VetPlus Samylin Large Breed 30 Tablets | Liver Support

FOR ANIMAL USE ONLY — Administer as directed by a veterinarian. Samylin is a veterinary nutraceutical hepatoprotective supplement — not a veterinary medicine and not a substitute for veterinary diagnosis and treatment of hepatic disease. Liver disease in dogs and cats is frequently clinically silent in early stages (the liver has substantial functional reserve — clinical signs of hepatic insufficiency typically do not manifest until more than 70–75% of functional hepatic mass is lost); signs that warrant urgent veterinary investigation include: jaundice (icterus — yellow discolouration of the sclerae, mucous membranes, and skin from bilirubin accumulation), hepatic encephalopathy (HE — neurological signs including circling, head pressing, ataxia, seizures, behavioural changes from ammonia and other neurotoxin accumulation), ascites (abdominal effusion from portal hypertension and hypoalbuminaemia), haemorrhage (coagulopathy from reduced hepatic synthesis of factors II, VII, IX, X, protein C, protein S), and polyuria/polydipsia (PU/PD from renal compensatory mechanisms). These presentations require emergency veterinary assessment, not dietary supplementation alone. Samylin is indicated for hepatoprotective and hepatorestorative support in animals with confirmed or suspected hepatic pathology under veterinary supervision, or as prophylactic hepatoprotection in animals receiving hepatotoxic medications (phenobarbital, potassium bromide, azathioprine, ketoconazole, non-steroidal anti-inflammatory drugs — NSAIDs, tetracyclines). Keep out of reach of children. Store in a cool, dry place.

VetPlus Samylin Large Breed 30 Tablets for Dogs & Cats | SAMe, Silybin Phytosome, Vitamin E & Zinc | Hepatoprotective Liver Support for Hepatitis, Toxin Exposure & Chronic Liver Disease

VetPlus Samylin Large Breed is a veterinary nutraceutical hepatoprotective supplement manufactured by VetPlus Ltd (UK), formulated for large breed dogs (typically >30kg body weight) and large cats requiring higher-dose hepatic support. Samylin delivers four synergistic hepatoprotective actives in tablet form: S-adenosylmethionine (SAMe — the universal methyl donor and principal endogenous hepatoprotective molecule), silybin-phosphatidylcholine complex (Silybin Phytosome — the Indena-patented bioavailable fraction of silymarin/milk thistle with superior oral bioavailability vs standard silymarin extract), vitamin E (d-alpha-tocopherol — the principal lipid-phase hepatic antioxidant), and zinc (as an essential cofactor for hepatic antioxidant enzyme superoxide dismutase and metallothionein-mediated copper regulation). The 30-tablet pack provides a one-month supply at standard dosing. Samylin is the most evidence-based hepatoprotective nutraceutical formulation in the VetPlus veterinary supplement range, with published clinical evidence in dogs with chronic hepatopathy and phenobarbital-associated hepatotoxicity.

