VetPlus Complivit 150g Multivitamin Paste for Dogs & Cats

FOR ANIMAL USE ONLY — Administer as directed by a veterinarian or as per label instructions. VetPlus Complivit is a veterinary nutraceutical multivitamin and mineral paste supplement — not a veterinary medicine. Complivit is not a substitute for veterinary diagnosis and treatment of the underlying condition causing anorexia, nutritional deficiency, weight loss, or illness. Animals with significant anorexia, weight loss, vomiting, or systemic illness require urgent veterinary investigation — do not delay veterinary assessment by initiating supplementation alone. In animals receiving therapeutic diets (renal, hepatic, cardiac, urological — which are precisely micronutrient-formulated), consult a veterinarian before adding Complivit to avoid exceeding target micronutrient levels. Fat-soluble vitamins A and D3 are stored and accumulate — do not exceed the recommended dose or duration without veterinary guidance. Keep out of reach of children. Store in a cool, dry place with the cap tightly secured.

VetPlus Complivit 150g Multivitamin Paste for Dogs & Cats | Complete Vitamins A, D3, E, C & B-Complex, Minerals, Amino Acids | Recovery, Convalescence, Anorexia & Nutritional Support

VetPlus Complivit 150g Paste is a veterinary nutraceutical broad-spectrum multivitamin, mineral, and amino acid supplement manufactured by VetPlus Ltd (UK), formulated for dogs and cats with increased nutritional requirements or reduced food intake. Complivit’s palatable paste format makes it suitable for administration to anorexic, recovering, post-surgical, or selective-eating animals that cannot consume adequate micronutrients through voluntary food intake alone. The paste may be administered directly into the mouth via syringe or offered on a finger, or mixed into a small amount of palatable food. Complivit provides a comprehensive micronutrient matrix covering all major vitamin groups (fat-soluble: A, D3, E; water-soluble: C, B1, B2, B3, B5, B6, B9, B12, biotin), essential and conditionally essential minerals (calcium, phosphorus, magnesium, iron, copper, manganese, zinc, iodine, selenium), essential amino acids (L-lysine, L-methionine), and an energy substrate (glucose/dextrose) to support metabolic function during periods of reduced caloric and nutrient intake.

