FOR VETERINARY USE — Administer as directed by a licensed veterinarian. Shake well before use. Use under veterinary supervision, especially in animals with confirmed hepatic disease or those receiving concurrent hepatically-metabolised medications. If your pet is pregnant, lactating, or on other medications, consult your veterinarian before use. Keep out of reach of children. Store in a cool, dry place away from direct sunlight.
Bionex Livfit Herbal Liver Health & Detox Syrup for Dogs, Cats & Pets | Hepatoprotective Supplement | Liver Support, Detox & Appetite Stimulant | 200ml
Bionex Livfit is a veterinary herbal hepatoprotective syrup formulated to support liver health, enhance hepatic detoxification, improve digestion, and stimulate appetite in dogs, cats, and other companion animals. Livfit combines time-validated Ayurvedic hepatoprotective botanicals — including Silymarin (Milk Thistle — Silybum marianum), Kutki (Picrorhiza kurroa), and Bhumi Amla (Phyllanthus niruri) — with synergistic herbal ingredients that together support the liver’s core functions: biotransformation of toxins and metabolic waste products, bile synthesis and secretion, albumin and clotting factor production, and glycogen/lipid metabolic regulation. Livfit is particularly indicated during periods of hepatic stress: prolonged antibiotic or NSAID use (drug-induced liver injury — DILI), post-illness hepatic recovery, hepatic lipidosis (especially in cats), chronic liver disease, and nutritional debilitation. Administer as directed by a licensed veterinarian.
Key Active Botanicals & Mechanisms of Action
-
Silymarin — Milk Thistle (Silybum marianum) seed extract (principal hepatoprotective component): Silymarin is a polyphenolic flavonolignan complex (principal bioactive: Silybin A and B — diastereomeric 2,3-dihydro-3-(4-hydroxy-3-methoxyphenyl)-2-(hydroxymethyl)-1,4-benzodioxin-6-yl flavonolignans, comprising ~50–60% of Silymarin by weight; minor flavonolignans: Silychristin, Silydianin, Isosilybin A and B) extracted from Silybum marianum seeds; hepatoprotective mechanisms: (1) Free radical scavenging and lipid peroxidation inhibition — Silybin directly scavenges reactive oxygen species (ROS: superoxide anion O2•−, hydroxyl radical HO•, peroxyl radical ROO•, and singlet oxygen 1O2) via electron donation from the electron-rich catechol B-ring of the flavonolignan scaffold; hepatocyte oxidative stress — arising from CYP450-mediated bioactivation of hepatotoxins (paracetamol/acetaminophen → N-acetyl-p-benzoquinone imine NAPQI by CYP2E1; aflatoxin B1 → AFB1-8,9-epoxide by CYP3A4/CYP1A2; CCl4 → CCl3• radical by CYP2E1), chronic alcohol metabolism (NADH/NAD+ redox imbalance → mitochondrial dysfunction), and inflammatory cytokine-mediated Kupffer cell NADPH oxidase (NOX2) activation → hepatocellular superoxide burst — drives lipid peroxidation of polyunsaturated fatty acids (PUFA) in hepatocyte plasma membrane phospholipids generating electrophilic 4-hydroxynonenal (4-HNE) and malondialdehyde (MDA) as cytotoxic lipid peroxidation end-products that form protein adducts with hepatocellular enzymes and structural proteins; Silybin intercepts and terminates the lipid peroxidation propagation chain by scavenging propagating peroxyl radicals (ROO•) before they abstract hydrogen from adjacent PUFA to initiate a new peroxidation chain; (2) Upregulation of endogenous hepatic antioxidant defences — Silybin activates the Nrf2 (nuclear factor erythroid 2-related factor 2) transcription factor pathway: cytoplasmic Nrf2 is normally sequestered by Keap1 (Kelch-like ECH-associated protein 1) — a Cullin3-based E3 ubiquitin ligase adaptor that continuously polyubiquitinates Nrf2 → 26S proteasomal degradation; Silybin and other electrophilic/pro-oxidant molecules modify critical cysteine thiols (Cys273, Cys288, Cys151) on Keap1 → conformational change in Keap1 → disruption of Keap1-Cullin3 interaction → Nrf2 escape from ubiquitination → nuclear translocation of Nrf2 → heterodimerisation with