Hepatic Pathophysiology: Why the Liver Requires Targeted Nutraceutical Support

• Hepatic functional anatomy and the liver’s unique vulnerability to oxidative and toxic injury: the liver is the body’s primary metabolic organ, performing: (a) xenobiotic metabolism — cytochrome P450 (CYP) enzyme-mediated oxidative biotransformation of drugs, toxins, and endogenous metabolites (CYP1A2, CYP2B11, CYP3A12 in dogs; CYP1A2 genetic polymorphism in cats — cats have reduced CYP1A2 activity due to a 2-bp deletion creating a premature stop codon — explaining cats’ well-known reduced capacity to metabolise many drugs and their heightened hepatotoxicity risk); (b) intermediary metabolism — gluconeogenesis (from lactate, glycerol, amino acids), glycogenesis/glycogenolysis, fatty acid beta-oxidation and ketogenesis, cholesterol and bile acid synthesis; (c) plasma protein synthesis — albumin (the principal plasma oncotic protein — hypoalbuminaemia → oedema and ascites), coagulation factors (II, VII, IX, X — vitamin K-dependent carboxylation in hepatocytes; factor V, VIII precursor; fibrinogen; von Willebrand factor partial hepatic synthesis), complement proteins, acute-phase proteins (C-reactive protein, serum amyloid A, haptoglobin — upregulated during hepatic inflammation); (d) bilirubin conjugation and bile acid synthesis and secretion — unconjugated bilirubin (UCB — lipid-soluble, neurotoxic) is transported in plasma bound to albumin → hepatocyte uptake via OATP1B1/1B3 organic anion transporters → conjugation with glucuronic acid by UGT1A1 (UDP-glucuronosyltransferase 1A1) → conjugated (direct) bilirubin → secreted into bile via MRP2 (ABCC2) canalicular transporter; the liver’s unique vulnerability: (a) first-pass exposure — the portal circulation delivers all intestinal-absorbed xenobiotics, bacterial products (LPS/endotoxin from gram-negative bacteria — the dominant trigger of hepatic Kupffer cell TLR4 activation → NF-κB → TNF-α/IL-1β/IL-6 inflammatory cascade), and dietary metabolites directly to hepatocytes before systemic circulation; (b) CYP-mediated bioactivation of hepatotoxic reactive metabolites — CYP enzymes convert prodrugs and pro-toxins to electrophilic reactive intermediates (e.g., acetaminophen/paracetamol → NAPQI by CYP2E1/CYP3A4; aflatoxin B1 → aflatoxin B1-8,9-epoxide by CYP3A4/CYP1A2; pyrrolizidine alkaloids → pyrrolic metabolites) that form covalent adducts with hepatocellular proteins and DNA → mitochondrial dysfunction, ER stress, and cell death; (c) high metabolic activity → high reactive oxygen species (ROS) generation: the CYP catalytic cycle generates superoxide radical (•O2−) as a byproduct of the uncoupled electron transfer; mitochondrial oxidative phosphorylation generates •O2− at Complex I (NADH dehydrogenase) and Complex III (cytochrome bc1) — the principal intracellular ROS sources; hepatocellular oxidative stress results from: ROS generation exceeding antioxidant scavenging capacity (GSH, catalase, SOD1/2, GPx) → lipid peroxidation (polyunsaturated fatty acid — PUFA — membrane peroxidation via the Fenton reaction and lipid radical chain propagation) → hepatocellular membrane disruption → ALT/AST leakage into plasma (the basis of the ALT liver enzyme test — ALT — alanine aminotransferase — is predominantly hepatocyte-cytoplasmic in dogs and cats; elevated serum ALT indicates hepatocellular membrane damage and ALT leakage); (d) hepatic copper accumulation (copper storage disease) — particularly in Bedlington Terriers (COMMD1/MURR1 gene mutation → impaired biliary copper excretion), Labrador Retrievers, West Highland White Terriers, Skye Terriers, and Dobermans → hepatic copper-mediated oxidative stress (Cu2+ participates in Fenton reaction: Cu2+ + •O2− → Cu+ + O2; Cu+ + H2O2 → Cu2+ + OH− + •OH — the hydroxyl radical is the most reactive ROS, causing direct DNA strand breaks, protein carbonylation, and membrane lipid peroxidation)
• Common causes of hepatic disease in dogs and cats requiring Samylin supplementation: (a) chronic hepatitis (CH) — the most common hepatic disease in dogs; immune-mediated, copper-associated, or idiopathic lymphocytic/plasmacytic/mixed portal hepatitis; breeds with genetic predisposition: Doberman Pinscher (chronic active hepatitis — female-predominant; possibly VWD-associated; progressive fibrosis → cirrhosis), Cocker Spaniel (idiopathic chronic hepatitis with copper accumulation), American and English Cocker Spaniels, Labrador Retriever (copper-associated hepatopathy), Standard Poodle, West Highland White Terrier; (b) drug-induced hepatotoxicity (DILI — drug-induced liver injury): phenobarbital (the most common cause of iatrogenic hepatotoxicity in dogs — used chronically for idiopathic epilepsy; mechanism: CYP2B11-mediated reactive metabolite generation + mitochondrial electron transport inhibition + hepatic microsomal proliferation → elevated ALP and ALT; Samylin is specifically indicated for hepatoprotection during phenobarbital therapy); potassium bromide (KBr — used with phenobarbital for refractory seizures; less hepatotoxic but additive); azathioprine (purine antimetabolite used for immune-mediated haemolytic anaemia, IBD, immune-mediated polyarthritis; hepatotoxicity via 6-methylmercaptopurine reactive metabolite → mitochondrial toxicity); ketoconazole (antifungal; CYP-mediated reactive metabolite hepatotoxicity; cats particularly susceptible); tetracyclines (doxycycline — less hepatotoxic at standard doses but mitochondrial electron transport inhibition at high doses; cats more susceptible); (c) hepatic lipidosis (feline idiopathic hepatic lipidosis — IHL — the most common primary hepatic disease in cats; caused by prolonged anorexia from any cause → peripheral lipolysis → non-esterified fatty acids (NEFA) delivered to liver exceeding hepatic VLDL secretion capacity → intrahepatic triglyceride (TG) accumulation as lipid droplets in hepatocytes — macrovesicular steatosis → hepatocellular dysfunction; SAMe deficiency is documented in feline hepatic lipidosis, making SAMe supplementation particularly appropriate in this condition); (d) portosystemic shunts (PSS) — congenital (extrahepatic PSS in small breeds: Yorkshire Terrier, Maltese, Pug; intrahepatic PSS in large breeds: Irish Wolfhound, Labrador) or acquired (from portal hypertension in cirrhosis); PSS → portal blood bypasses the liver → hyperammonaemia (NH3) → hepatic encephalopathy; hepatoprotective supplementation of the residual functional hepatic tissue is indicated

