VetPlus Samylin Medium 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. Signs warranting urgent veterinary investigation include: jaundice (icterus — yellow discolouration of sclerae, mucous membranes, and skin), hepatic encephalopathy (circling, head pressing, ataxia, seizures, behavioural changes from ammonia accumulation), ascites (abdominal effusion from portal hypertension and hypoalbuminaemia), haemorrhage (coagulopathy from reduced hepatic synthesis of clotting factors II, VII, IX, X), and polyuria/polydipsia. These presentations require emergency veterinary assessment. 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, NSAIDs, tetracyclines). Keep out of reach of children. Store in a cool, dry place.

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

VetPlus Samylin Medium Breed is a veterinary nutraceutical hepatoprotective supplement manufactured by VetPlus Ltd (UK), formulated for medium breed dogs (typically 10–30kg body weight) and cats requiring hepatic support at medium-breed dosing. Samylin delivers four synergistic hepatoprotective actives in a palatable coated tablet: S-adenosylmethionine (SAMe — the universal methyl donor, principal endogenous hepatoprotective molecule, and glutathione precursor), silybin-phosphatidylcholine complex (Silybin Phytosome — the Indena-patented bioavailable fraction of silymarin/milk thistle with 4–10× superior oral bioavailability vs standard silymarin extract), vitamin E (d-alpha-tocopherol — the principal lipid-phase hepatic antioxidant), and zinc (essential cofactor for hepatic antioxidant enzyme SOD1 and metallothionein-mediated copper regulation). The 30-tablet pack provides approximately one month’s supply at standard medium-breed dosing. Tablets may be given with or without food and are coated for palatability.

Why the Liver Requires Targeted Nutraceutical Support

• Hepatic functional vulnerability and oxidative stress: the liver is the body’s primary metabolic organ — performing xenobiotic biotransformation (cytochrome P450 — CYP — enzyme-mediated drug and toxin metabolism), intermediary metabolism (gluconeogenesis, glycogenolysis, fatty acid beta-oxidation), plasma protein synthesis (albumin, coagulation factors II/VII/IX/X, complement), and bilirubin conjugation (UGT1A1-mediated glucuronidation → MRP2 biliary secretion); the CYP catalytic cycle generates superoxide radical (•O2−) as a byproduct — and mitochondrial oxidative phosphorylation generates additional •O2− at Complex I and Complex III; high CYP activity → high ROS generation → hepatocellular oxidative stress when antioxidant capacity (GSH, SOD1, catalase, GPx) is overwhelmed → lipid peroxidation (PUFA membrane peroxidation via Fenton reaction → ALT/AST leakage → elevated serum liver enzymes); note: cats have reduced CYP1A2 activity due to a 2-bp deletion creating a premature stop codon — explaining their heightened hepatotoxicity risk and inherently lower hepatic SAMe synthesis capacity
• Common indications in medium breed dogs and cats: (a) chronic hepatitis (CH) — idiopathic, immune-mediated, or copper-associated hepatopathy in medium breed dogs; breeds with predisposition in the medium-breed weight class include American Cocker Spaniel, English Springer Spaniel, Standard Poodle, and Samoyed; (b) drug-induced hepatotoxicity (DILI) — phenobarbital-associated hepatotoxicity in epileptic dogs (the most common indication — phenobarbital is the first-line anticonvulsant for canine idiopathic epilepsy; CYP2B11-mediated reactive metabolite generation + hepatic microsomal proliferation → elevated ALP and ALT; Samylin is specifically indicated for concurrent hepatoprotection during phenobarbital therapy); azathioprine, ketoconazole, NSAIDs (particularly carprofen-associated hepatotoxicity in Labrador Retrievers and English Bulldogs), and tetracyclines; (c) feline hepatic lipidosis (IHL) — the most common primary hepatic disease in cats; prolonged anorexia → peripheral lipolysis → NEFA hepatic delivery exceeding VLDL secretion capacity → intrahepatic TG accumulation → macrovesicular steatosis; SAMe deficiency is documented in feline IHL (low MAT1A expression in cats → reduced endogenous SAMe synthesis → impaired PEMT-mediated PC synthesis → reduced VLDL-TG export capacity); (d) portosystemic shunts (PSS) — extrahepatic PSS in small-to-medium breeds (Yorkshire Terrier, Maltese, Pug — which may be in the lower end of the medium-breed weight range); (e) hepatic copper accumulation in predisposed medium breeds

