VetPlus Coatex EFA Blister Capsules for Dogs & Cats

FOR ANIMAL USE ONLY — Administer as directed by a veterinarian or as per label instructions. Coatex is a veterinary nutraceutical supplement — not a veterinary medicine; it does not require a prescription but veterinary guidance is strongly recommended, particularly for dogs and cats with active atopic dermatitis, seborrhoeic skin disease, or other diagnosed dermatological conditions requiring concurrent medical management. Do not use as a substitute for veterinary-prescribed immunomodulatory therapy (ciclosporin, oclacitinib/Apoquel, lokivetmab/Cytopoint) in moderate-to-severe canine atopic dermatitis — EFA supplementation is an adjunct, not a monotherapy for established CAD. Allow 6–8 weeks of continuous supplementation for skin and coat improvement to become apparent. Use with caution in dogs or cats with known fish allergy. Keep out of reach of children. Store in a cool, dry place away from direct sunlight; refrigeration may extend shelf life of the fish oil component.

VetPlus Coatex EFA Blister Capsules for Dogs & Cats | Evening Primrose Oil, Fish Oil, Vitamin E, Biotin & Zinc | Skin Barrier, Coat Gloss & Atopic Dermatitis Support | 60 & 240 Capsules

VetPlus Coatex EFA Blister Capsules are a veterinary nutraceutical skin and coat supplement manufactured by VetPlus Ltd (UK) for dogs and cats. The formula delivers a synergistic combination of essential fatty acids (EFAs) from two complementary sources — Evening Primrose Oil (rich in GLA — gamma-linolenic acid, an n-6 EFA) and Fish Oil (rich in EPA and DHA — n-3 EFAs) — alongside co-factor micronutrients (Vitamin E as d-α-tocopherol, Biotin, and Zinc) that are required for normal EFA metabolism, keratinocyte differentiation, and stratum corneum barrier formation. Coatex EFA addresses the well-documented EFA deficiency and altered desaturase enzyme activity in canine atopic dermatitis (CAD) and feline skin disease, restoring the skin’s epidermal lipid barrier, reducing transepidermal water loss (TEWL), and modulating the cutaneous inflammatory response through the arachidonic acid/eicosanoid pathway. The blister capsule format protects the EFA content from oxidation between uses (critical for maintaining the biological activity of polyunsaturated fatty acids). Available in 60-capsule (approximately 1–2 month) and 240-capsule (approximately 4–8 month) packs.

Canine & Feline Skin Barrier Pathophysiology Relevant to EFA Supplementation

• Normal stratum corneum lipid barrier: the stratum corneum (SC) — the outermost layer of the epidermis (10–15 stacked layers of anucleate, terminally differentiated corneocytes embedded in a lipid-rich extracellular matrix) — is the primary physical and chemical barrier of the skin; the SC extracellular lipid lamellae are composed of a precisely structured mixture of ceramides (~50% by weight), free fatty acids (~10–20%), and cholesterol (~25%), organised in lamellar bodies (Odland bodies) secreted by stratum granulosum keratinocytes at the stratum granulosum–stratum corneum interface; the lamellar body membrane is rich in glucosylceramides and phosphatidylcholine, which are processed by secreted β-glucocerebrosidase and secreted phospholipase A2 in the SC extracellular space into the ceramide and free fatty acid components of the lamellar membranes; ceramides (particularly ceramide 1/CER[EOS] — acylceramide — which contains a very long chain ω-linked linoleic acid — LA — at the terminus of the sphingosine base) are essential structural components of the SC lipid lamellae that determine their lamellar packing order — gel-phase orthorhombic packing provides optimal barrier function and low water permeability; in EFA deficiency, linoleic acid (LA — 18:2n-6) is replaced by oleic acid (OA — 18:1n-9) in ceramide 1 → disruption of the orthorhombic lamellar packing → liquid-crystalline phase → markedly increased TEWL (transepidermal water loss — the diffusion of water vapour through the SC) → skin dehydration and ‘dry coat’
• Atopic dermatitis EFA defect: canine atopic dermatitis (CAD) is a genetically predisposed inflammatory and pruritic allergic skin disease characterised by: (a) a primary epidermal barrier defect (reduced filaggrin expression — filaggrin is a structural protein that cross-links keratin intermediate filaments in corneocytes and serves as a precursor for natural moisturising factor — NMF components including urocanic acid and pyrrolidone carboxylic acid; filaggrin gene mutations FLG-R501X and FLG-2282del4 are the strongest genetic risk factors for human atopic eczema; similar filaggrin mutations are described in West Highland White Terriers and other atopic breeds); (b) altered SC ceramide composition — atopic dogs and cats have reduced total ceramide content and an altered ceramide subclass profile with relatively lower ceramide 1 (CER[EOS]) content compared to healthy animals → impaired lamellar packing → elevated TEWL; (c) Th2-skewed immune deviation: allergen penetration through the leaky SC barrier activates Langerhans cells and dermal dendritic cells → allergen peptide presentation to naïve CD4+ T cells in draining lymph nodes → TSLP (thymic stromal lymphopoietin — released from barrier-disrupted keratinocytes), IL-33, and IL-25 from epithelial cells drive Th2 polarisation of naive T cells → Th2 CD4+ cells produce IL-4, IL-13 (which upregulate IgE class switching in B cells → atopic IgE production against environmental allergens — house dust mite, pollens, mould spores), IL-5 (eosinophil growth and activation), and IL-31 (the key pruritogenic cytokine in CAD — IL-31 acts on IL-31RA/OSMR heterodimer on sensory C-fibre nociceptors in the skin → TRPA1 and TRPV1 channel activation → itch; lokivetmab/Cytopoint targets IL-31 with a monoclonal antibody; oclacitinib/Apoquel targets JAK1-dependent IL-31 receptor signalling)