Clinical Indications: When Micronutrient Sufficiency Is Compromised

• Anorexia and reduced voluntary food intake — the primary indication: anorexia (complete absence of voluntary eating) and hyporexia (reduced voluntary eating) are extremely common presenting signs across virtually all feline and canine disease categories; the consequences of sustained anorexia extend beyond caloric deficit: (a) water-soluble vitamin depletion — B vitamins (thiamine B1, riboflavin B2, niacin B3, pantothenic acid B5, pyridoxine B6, folic acid B9, cyanocobalamin B12, biotin) have no significant body stores (unlike fat-soluble vitamins A/D/E which are stored in adipose and liver); hepatic B vitamin reserves are depleted within days to weeks of anorexia; thiamine (B1) deficiency is the most acute risk — manifesting as: in cats: thiamine-deficiency polioencephalomyelopathy (vestibular signs, cervical ventroflexion, ataxia, seizures — from selective brain stem neuronal necrosis at the olivary nuclei and caudal colliculi requiring thiamine’s role as cofactor for pyruvate dehydrogenase [PDH] and alpha-ketoglutarate dehydrogenase [α-KGDH] in mitochondrial oxidative phosphorylation; the feline brain has a 50-fold higher glucose oxidation rate than canine brain and is therefore exquisitely sensitive to thiamine-dependent PDH impairment); in dogs: thiamine-deficiency neuropathy with cardiovascular signs (Wernicke’s encephalopathy equivalent); (b) cobalamin (B12) — feline and canine hypocobalaminaemia is common in GI disease (EPI, IBD, pancreatitis) and predicts poor prognosis without supplementation; cobalamin is required for methionine synthase (methionine cycle: homocysteine + 5-MTHF → methionine + THF, where cobalamin is the methyl carrier) and for methylmalonyl-CoA mutase (propionate metabolism: methylmalonyl-CoA → succinyl-CoA, entering the TCA cycle); cobalamin deficiency → methylmalonic acidaemia (MMA) → propionate accumulation → CNS and hepatic toxicity; (c) vitamin C (ascorbate) — dogs and cats synthesise ascorbate endogenously (from UDP-glucuronate via GULO — L-gulonolactone oxidase; unlike primates and guinea pigs which are GULO-null); however, in critical illness, sepsis, and hepatic disease, endogenous synthesis capacity may be overwhelmed → relative ascorbate deficiency → reduced collagen hydroxylation (prolyl hydroxylase and lysyl hydroxylase require ascorbate as the reductant for Fe2+ catalytic cycling) → impaired wound healing and tissue repair
• Recovery and convalescence — post-surgical, post-infectious, and post-inflammatory nutrient demands: healing and recovery dramatically increase micronutrient requirements: (a) zinc — wound healing requires zinc as cofactor for matrix metalloproteinases (MMPs — collagen remodelling enzymes), RNA polymerase (for keratinocyte and fibroblast proliferation), and zinc finger transcription factors (controlling inflammatory resolution and tissue remodelling gene expression); (b) vitamin A (retinol) — required for fibroblast differentiation, collagen synthesis (RAR/RXR-mediated fibronectin and TGF-β transcriptional regulation), and epithelial barrier restoration; (c) copper — copper-dependent lysyl oxidase (LOX) cross-links collagen and elastin (oxidative deamination of lysine/hydroxylysine side chains → allysine → Schiff base cross-links) → without adequate copper, newly synthesised collagen has reduced tensile strength and wound dehiscence risk increases; (d) iron — erythropoiesis and tissue oxygenation: iron is the prosthetic group metal of haemoglobin (the haem moiety — Fe2+ chelated by protoporphyrin IX in haemoglobin) and myoglobin; post-surgical/post-inflammatory anaemia depletes iron stores; iron is also a cofactor for prolyl hydroxylase (collagen proline hydroxylation) and ribonucleotide reductase (the rate-limiting enzyme of DNA synthesis − required for rapidly dividing fibroblasts, keratinocytes, and immune cells at the wound); (e) selenium and vitamin E — the GPx/TrxR antioxidant system: selenium is the catalytic selenocysteine residue (the 21st amino acid, encoded by the UGA stop codon read-through mechanism requiring SECIS element in the 3’-UTR of selenoprotein mRNAs) of glutathione peroxidases (GPx1–4 — the H2O2/LOOH-reducing enzymes) and thioredoxin reductase (TrxR1/2/3 — the NADPH-dependent disulfide reductases regenerating the thioredoxin [Trx] antioxidant/reducing system); in post-inflammatory recovery, oxidative stress from residual neutrophil respiratory burst activity (NADPH oxidase → •O2− → SOD → H2O2 → GPx reduction, requiring Se-GPx) damages healing tissue; selenium + vitamin E together protect healing tissue from ROS-mediated oxidative injury
• Pregnancy, lactation, and neonatal growth: pregnancy dramatically increases demands for folic acid (B9 — required for neural tube closure and DNA methylation; 5,10-MTHF → thymidylate synthase → dTMP for DNA synthesis in rapidly dividing foetal cells), calcium and phosphorus (foetal skeletal mineralisation), zinc (foetal organogenesis), iodine (foetal thyroid hormone synthesis: T4 → T3, essential for foetal brain development), vitamin D3 (trans-placental calcium transport for foetal bone mineralisation → CaBP/calbindin D9k induction by calcitriol in placental syncytiotrophoblasts), and cobalamin/methionine (neural tube and neurodevelopment); lactation further increases calcium, phosphorus, and energy demands − periparturient hypocalcaemia (eclampsia) is a risk in high-milk-volume small breed bitches
• Senior animals and age-associated nutrient depletion: ageing dogs and cats have impaired nutrient absorption (reduced intestinal villus height, reduced brush border enzyme activity, reduced gastric acid secretion → impaired B12 release from food protein), reduced hepatic B vitamin activation, and increased oxidative stress from mitochondrial uncoupling and reduced antioxidant enzyme expression; L-methionine and cobalamin are particularly important in senior animals for maintaining the SAMe methylation cycle → cognitive function (SAMe is a methyl donor for myelin and neurotransmitter synthesis) and glutathione synthesis (transsulfuration: SAMe → cysteine → γ-GCL → GSH)

