta-6-desaturase — encoded by FADS2 — the rate-limiting enzyme of PUFA elongation/desaturation; requires pyridoxine B6, magnesium, zinc as cofactors; α6 desaturation inserts a double bond between C6 and C7 of LA) → gamma-linolenic acid (GLA, 18:3n-6) → elongase-5 (ELOVL5) → dihomo-gamma-linolenic acid (DGLA, 20:3n-6) → delta-5-desaturase (D5D/FADS1) → arachidonic acid (AA, 20:4n-6); D6D is the rate-limiting step; in atopic dogs, D6D activity is reduced (the specific mechanism has not been fully characterised in dogs — in human atopic eczema, multiple FADS2 promoter SNPs reduce D6D mRNA expression; analogous polymorphisms likely exist in dog breeds with high CAD prevalence including West Highland White Terriers, Golden Retrievers, Labrador Retrievers, French Bulldogs, Pugs, Boxers, and German Shepherds); the consequence of impaired D6D: LA → GLA conversion is blocked → GLA is deficient despite adequate dietary LA intake → downstream DGLA and eicosanoid products of the DGLA pathway (15-HETrE, PGE1 — the anti-inflammatory prostaglandin) are deficient; evening primrose oil in Coatex bypasses the D6D bottleneck by delivering pre-formed GLA (Oenothera biennis seed oil contains approximately 8–10% GLA) → GLA is directly elongated to DGLA by ELOVL5 without requiring D6D → DGLA → anti-inflammatory eicosanoids (15-HETrE, PGE1) and DGLA incorporation into membrane phospholipids → competing with AA for cyclooxygenase (COX-1/2) and 5-lipoxygenase (5-LOX) → reduced AA-derived pro-inflammatory eicosanoids (PGE2, LTB4, LTC4, TXA2); cats have additional FADS2 constraints: cats express the FADS2 enzyme (unlike historically reported) but at reduced activity for delta-6-desaturation — cats must obtain pre-formed long-chain PUFAs (GLA, AA, EPA, DHA) from the diet; this makes Coatex supplementation particularly important in cats on low-EFA or plant-protein-based diets
• n-3 PUFA anti-inflammatory mechanisms — EPA and DHA from fish oil: fish oil in Coatex provides EPA (eicosapentaenoic acid, 20:5n-3) and DHA (docosahexaenoic acid, 22:6n-3); mechanisms: (a) competitive inhibition of AA eicosanoid synthesis: EPA competes with AA for COX-1/2 (prostaglandin H synthase 1/2) and 5-LOX (arachidonate 5-lipoxygenase) active sites; EPA-derived eicosanoids (PGE3 from COX, LTB5 from 5-LOX) are 10–100-fold less pro-inflammatory than the equivalent AA-derived eicosanoids (PGE2, LTB4); AA-derived LTB4 is the primary neutrophil chemoattractant in allergic skin inflammation (LTB4 binds BLT1 receptor on neutrophils → chemotaxis, reactive oxygen species generation, and granule release at the allergic skin site); EPA-derived LTB5 binds BLT1 with approximately 10× lower affinity → reduced neutrophil recruitment; (b) specialised pro-resolving mediators (SPMs) — the active resolution of inflammation: DHA and EPA are the substrate precursors for a family of endogenous lipid mediators that actively resolve inflammation (not merely suppress it); EPA-derived SPMs: resolvins of the E-series (RvE1, RvE2, RvE3 — produced from EPA via aspirin-acetylated COX-2 or CYP450 → 18-HEPE → further 5-LOX-mediated conversion in leukocytes); DHA-derived SPMs: resolvins of the D-series (RvD1–RvD6 — from 17-HpDHA via 5-LOX), protectins/neuroprotectins (PD1/NPD1 from 17-HpDHA via 15-LOX → 17S,18R-diHDHA), and maresins (MaR1, MaR2 from 14-HpDHA via 12-LOX); resolvin and protectin mechanisms in allergic skin: (i) neutrophil recruitment shutdown — resolvins inhibit integrin activation and reduce CXCL8 (IL-8) production → reducing neutrophil transmigration into the skin; (ii) M2 macrophage polarisation — resolvins promote the switch from M1 pro-inflammatory (TNF-α, IL-12, IL-23) to M2 anti-inflammatory (IL-10, TGF-β, arginase-1) macrophage phenotype in the resolving skin lesion; (iii) eosinophil apoptosis induction — resolvins activate caspase-3-mediated eosinophil apoptosis → reducing eosinophil-mediated MBP (major basic protein) release in allergic skin; (iv) mast cell histamine and prostaglandin release inhibition — resolvins and protectins inhibit mast cell FceRI cross-linking-induced degranulation → reduced immediate-phase allergic skin response; (c) membrane phospholipid remodelling: EPA and DHA incorporate into skin keratinocyte and immune cell phospholipids (at the sn-2 position of phosphatidylcholine and phosphatidylethanolamine — the primary AA substrate reservoir) → displacing AA from membrane phospholipids → reducing the AA pool available for eicosanoid synthesis during inflammatory activation; this membrane remodelling effect requires weeks of supplementation to fully manifest — consistent with the 6–8 week minimum supplementation period recommended for EFA skin supplements in dogs