Active Ingredients & Mechanisms of Action

• Evening Primrose Oil (EPO) — rich source of Gamma-Linolenic Acid (GLA, 18:3n-6) and Linoleic Acid (LA, 18:2n-6): Evening Primrose (Oenothera biennis) seed oil contains approximately 70–74% LA and 8–10% GLA; LA is the parent n-6 EFA and the critical substrate for ceramide 1 (CER[EOS]) synthesis — LA is incorporated into acylceramides via the FATP4 (fatty acid transport protein 4) transporter in keratinocytes and esterified to the ω-hydroxyl of ceramide long chains by the fatty acid elongase ELOVL4 and acyltransferases to form the acylceramide structure essential for SC lamellar packing; GLA bypasses the Δ-6-desaturase enzymatic bottleneck: in healthy skin, LA → GLA requires Δ-6-desaturase (FADS2 — fatty acid desaturase 2; the rate-limiting enzyme of the n-6 pathway; Δ-6-desaturase activity is impaired in atopic skin due to genetic variation in FADS gene cluster, high saturated fat intake, insulin resistance, and aging); GLA is directly further metabolised to DGLA (dihomo-γ-linolenic acid — 20:3n-6 — the anti-inflammatory eicosanoid precursor) by ELOVL5 elongase without requiring Δ-6-desaturase; DGLA → PGE1 (prostaglandin E1) via COX-1/COX-2 and PGE1 synthase: PGE1 is a potent anti-inflammatory prostanoid that: (a) activates EP2 and EP4 receptors on T cells → cAMP elevation → PKA → reduced IL-2 production and T cell proliferation → immunomodulation; (b) inhibits mast cell degranulation (reducing histamine release); (c) suppresses LTB4 production by competing with AA for 5-LOX; DGLA also directly competes with arachidonic acid (AA — 20:4n-6) for 5-LOX (5-lipoxygenase) → DGLA-5-LOX interaction produces 15-HETrE (15-hydroxyeicosatrienoic acid) rather than LTB4 — LTB4 (leukotriene B4) is the most potent endogenous neutrophil and eosinophil chemotactic agent and a key amplifier of cutaneous inflammation in CAD; by reducing LTB4 production, DGLA reduces neutrophil and eosinophil skin infiltration; additionally, DGLA cannot be converted to AA (the conversion of DGLA → AA requires Δ-5-desaturase — FADS1; Δ-5-desaturase activity is also reduced in atopic skin) → GLA supplementation does not increase the AA pool
• Fish Oil (Marine Omega-3) — EPA (20:5n-3) and DHA (22:6n-3) anti-inflammatory EFAs: fish oil EPA and DHA competitively inhibit AA-derived eicosanoid production: EPA competes with AA for COX-2 and 5-LOX active sites → EPA-derived 3-series prostanoids (PGE3 — less potent than PGE2; TXA3 — weaker vasoconstrictor/platelet aggregator than TXA2) and 5-series leukotrienes (LTB5 — 100× less potent neutrophil chemotactic activity than LTB4) replace the pro-inflammatory 2-series/4-series products; in the skin, this translates to: reduced mast cell LTC4/LTD4 production (reducing vascular permeability and wheal formation), reduced keratinocyte and Langerhans cell inflammatory cytokine secretion, and reduced Th2 immune activation; DHA-derived protectin D1 (neuroprotectin D1/NPD1 — 10(S),17(S)-diHDHA) specifically inhibits Th2 cytokine production (IL-4, IL-13) and reduces allergen-driven IgE class switching; DHA is also incorporated into keratinocyte membrane phospholipids → modifies membrane fluidity and lipid raft composition → alters keratinocyte signalling (EGFR, STAT3, NF-κB pathway modulation); the EPO + Fish Oil EFA combination in Coatex provides both the n-6 pathway (LA/GLA → DGLA → PGE1; ceramide 1 structural repair) and the n-3 pathway (EPA/DHA → 3-series prostanoids, SPMs) simultaneously — dual EFA pathway supplementation is more effective than either source alone
• Vitamin E (d-α-tocopherol) — lipid-soluble antioxidant protecting EFAs from peroxidation: polyunsaturated fatty acids (PUFAs — GLA, EPA, DHA) are highly susceptible to lipid peroxidation (non-enzymatic and enzymatic oxidation of the bis-allylic methylene groups of PUFA carbon chains): the bis-allylic C-H bonds of PUFAs have low bond dissociation energy → hydrogen abstraction by lipid peroxyl radicals (ROO•) initiates chain reactions (lipid peroxidation propagation − Bolland–Gee chain mechanism) producing toxic lipid hydroperoxides (LOOH) and end-products including 4-hydroxynonenal (4-HNE) and malondialdehyde (MDA); d-α-tocopherol is the most biologically active form of Vitamin E and the principal lipid-soluble antioxidant in biological membranes: the tocopherol phenol ring donates an H