Active Ingredients & Mechanisms

• Fat-Soluble Vitamins: vitamin A (retinol — RAR/RXR nuclear receptor-mediated keratinocyte differentiation, filaggrin/loricrin/involucrin cornified envelope gene expression, collagen/fibronectin transcription, TGF-β wound repair regulation); vitamin D3 (cholecalciferol → hepatic 25-hydroxylase CYP2R1 → 25(OH)D3 → renal CYP27B1 1α-hydroxylase → 1,25(OH)2D3 calcitriol; VDR/RXRα/VDRE-mediated calcium absorption [TRPV6 intestinal calcium channel, calbindin D9k], immune Treg induction, cathelicidin/beta-defensin-2 AMP expression); vitamin E (d-alpha-tocopherol — LOO• radical chain termination, tocopheroxyl radical recycling by ascorbate/GSH, hepatic TTP-mediated skin sebum delivery)
• Water-Soluble Vitamins: vitamin C (ascorbate — prolyl/lysyl hydroxylase Fe2+ reductant for collagen − hydroxylation of proline at the Xaa-Pro-Gly triplet by P4H [prolyl-4-hydroxylase] and of lysine by LH [lysyl hydroxylase − procollagen-lysine,2-oxoglutarate 5-dioxygenase]; recycling of vitamin E tocopheroxyl radical; endogenous antioxidant); B1 thiamine (TPP cofactor for PDH and α-KGDH − the two mitochondrial decarboxylases linking glycolysis/amino acid catabolism to the TCA cycle; transketolase in the pentose phosphate pathway); B2 riboflavin (FAD/FMN cofactor for Complex I [NADH:ubiquinone oxidoreductase] and Complex II [succinate dehydrogenase] of the mitochondrial electron transport chain; fatty acid beta-oxidation [ACAD enzymes]); B3 niacinamide/niacin (NAD+/NADH and NADP+/NADPH cofactor for approximately 400 oxidoreductase reactions; SIRT1/3 deacylase substrate ‒ NAD+ → SIRT1 → PGC-1α deacetylation → mitochondrial biogenesis); B5 pantothenic acid (CoA biosynthesis precursor — the phosphopantetheine group of CoA is derived from pantothenate + cysteine via pantothenate kinase [PANK2]; CoA is the thioester carrier for acetyl-CoA, succinyl-CoA, and fatty acyl-CoA in the TCA cycle and fatty acid beta-oxidation); B6 pyridoxine (PLP cofactor for over 140 PLP-dependent enzymes: amino acid transaminases [AST, ALT], decarboxylases [DOPA decarboxylase → dopamine, tryptophan decarboxylase → tryptamine], CBS and cystathionase in the transsulfuration pathway → cysteine → GSH; GABA synthesis [glutamate decarboxylase − GAD]); B9 folic acid (5,6,7,8-THF − the one-carbon carrier; 5-MTHF → methionine synthase → methionine cycle; 5,10-MTHF → thymidylate synthase → dTMP for DNA synthesis; 10-formyl-THF → de novo purine synthesis; required for all rapidly dividing cells − critical in foetogenesis, wound healing, and immune cell proliferation); B12 cyanocobalamin (methionine synthase and methylmalonyl-CoA mutase cofactor; enterohepatically recirculated, absorbed by IF [intrinsic factor]-cubilin receptor in the ileum; deficiency in EPI/IBD dogs and cats); biotin/B7 (covalently attached to carboxylase enzymes via biotinyl-AMP + holocarboxylase synthetase [HCS]: pyruvate carboxylase [gluconeogenesis − pyruvate → oxaloacetate], propionyl-CoA carboxylase [propionate metabolism − propionyl-CoA → methylmalonyl-CoA], and acetyl-CoA carboxylase [fatty acid synthesis − acetyl-CoA → malonyl-CoA, the committed step of de novo lipogenesis])
• Minerals: calcium + phosphorus (hydroxyapatite [Ca10(PO4)6(OH)2] skeletal mineralisation; Ca2+ second messenger signalling; phosphorus in ATP, phospholipids, DNA/RNA backbone); magnesium (Mg2+ cofactor for over 300 ATP-dependent enzymes; Mg2+-ATP is the true substrate for kinases; NMDA receptor Mg2+ channel block [the voltage-dependent Mg2+ block of the NMDA receptor pore at resting membrane potential]; Mg2+ stabilises ribosomes and DNA polymerase); iron (haem [Fe2+-protoporphyrin IX] in haemoglobin/myoglobin; Fe-S clusters in mitochondrial Complex I/II/III and aconitase; prolyl hydroxylase Fe2+ cofactor; ribonucleotide reductase diferric-tyrosyl radical); copper (Cu/Zn-SOD1 •O2− dismutase; ceruloplasmin ferroxidase [Fe2+→Fe3+ for transferrin loading]; lysyl oxidase LOX [collagen/elastin cross-linking]; dopamine beta-hydroxylase [DBH − dopamine → noradrenaline]; cytochrome c oxidase Complex IV [the terminal electron acceptor of the mitochondrial ETC]); manganese (Mn-SOD2 [MnSOD − the mitochondrial matrix •O2− dismutase]; arginase [urea cycle]; pyruvate carboxylase [gluconeogenesis]); zinc (Zn2+ in over 300 zinc metalloenzymes: Cu/Zn-SOD1, MMP collagenases/gelatinases, alkaline phosphatase, carbonic anhydrase, alcohol dehydrogenase, and approximately 700 zinc finger transcription factors [Cys2His2 zinc fingers, RING domain proteins, LIM domain proteins]); iodine (thyroid hormone synthesis: TPO [thyroid peroxidase] iodination of tyrosine residues in thyroglobulin ’s Tyr-X-Tyr dipeptide → MIT + DIT → T3 and T4; T4 → T3 by deiodinase DIO2 in target tissues − T3 binds TRα/TRβ nuclear receptors → regulates basal metabolic rate, thermogenesis, cardiac output, and growth); selenium (catalytic selenocysteine [Sec − the 21st amino acid, UGA selenocodon] in GPx1-4 [H2O2/LOOH reduction with GSH] and TrxR1/2/3 [NADPH-dependent Trx regeneration]; selenoprotein P [SELENOP − the plasma selenium transporter, 10 Sec residues − delivers selenium to brain and testes]; iodothyronine deiodinase DIO1/2/3 − selenium-dependent T4→T3 conversion])
• Amino Acids: L-lysine (the essential amino acid most limiting in plant-based and cereal-heavy diets; required for collagen hydroxylysine formation [lysyl hydroxylase − LH1/2/3] → hydroxylysine cross-links [pyridinoline, deoxypyridinoline] in mature collagen fibrils; precursor for carnitine biosynthesis [L-lysine + L-methionine → ε-N-trimethyllysine → 4-hydroxy-TML → 3-hydroxy-6-N-trimethylaminobutyraldehyde → 4-N-trimethylaminobutyrate → γ-butyrobetaine → carnitine via γ-butyrobetaine hydroxylase (BBOX1) requiring ascorbate as cofactor] − carnitine is the obligate shuttle for long-chain fatty acyl-CoA across the inner mitochondrial membrane [via CPT1/CAT/CPT2] for beta-oxidation − critical for energy metabolism during anorexia); L-methionine (the initiating amino acid of all protein synthesis [AUG start codon] and the endogenous methyl group donor via its activated form S-adenosylmethionine [SAMe]; the transsulfuration pathway substrate for cysteine and GSH synthesis via CBS and cystathionase; precursor for taurine [via CDO1 − cysteine dioxygenase] which is the obligate bile acid conjugate in cats [BAAT with taurine rather than glycine] and an essential dietary requirement in cats due to limited CDO1 and sulfinoalanine decarboxylase [CSAD] activity; methionine is also the precursor for L-lysine’s first step in carnitine biosynthesis via methyl donation to form trimethyllysine via protein methyltransferases METTL1/2)
• Energy Substrate (Glucose/Dextrose): provides an immediately bioavailable monosaccharide energy source for compromised animals with reduced glycogen reserves; glucose → glycolysis → pyruvate → PDH (thiamine-dependent) → acetyl-CoA → TCA cycle → mitochondrial OXPHOS → ATP; the glucose component of Complivit paste supports palatability and provides immediate energy to anorexic animals during the critical early phases of nutritional recovery