Active Ingredients & Mechanisms

• Evening Primrose Oil (Oenothera biennis seed oil — approximately 8–10% GLA) — the D6D-bypass GLA source: provides pre-formed GLA (18:3n-6) → ELOVL5 elongation → DGLA (20:3n-6) → anti-inflammatory eicosanoids (15-HETrE, PGE1) and competitive COX/5-LOX substrate displacement of AA → reduced PGE2, LTB4, TXA2; addresses the specific D6D impairment in atopic dogs and cats; LA from EPO also contributes to the SC ceramide acylceramide LA pool (SC ceramide EOS − linoleic acid esterified at the omega-OH of the ULCFA component) → restores SC lamellar lipid bilayer integrity
• Fish Oil (EPA 20:5n-3 & DHA 22:6n-3) — eicosanoid competition and SPM precursors: EPA competes with AA at COX-1/2 and 5-LOX active sites → PGE3 and LTB5 (10–100× less pro-inflammatory than PGE2 and LTB4); DHA → D-series resolvins (RvD1–RvD6), protectins (PD1/NPD1), and maresins (MaR1/MaR2) → active pro-resolution of allergic skin inflammation; EPA → E-series resolvins (RvE1–RvE3) → neutrophil shutdown, M2 macrophage polarisation, eosinophil apoptosis, mast cell degranulation inhibition; membrane phospholipid sn-2 position remodelling → displacement of AA from the membrane-bound eicosanoid substrate pool
• Vitamin E (d-alpha-tocopherol) — dual-function PUFA antioxidant and membrane protector: (a) in-product antioxidant: protects the highly oxidation-susceptible PUFAs (GLA, EPA, DHA — each additional double bond approximately doubles the rate of lipid autoxidation) in the liquid formulation from oxidative rancidity during storage; (b) in vivo lipid-phase antioxidant: d-alpha-tocopherol (RRR stereoisomer; preferentially secreted by hepatic TTP into VLDL for delivery to skin) intercalates into keratinocyte and immune cell plasma membranes → phenolic OH donates H• to LOO• (lipid peroxyl radicals) → terminates PUFA lipid radical chain propagation in skin membranes; the tocopheroxyl radical is recycled by ascorbate (vitamin C) and GSH → restoring vitamin E antioxidant capacity; vitamin E is concentrated in the skin sebaceous glands and secreted onto the SC surface via sebum → providing epidermal surface antioxidant protection against UV-generated ROS
• Vitamin A (retinol) — keratinocyte differentiation regulator and epidermal barrier gene regulator: retinol is esterified in the liver (LRAT — lecithin:retinol acyltransferase) → stored as retinyl esters; mobilised as retinol → oxidised in target tissues (skin keratinocytes) by RDH (retinol dehydrogenase) → retinaldehyde → RALDH (retinaldehyde dehydrogenase) → all-trans-retinoic acid (atRA); atRA binds nuclear RAR (α, β, γ isoforms — the retinoic acid receptors) and RXR (retinoid X receptors) → RAR/RXR heterodimer binds RARE (retinoic acid response elements) in the promoters of: (a) filaggrin (FLG) → filaggrin is the precursor protein of the natural moisturising factor (NMF — the SC hygroscopic amino acid and metabolite pool maintaining SC hydration; FLG is proteolytically processed in the SC by caspase-14 and kallikreins to release free amino acids − mainly histidine → urocanic acid [UCA], and arginine → citrulline, and NMF hygroscopic components pyrrolidone carboxylic acid [PCA], lactate, urea); filaggrin deficiency (the FLG R501X/2282del loss-of-function mutations in human AD — analogous mutations in West Highland White Terriers and other breeds with CAD) is the most important genetic determinant of SC barrier defect in atopic dermatitis — vitamin A supports FLG gene expression via RARE-mediated transcriptional activation; (b) loricrin and involucrin (the structural proteins of the cornified envelope — CE — the 15nm protein scaffold beneath the SC lipid layer that forms after caspase-14-mediated cross-linking by transglutaminase 1 [TGM1] and 3 [TGM3]); (c) keratin K1/K10 (the intermediate filament proteins of the differentiating corneocyte that provide mechanical SC rigidity); vitamin A deficiency → squamous metaplasia, hyperkeratosis, follicular plugging, sebaceous gland atrophy — clinically manifesting as dry, scaly, flaky coat in dogs and cats
• Vitamin D3 (cholecalciferol) — skin immune regulation and keratinocyte antimicrobial peptide induction: cholecalciferol (D3) is the precursor to the active secosteroid hormone 1,25-dihydroxyvitamin D3 (calcitriol; 1,25(OH)2D3); in the skin: keratinocytes express both 25-hydroxylase (CYP2R1) and 1α-hydroxylase (CYP27B1) → capable of locally activating vitamin D3 to calcitriol within the epidermis; calcitriol binds the nuclear vitamin D receptor (VDR) → VDR/RXRα heterodimer → VDRE (vitamin D response element) binding in gene promoters: (a) cathelicidin (CAMP — the only human/canine cathelicidin; dog: cath-2, also termed CRAMP — the murine ortholog; cathelicidins are cationic, amphipathic antimicrobial peptides [AMPs] that disrupt bacterial membrane integrity via membrane poration; cathelicidin in the skin provides innate antimicrobial defence against Staphylococcus pseudintermedius [the primary canine pyoderma pathogen], S. aureus, and Malassezia pachydermatis [the yeast opportunist in atopic dogs] at the epidermal surface) — VDR/VDRE transcriptional activation of cathelicidin explains why vitamin D3-deficient atopic dogs and cats are at increased risk of bacterial pyoderma and Malassezia overgrowth; (b) beta-defensin-2 (BD-2/HBD-2) induction → additional AMP activity against gram-negative skin bacteria; (c) filaggrin expression (VDR/VDRE element in the FLG promoter — synergistic with RAR from vitamin A → dual nuclear receptor regulation of SC barrier gene expression); (d) Treg induction: calcitriol in the skin dendritic cell context promotes FoxP3+ Treg differentiation → suppression of Th2-skewed allergic skin inflammation (IL-4, IL-13, IL-31 — the itch cytokine in CAD − are Th2 cytokines suppressed by local calcitriol-induced Treg activity); vitamin D deficiency is documented in atopic dogs (Titmarsh et al., Vet Dermatol 2015 — significantly lower serum 25(OH)D in dogs with CAD vs controls)