atom to a lipid peroxyl radical (ROO•) → generating a lipid hydroperoxide (LOOH) and the relatively stable tocopheroxyl radical (Toc•); Toc• is regenerated to tocopherol by ascorbic acid (Vitamin C) in the aqueous phase (the tocopherol-ascorbate electron transfer cycle); Vitamin E in Coatex serves two functions: (a) protects the co-administered GLA and EPA/DHA in the capsule from oxidation (maintaining EFA biological activity during storage); (b) reduces oxidative stress in keratinocyte and SC membranes, preventing PUFA peroxidation-driven membrane damage in atopic skin (atopic skin has elevated reactive oxygen species from inflammatory cell infiltration — neutrophil and eosinophil NADPH oxidase/NOX2 •O2− production → dismutation to H2O2 → Fenton reaction → •OH → PUFA peroxidation)
• Biotin (Vitamin B7/H) — coenzyme for fatty acid synthesis and keratinocyte differentiation: Biotin is an essential water-soluble B-vitamin that serves as a covalently attached prosthetic group (via an amide bond to a specific lysine residue) of carboxylase enzymes; the biotin-dependent carboxylases critical for skin health: (a) Acetyl-CoA carboxylase (ACC1 and ACC2 — the rate-limiting enzymes of de novo fatty acid synthesis): ACC catalyses the ATP-dependent carboxylation of acetyl-CoA to malonyl-CoA (the 2-carbon donor for FAS — fatty acid synthase elongation cycles) → malonyl-CoA is the direct substrate for FA chain elongation; biotin deficiency → impaired ACC activity → reduced de novo fatty acid synthesis in keratinocytes → reduced ceramide and free fatty acid availability for SC barrier formation; (b) Propionyl-CoA carboxylase (PCC): carboxylates propionyl-CoA to methylmalonyl-CoA (substrate for mitochondrial succinyl-CoA — TCA cycle entry); biotin deficiency → PCC dysfunction → propionyl-CoA accumulation → propionate incorporation into odd-chain fatty acids → abnormal membrane lipid composition; classic signs of biotin deficiency in dogs and cats: alopecia, seborrhoea, hyperkeratosis, and poor coat condition — biotin supplementation in animals with subclinical deficiency (which can occur secondary to raw egg white consumption — avidin protein in egg white binds biotin with extremely high affinity — Kd ∼10−15 M — preventing intestinal absorption) or intestinal dysbiosis (gut bacteria normally synthesise biotin) rapidly restores coat quality
• Zinc (as Zinc sulphate or Zinc amino acid chelate) — essential trace mineral for keratinocyte differentiation, EFA desaturase co-factor, and skin barrier enzyme function: Zinc is the second most abundant trace mineral in the body after iron; in the skin, Zinc is essential for: (a) keratinocyte proliferation and differentiation — Zinc activates multiple transcription factors (Sp1 — which regulates keratinocyte differentiation gene promoters including filaggrin, loricrin, and involucrin) via Zinc-finger domain protein folding; (b) Δ-6-desaturase (FADS2) co-factor — FADS2, the rate-limiting enzyme converting LA → GLA, is a membrane-bound fatty acid desaturase that requires Zinc as a structural and catalytic co-factor (along with Cytochrome b5 as the electron donor); Zinc deficiency directly impairs Δ-6-desaturase activity → reduces GLA synthesis from LA − even in the presence of adequate LA substrate → EFA processing bottleneck; this is why Zinc co-supplementation with EFAs in Coatex is synergistic — Zinc restores the FADS2 enzyme activity required to process LA to GLA from both endogenous LA and supplemented LA; (c) matrix metalloproteinase regulation — Zinc is the catalytic metal of MMP active sites; MMP-1, MMP-2, and MMP-9 are expressed in keratinocytes and participate in normal skin remodelling; Zinc availability regulates MMP activity in the skin; (d) antioxidant metalloenzymes — Zinc is a structural component of Cu/Zn-SOD (copper/zinc superoxide dismutase — SOD1) which dismutates •O2− to H2O2 (then detoxified by catalase and GPx) — reducing oxidative burden in inflamed skin; Zinc-responsive dermatoses in dogs: two distinct syndromes — Zinc Responsive Dermatosis Type I (Northern breeds — Siberian Husky, Alaskan Malamute — due to reduced intestinal Zinc absorption; responds to oral Zinc supplementation) and Type II (rapidly growing large breed puppies on high-cereal/phytate diets — phytate chelates dietary Zinc reducing bioavailability; responds to diet correction)