Active Ingredients & Mechanisms of Action

• S-Adenosylmethionine (SAMe) — glutathione precursor, methylation substrate, and antifibrotic agent: SAMe is synthesised in hepatocytes from L-methionine + ATP by methionine adenosyltransferase (MAT — hepatic isoform MATIA); SAMe’s hepatoprotective mechanisms: (a) GSH biosynthesis — SAMe → homocysteine → cysteine (transsulfuration: CBS → cystathionase) → γ-glutamylcysteine (GCL — rate-limiting, cysteine-limited) → GSH; GSH is the hepatocyte’s primary defence against reactive electrophiles (via GST conjugation), H2O2 (via GPx), and lipid hydroperoxides (GPx4/ferroptosis defence); in DILI, hepatic GSH is severely depleted (NAPQI from paracetamol/CYP2E1 overwhelms GSH → hepatocellular protein adducts → Kupffer cell TLR4/NF-κB inflammatory amplification); (b) PEMT transmethylation — SAMe is the methyl donor for phosphatidylethanolamine N-methyltransferase (PEMT − the hepatocyte-specific three-step PE→PC methylation consuming 3 SAMe per PC); PC is the structural phospholipid of VLDL particles secreted by the liver — impaired PC synthesis in hepatic disease reduces VLDL-TG export → hepatic steatosis (recapitulating feline hepatic lipidosis pathophysiology); SAMe restores hepatic PC synthesis capacity; (c) antifibrotic activity — SAMe methylates and inactivates Sp1 transcription factor binding sites in the COL1A1 promoter → reduces collagen I transcription in activated hepatic stellate cells (HSCs); also restores HSC apoptosis sensitivity via caspase-3 methylation-dependent mechanisms; (d) taurine synthesis (via transsulfuration → cysteine → cysteine dioxygenase → taurine) — critical in cats, which conjugate bile acids almost exclusively with taurine (low glycine-N-acyltransferase activity) and have an absolute dietary taurine requirement; clinical evidence: Proot et al. (JVIM 2009) — SAMe reduced ALT, ALP, and GGT in dogs with chronic hepatopathy; Webb et al. (JVIM 2011) — SAMe + vitamin E reduced ALT in dogs on phenobarbital; Center et al. — SAMe improved hepatic GSH in cats with hepatic lipidosis
• Silybin Phosphatidylcholine Complex (Silybin Phytosome — Indena patent) — bioavailable silymarin fraction with 4–10× superior oral bioavailability: standard silymarin (the flavonolignan complex from Silybum marianum — milk thistle seed; principal component silybin A+B, accounting for approximately 50–60% of silymarin) has poor oral bioavailability due to limited aqueous solubility and extensive first-pass phase II metabolism; Silybin Phytosome (1:2 silybin:phosphatidylcholine molar complex — Indena S.p.A.) achieves 4–10× higher peak plasma silybin Cmax and 3–6× higher AUC vs standard silymarin in pharmacokinetic studies in dogs; silybin hepatoprotective mechanisms: (a) free radical scavenging — catechol ring (ortho-dihydroxyphenyl) donates H• to lipid peroxyl radicals (LOO•) → terminates lipid radical chain propagation; scavenges peroxynitrite (ONOO− — from NO• + •O2− in activated Kupffer cells); (b) Fe3+ chelation — catechol groups chelate redox-active iron (log K ∼20 for Fe3+-catechol complexes) → prevents Fenton •OH generation; (c) antifibrotic — inhibits TGF-β1 via ALK5/Smad2-3 suppression → reduces CTGF and COL1A1 transcription; inhibits PDGFRβ tyrosine kinase (the principal HSC mitogen receptor) → reduces HSC proliferation; restores MMP-2/MMP-9 activity by reducing TIMP-1 → increases collagen degradation in established fibrosis; (d) anti-inflammatory — inhibits NF-κB p65/p50 via IKKβ suppression → reduces TNF-α, IL-1β, IL-6 in Kupffer cells; (e) PC membrane stabilisation — the PC component of Silybin Phytosome intercalates into hepatocyte membranes, restoring fluidity and reducing toxin permeability; clinical evidence: Mazzaferro et al. (JVIM 2011) — Silybin Phytosome improved liver enzymes in dogs with chronic hepatopathy; Favole et al. (JVIM 2016) — SAMe + Silybin Phytosome (the Samylin formula) significantly reduced ALT and ALP in dogs with chronic hepatopathy
• Vitamin E (d-alpha-tocopherol) — lipid-phase hepatic antioxidant and membrane protector: RRR-alpha-tocopherol (the natural stereoisomer, preferentially secreted by hepatic tocopherol transfer protein — TTP — into VLDL) is incorporated into hepatocyte plasma and ER membranes; the chroman ring phenolic OH donates H• to LOO• → terminates lipid radical chain reactions; the resulting tocopheroxyl radical is recycled by ascorbate (vitamin C), GSH/GPx, and NADPH-dependent tocopherolquinone reductase; vitamin E also inhibits NF-κB via PKC-α/δ/ε suppression → IKKβ attenuation; vitamin E and SAMe/GSH provide complementary antioxidant protection: vitamin E in the membrane lipid phase, GSH in the aqueous cytoplasmic phase
• Zinc — metallothionein inducer, SOD1 cofactor, and hepatic copper regulator: Zn2+ activates MTF1 → induces hepatic and intestinal MT1A/MT2A expression; MT (the cysteine-rich metal-binding protein, MW ∼7 kDa, 20 cysteine residues) binds Cu2+ with higher affinity than Zn2+ (log K ∼17 vs ∼12) → copper is sequestered and excreted — the mechanism of zinc therapy for copper storage hepatopathy (intestinal MT → dietary copper trapped in enterocytes → excreted in faeces); Zn2+ is also the structural cofactor for Cu/Zn-SOD (SOD1 — cytoplasmic •O2− dismutase − Zn2+ required for SOD1 stability and Cu2+ catalytic site geometry) and for >300 zinc finger transcription factors controlling hepatocyte proliferation and regeneration

Indications

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

Directions for Use

• Administer as directed by a veterinarian; dosing is based on body weight per VetPlus label instructions (the Medium Breed formulation is designed for dogs typically 10–30kg)
• Coated tablets may be given with or without 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 medium-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 with the container tightly closed