Indications

• Canine and feline atopic dermatitis (CAD/FAD) — adjunctive EFA and fat-soluble vitamin support alongside veterinary dermatology management
• Dry, flaky, or scaling skin — dry coat syndrome, seborrhoea sicca, ichthyosis
• Poor coat condition — dull, brittle, or excessively shedding coat
• Seasonal coat changes with reduced sebum and skin moisture
• Post-illness or post-nutritional-deficiency coat recovery
• Essential fatty acid and fat-soluble vitamin supplementation in dogs and cats on low-fat or plant-based diets with inadequate PUFA content
• Prophylactic skin barrier support in breeds with genetic predisposition to atopic dermatitis: West Highland White Terrier, Labrador Retriever, Golden Retriever, French Bulldog, Pug, Boxer, German Shepherd, Cavalier King Charles Spaniel

Directions for Use

• Administer as directed by a veterinarian or per VetPlus label instructions; add the appropriate dose to food daily
• Shake well before use to resuspend the oil components
• Available in 65ml (suitable for smaller dogs, cats, or trial use) and 150ml (suitable for larger dogs or extended use)
• Allow a minimum of 6–8 weeks of daily supplementation for full skin barrier and coat condition benefits to manifest (reflecting the time required for membrane phospholipid remodelling and SC ceramide pool replenishment)
• Store in a cool, dry place away from direct sunlight with the cap tightly sealed after each use to prevent PUFA oxidative rancidity

Safety Information

• For animal use only — keep out of reach of children
• Not a substitute for veterinary diagnosis and treatment of dermatological conditions
• Do not exceed the recommended dose; fat-soluble vitamins A and D3 are stored and may accumulate with excessive dosing — follow label directions
• Store with cap tightly sealed to protect PUFAs from oxidative degradation; discard if the product smells rancid