Indications

• Canine atopic dermatitis (CAD) — adjunctive EFA supplementation to support skin barrier repair and reduce inflammatory cytokine/eicosanoid production; use alongside oclacitinib/Apoquel, lokivetmab/Cytopoint, ciclosporin, or allergen-specific immunotherapy (ASIT) as directed by veterinarian
• Feline atopic skin syndrome (FASS) and feline eosinophilic granuloma complex (EGC)
• Dry, flaky, or seborrhoeic skin in dogs and cats of any breed
• Dull, brittle, or poor-condition coat — excessive shedding, loss of coat gloss, coat texture changes
• Pruritic skin conditions (itchy skin) with inflammatory aetiology
• Zinc-responsive dermatosis in Northern breeds
• Post-clipping alopecia and poor coat regrowth in dogs
• General skin and coat maintenance in large breed, giant breed, and senior dogs with age-related skin changes

Directions for Use

• Administer orally as directed by a veterinarian or per VetPlus label instructions
• Capsules can be given whole, or punctured and squeezed onto food — the EFA oil content is palatable to most dogs and cats
• Allow 6–8 weeks of continuous supplementation before assessing coat and skin improvement — do not discontinue prematurely
• For best results, supplement long-term continuously
• 240-capsule pack — approximately 4–8 month supply depending on prescribed dose

Safety Information

• For animal use only — keep out of reach of children
• Use with caution in dogs or cats with known fish or shellfish allergy
• Not a substitute for veterinary-prescribed immunomodulatory therapy in moderate-to-severe CAD
• Can be used concurrently with NSAIDs, ciclosporin, oclacitinib, and lokivetmab under veterinary guidance
• Store in a cool, dry place; blister packaging protects EFAs from oxidation — do not remove capsules from blisters until immediately before use; refrigeration may extend EFA stability