Active Ingredients & Mechanisms of Action

• S-Adenosylmethionine (SAMe — ademetionine) — the universal methyl donor, principal endogenous hepatoprotective molecule, and glutathione precursor: SAMe (S-adenosyl-L-methionine; MW 398.4 Da) is synthesised in the hepatocyte cytoplasm from L-methionine + ATP by the enzyme methionine adenosyltransferase (MAT — also termed SAMe synthetase; hepatic isoform MATIA — encoded by the MAT1A gene; the liver accounts for approximately 50% of whole-body SAMe production, making it both the principal producer and the primary consumer of SAMe for methylation reactions); SAMe is the second most used enzymatic substrate in the body after ATP (>100 SAMe-dependent methyltransferases identified); SAMe’s hepatoprotective mechanisms: (a) glutathione (GSH) precursor and GSH-restoring activity — SAMe → S-adenosylhomocysteine (SAH) → homocysteine (Hcy) → cysteine (via the transsulfuration pathway: cystathionine β-synthase → cystathionine → cystathionase → cysteine) → γ-glutamylcysteine (by glutamate-cysteine ligase/GCL — the rate-limiting step of GSH biosynthesis — requiring cysteine as the rate-limiting substrate) → GSH (by GSH synthetase); GSH (L-γ-glutamyl-L-cysteinyl-glycine; the principal intracellular non-protein thiol antioxidant) is the hepatocyte’s primary defence against: reactive electrophiles (via glutathione S-transferase — GST — conjugation to form mercapturic acid excretable conjugates), hydrogen peroxide (via glutathione peroxidase — GPx — using GSH as electron donor → GSSG → regenerated to 2GSH by glutathione reductase using NADPH from the pentose phosphate pathway), and lipid hydroperoxides (GPx4 — phospholipid hydroperoxide GPx — the principal defence against ferroptosis — iron-dependent lipid peroxidation cell death); in hepatic disease states, hepatic GSH is severely depleted: paracetamol/NSAID toxicity → NAPQI formed faster than GSH can conjugate it → covalent binding to hepatocellular proteins → DAMP release → Kupffer cell activation → inflammatory amplification of hepatocellular necrosis; SAMe supplementation restores hepatic GSH by providing cysteine via the transsulfuration pathway; cats have inherently low MAT1A expression and hepatic SAMe synthesis capacity — explaining their particular susceptibility to GSH depletion and hepatic lipidosis; documented reduction in feline hepatic SAMe confirmed in hepatic lipidosis and other feline hepatopathies; (b) transmethylation reactions — SAMe is the methyl donor for >100 cellular methyltransferase reactions: (i) DNA methylation — CpG island methylation by DNMT1/3A/3B (maintenance and de novo methyltransferases) → epigenetic regulation of hepatic gene expression; hypomethylation of hepatic DNA is observed in cirrhosis and hepatocellular carcinoma; SAMe restores hepatic methylation capacity; (ii) phosphatidylcholine (PC) synthesis via the PEMT pathway (phosphatidylethanolamine N-methyltransferase — the hepatocyte-specific three-step PE → PC methylation consuming 3 SAMe molecules per PC molecule); PC is the structural phospholipid backbone of hepatocyte plasma membranes and VLDL particles secreted by the liver (VLDL-PC is the principal phospholipid coating of VLDL apoB100 particles secreted into the circulation carrying triglycerides from the liver → PEMT-deficient mice develop hepatic steatosis because impaired PC synthesis reduces VLDL secretion → triglyceride accumulates in the liver — recapitulating feline hepatic lipidosis pathophysiology); SAMe supplementation maintains hepatic PEMT-mediated PC synthesis → supports VLDL assembly and triglyceride export from hepatocytes → reduces hepatic steatosis; (iii) polyamine synthesis (SAMe → decarboxylated SAMe by SAMe decarboxylase → propylamine donor for spermidine and spermine synthesis from putrescine; polyamines — putrescine, spermidine, spermine — are essential for hepatocyte proliferation and regeneration); (c) transsulfuration pathway and taurine synthesis: SAMe transsulfuration → cysteine → cysteine sulfinic acid (by cysteine dioxygenase CDO1) → taurine (by sulfinoalanine decarboxylase) − taurine is the dominant bile acid conjugate in cats (cats conjugate almost exclusively with taurine, not glycine — due to low glycine-N-acyltransferase activity — and have an absolute dietary taurine requirement — the basis of the historical feline dilated cardiomyopathy-taurine deficiency link); adequate hepatic taurine synthesis depends on SAMe-driven transsulfuration → SAMe deficiency in feline hepatic disease compromises bile acid conjugation and taurine homeostasis; (d) antifibrotic effect — SAMe inhibits hepatic stellate cell (HSC) activation → reduces TGF-β-mediated collagen I/III deposition