Indications

• Anorexia and hyporexia — any cause; daily micronutrient maintenance during periods of reduced voluntary food intake
• Post-surgical and post-infectious convalescence and recovery
• Illness-associated nutritional depletion — GI disease (EPI, IBD, pancreatitis), hepatic disease, renal disease (under veterinary guidance), infectious disease
• Pregnancy and lactation — increased micronutrient demands
• Neonatal and growth-phase nutritional support
• Senior dogs and cats (≥08 years) with age-associated reduced absorption and micronutrient depletion
• Picky or selective eaters with demonstrated nutritional inadequacy
• Animals on restricted or therapeutic diets with confirmed micronutrient gaps (under veterinary guidance)

Directions for Use

• Administer as directed by a veterinarian or per VetPlus label instructions
• The paste may be administered directly from the tube or syringe into the mouth, offered on a finger or spoon, or mixed into a small amount of palatable food
• 150g tube provides an extended supply at standard daily dosing
• Store in a cool, dry place with the cap tightly secured; do not refrigerate unless specified on the label

Safety Information

• For animal use only — keep out of reach of children
• Not a substitute for veterinary assessment of the underlying condition causing anorexia or nutritional deficiency
• Do not exceed the recommended dose; fat-soluble vitamins A and D3 accumulate with excessive long-term dosing
• Consult a veterinarian before use in animals on therapeutic renal, hepatic, or cardiac diets