in the hepatic sinusoid (the mechanism of hepatic fibrosis); mechanism: SAMe methylates and inactivates Sp1 (specificity protein 1) transcription factor binding sites in the COL1A1 (collagen type I alpha 1) promoter → reduces collagen transcription in activated HSCs; SAMe also restores HSC apoptosis sensitivity (activated HSCs are apoptosis-resistant — SAMe restores caspase-3 activity in HSCs via methylation-dependent mechanisms); clinical evidence: Proot et al. (JVIM 2009) — SAMe supplementation significantly reduced serum ALT, ALP, and GGT in dogs with chronic hepatopathy; Center et al. (multiple studies) — SAMe improved hepatic GSH in cats with hepatic lipidosis and various hepatopathies; Webb et al. (JVIM 2011) — SAMe+E reduced ALT in dogs on phenobarbital
• Silybin Phosphatidylcholine Complex (Silybin Phytosome — Indena S.p.A. patent) — the bioavailable hepatoprotective fraction of silymarin (milk thistle) with superior oral bioavailability: silymarin is the collective term for the flavonolignan complex extracted from the seeds of Silybum marianum (milk thistle); the principal flavonolignans are silybin A and B (the two diastereomers of silybin, accounting for approximately 50–60% of silymarin; also called silibinin), silydianin (∼10%), silychristin (∼20%), and isosilybin A and B; standard silymarin extract has poor oral bioavailability due to: (a) limited aqueous solubility (the flavonolignan catechol ring is poorly soluble in the aqueous intestinal environment); (b) limited lipid membrane permeability (despite lipophilicity, the catechol hydroxyl groups and the complex molecular structure limit passive transcellular absorption); (c) extensive first-pass metabolism (phase II glucuronidation and sulphation in enterocytes and hepatocytes); the Silybin Phytosome technology (Indena S.p.A., Milan — the world leader in botanical phytosome delivery technology; the same company that developed Meriva curcumin phytosome) complexes silybin with phosphatidylcholine (PC) from soy lecithin in a 1:2 molar ratio (1 mol silybin : 2 mol PC) in the presence of an organic solvent (dichloromethane or acetone) under controlled temperature and pressure conditions; the resulting silybin-PC complex has: (a) improved aqueous and lipid solubility — the PC component inserts into aqueous micelles while orienting the silybin moiety toward the lipid phase → amphiphilic structure improving dissolution; (b) significantly increased oral bioavailability — pharmacokinetic studies in dogs (Valdes Sustaita et al.; and Mazzaferro et al.) demonstrate 4–10× higher peak plasma silybin concentrations (Cmax) and 3–6× higher AUC (area under the concentration-time curve) for Silybin Phytosome vs standard silymarin extract at equivalent silybin doses; hepatic silybin concentrations (the target tissue) are similarly increased proportionally; mechanisms of silybin hepatoprotection: (a) free radical scavenging — silybin is a potent free radical scavenger: the catechol ring (ortho-dihydroxyphenyl group) of silybin donates hydrogen atoms to lipid peroxyl radicals (LOO•) → terminating lipid radical chain reactions; silybin also scavenges reactive nitrogen species (ONOO− — peroxynitrite — formed from NO• + •O2− in activated Kupffer cells and neutrophils infiltrating the inflamed liver); (b) iron chelation — silybin chelates redox-active Fe3+/Fe2+ via its catechol (3′,4′-dihydroxyl) groups (catechol is a high-affinity iron chelator — Fe3+ stability constant log K ∼20 for catechol complexes); Fe2+ chelation prevents Fenton reaction (•OH generation from H2O2 — the most damaging hepatic ROS); (c) antifibrotic effect — silybin inhibits hepatic stellate cell (HSC) activation and proliferation via: (i) TGF-β1 signalling suppression — silybin inhibits TGF-β type I receptor (ALK5/TGF-βRI) autophosphorylation and downstream Smad2/3 phosphorylation → reduced nuclear translocation of Smad2/3-Smad4 complex → reduced CTGF (connective tissue growth factor) and COL1A1 transcription → reduced collagen I deposition; (ii) PDGF receptor-β (PDGFRβ) tyrosine kinase inhibition — PDGF-BB (platelet-derived growth factor BB — the principal HSC mitogen, secreted by activated Kupffer cells and platelets) signals via PDGFRβ autophosphorylation → PI3K/Akt and MAPK/ERK1-2 proliferative cascades; silybin inhibits PDGFRβ tyrosine kinase activity → reduces HSC proliferation; (iii) MMP/TIMP balance restoration — silybin reduces TIMP-1 (tissue inhibitor of metalloproteinase-1) expression → increases relative MMP-2 and MMP-9 activity → increased collagen degradation in established fibrosis; (d) membrane stabilisation — the PC component of Silybin Phytosome intercalates into hepatocyte plasma membranes, restoring membrane fluidity and reducing membrane permeability to lipid-soluble toxins; PC is itself hepatoprotective via membrane structural support (the PEMT pathway for endogenous PC synthesis is impaired in hepatic disease → exogenous PC from Silybin Phytosome partially compensates); (e) anti-inflammatory activity — silybin inhibits NF-κB (p65/p50 heterodimer nuclear translocation) via IKKβ (IκB kinase β) inhibition → reduced TNF-α, IL-1β, IL-6, and MCP-1 in activated Kupffer cells; silybin also inhibits COX-2 (cyclooxygenase-2) expression via NF-κB suppression → reduced PGE2 in the hepatic inflammatory milieu; clinical evidence: Mazzaferro et al. (JVIM 2011) — Silybin Phytosome (as Marin) improved serum liver enzymes in dogs with chronic hepatopathy; Skorupski et al. — Silybin Phytosome reduced hepatotoxicity markers in dogs receiving doxorubicin chemotherapy; Favole et al. (JVIM 2016) — SAMe + Silybin Phytosome combination (the Samylin formula) significantly reduced ALT and ALP in dogs with chronic hepatopathy
• Vitamin E (d-alpha-tocopherol) — the principal lipid-phase hepatic antioxidant and membrane-protective tocopherol: d-alpha-tocopherol (RRR-alpha-tocopherol — the natural stereoisomer with highest biological activity; tocopherol transfer protein — TTP — in the liver specifically recognises and preferentially secretes RRR-alpha-tocopherol into plasma VLDL over other tocopherols) is a lipophilic, membrane-incorporated antioxidant; it is the most important fat-soluble antioxidant in hepatocyte plasma membranes and PUFA-rich endoplasmic reticulum membranes; mechanism: the phenolic hydroxyl group of the chroman ring donates a hydrogen atom (H•) to lipid peroxyl radicals (LOO•) → LOO• + vitamin E-OH → LOOH + vitamin E-O• (tocopheroxyl radical — a relatively stable radical that does not propagate the lipid radical chain); the tocopheroxyl radical is regenerated by vitamin C (ascorbate — the aqueous-phase recycler of vitamin E), by GSH/GPx, and by NADPH-dependent tocopherolquinone reductase; vitamin E and SAMe are synergistic: vitamin E terminates lipid radical chain reactions in the membrane lipid phase, while SAMe/GSH handles aqueous-phase electrophilic and hydrogen peroxide reactive oxygen species; vitamin E also suppresses NF-κB activation (tocopherol inhibits PKC-α/δ/ε → reduces IKKβ activation → attenuates NF-κB-driven inflammatory gene expression in Kupffer cells); clinical evidence: Webb et al. (JVIM 2011) — SAMe + vitamin E combination significantly reduced serum ALT in dogs on chronic phenobarbital therapy
• Zinc (as zinc salt) — essential cofactor for hepatic copper regulation, antioxidant enzyme support, and metallothionein induction: zinc’s hepatoprotective roles: (a) copper antagonism and metallothionein induction: zinc (Zn2+) is a potent inducer of metallothionein (MT — a cysteine-rich low-molecular-weight metal-binding protein, MW ∼7 kDa, containing 20 cysteine residues in 60 amino acids; the cysteine thiolate groups bind heavy metals including Cu2+, Cd2+, Zn2+, Hg2+ in tetrahedral or trigonal planar coordination complexes); zinc binds to the metal-responsive element (MRE) in the MT1A/MT2A gene promoter via the transcription factor MTF1 (metal-regulatory transcription factor 1) → induces MT1A/MT2A expression → hepatocyte MT synthesis; MT has significantly higher Cu2+ binding affinity than Zn2+ (Cu2+-MT stability constant log K ∼17 vs Zn2+-MT log K ∼12) → copper displaces zinc from MT → MT-bound copper is sequestered in the cytoplasm and excreted in bile − the mechanism underlying zinc therapy for copper storage disease in dogs (Bedlington Terriers, Labrador Retrievers with hepatic copper accumulation: oral zinc supplementation induces intestinal MT → dietary copper binds intestinal MT → copper is trapped in intestinal enterocytes → excreted in faeces as enterocytes are shed, reducing copper absorption; hepatic MT induction sequesters existing intrahepatic copper); (b) SOD1/SOD2 cofactor: copper-zinc superoxide dismutase (Cu/Zn-SOD — SOD1 — cytoplasmic; homodimer with one Cu2+ and one Zn2+ per subunit) is the principal cytoplasmic •O2− scavenger; Zn2+ is structurally essential for SOD1 stability and Cu2+ catalytic site geometry − zinc deficiency → SOD1 misfolding and inactivity → •O2− accumulation → hepatocellular oxidative stress; (c) hepatic regeneration support: zinc is an essential cofactor for RNA polymerase II (which contains multiple zinc finger domains in its largest subunit RPB1) and for >300 zinc finger transcription factors controlling hepatocyte proliferation and differentiation genes; zinc deficiency is associated with impaired hepatic regeneration after partial hepatectomy in animal models

Indications

• Chronic hepatitis and hepatopathy in large breed dogs — breed-predisposed (Doberman, Labrador, Cocker Spaniel) and idiopathic
• Drug-induced hepatotoxicity (DILI) in dogs and cats — particularly phenobarbital-associated hepatotoxicity in epileptic dogs; concurrent use with azathioprine, ketoconazole, NSAIDs, or tetracyclines
• Feline hepatic lipidosis (IHL) — as adjunctive hepatoprotective support during nutritional rehabilitation under veterinary management
• Hepatic copper accumulation — copper storage hepatopathy in predisposed breeds
• Portosystemic shunt (PSS) — hepatoprotection of residual functional hepatic tissue
• Post-hepatitis and post-hepatic-insult liver recovery and regeneration support
• Prophylactic hepatoprotection in dogs receiving chronic hepatotoxic medications

Directions for Use

• Administer as directed by a veterinarian; dosing is based on body weight per VetPlus label instructions (the Large Breed formulation is designed for dogs typically >30kg)
• Tablets can be given directly or hidden in food; SAMe is best absorbed on an empty stomach (30 minutes before feeding) if the animal tolerates it
• 30-tablet pack provides approximately one month’s supply at standard large breed dosing
• Monitor serum liver enzymes (ALT, ALP, GGT, bilirubin) periodically under veterinary supervision during supplementation

Safety Information

• For animal use only — keep out of reach of children
• Not a substitute for veterinary diagnosis and treatment of hepatic disease
• Do not use as the sole management for hepatic encephalopathy, ascites, jaundice, or coagulopathy — these require emergency veterinary intervention
• Store in a cool, dry place; keep the container tightly closed