sMaf proteins and binding to Antioxidant Response Elements (AREs — consensus sequence 5’-TGAC/GnnnGC-3’) in the promoter regions of cytoprotective genes → transcriptional upregulation of: glutamate-cysteine ligase (GCL — catalytic and modifier subunits GCLc/GCLm — rate-limiting enzyme for GSH synthesis from glutamate + cysteine), glutathione S-transferases (GSTs — conjugate electrophilic toxin metabolites with GSH for biliary excretion), heme oxygenase-1 (HO-1 — catabolises pro-oxidant heme to cytoprotective biliverdin + CO + Fe2+ released for ferritin sequestration), NAD(P)H quinone oxidoreductase 1 (NQO1 — 2-electron reductase that detoxifies quinone electrophiles), thioredoxin reductase (TrxR — maintains thioredoxin in reduced form for ROS detoxification), and superoxide dismutase (SOD1/2); (3) Hepatocyte membrane stabilisation and hepatotoxin uptake inhibition — Silybin competitively inhibits the organic anion transport system on the hepatocyte sinusoidal membrane used by phalloidin (Amanita phalloides — death cap mushroom amatoxin), α-amanitin, and other hepatotoxins to enter hepatocytes — reducing toxin-induced hepatocellular necrosis; Silybin also inhibits LPS-stimulated Kupffer cell activation → reduced Kupffer cell-derived TNF-α and ROS production → reduced inflammatory hepatocellular injury; (4) Hepatocyte regeneration stimulation — Silybin stimulates RNA polymerase I (Pol I) activity specifically in non-neoplastic hepatocytes → increased ribosomal RNA (rRNA 28S, 18S, 5.8S) transcription at RNA Pol I-dedicated rDNA gene clusters in the nucleolus → enhanced ribosome biogenesis → increased translational capacity → accelerated hepatocyte protein synthesis and hepatocellular regeneration; (5) Anti-fibrotic hepatic activity — Silybin inhibits TGF-β-mediated transcriptional activation of hepatic stellate cells (HSCs — activated by TGF-β1 via Smad2/3 phosphorylation → α-SMA expression → myofibroblast transdifferentiation → collagen I/III/IV and fibronectin ECM deposition → hepatic fibrosis progression); Silybin inhibits Smad3 nuclear translocation and upregulates MMP-2/9 (matrix metalloproteinases) that degrade excess collagen ECM, collectively retarding fibrogenesis
-
Kutki — Picrorhiza kurroa root (Kutkin glycosides — Picroside I, II, III and Kutkoside): Picrorhiza kurroa is an Ayurvedic bitter tonic herb from the Himalayan region; principal bioactives are Kutkin (an equal molar mixture of Picroside I and Kutkoside — iridoid glycosides) and Picroside II and III; hepatoprotective mechanisms: (1) Anti-inflammatory hepatoprotection via NF-κB inhibition — Kutkin suppresses IκB kinase (IKKβ) activation, preventing IκBα phosphorylation and degradation → retaining NF-κB (p65/p50 heterodimer) in the cytoplasm → reduced NF-κB-driven transcription of pro-inflammatory hepatic genes (TNF-α, IL-1β, IL-6, COX-2, iNOS); (2) Choleretic activity — Picrorhiza kurroa stimulates bile flow (choleresis) and bile acid secretion → enhanced biliary excretion of conjugated toxins and bilirubin → reduced hepatic toxin accumulation and improved fat-soluble vitamin absorption; (3) Hepatocyte regeneration — Picroside II stimulates hepatocyte proliferation; (4) Antioxidant activity — Kutkin upregulates hepatic catalase, SOD, and GPx activities
-
Bhumi Amla — Phyllanthus niruri (Chanca Piedra — stonebreaker) aerial parts: Phyllanthus niruri is an Ayurvedic hepatoprotective herb with a broad phytochemical profile including lignans (Phyllanthin, Hypophyllanthin), flavonoids (Quercetin, Rutin), ellagitannins (Geraniin, Corilagin), and alkaloids (Phyllanthusine); hepatoprotective mechanisms: (1) CYP2E1 inhibition — Phyllanthin inhibits CYP2E1 (the primary CYP450 isoform responsible for paracetamol → NAPQI bioactivation and ethanol oxidation → acetaldehyde → ROS), reducing CYP2E1-mediated hepatotoxin bioactivation and oxidative hepatocellular injury; (2) Direct antioxidant activity — Quercetin and Rutin are potent radical-scavenging flavonoids; (3) Anti-fibrotic activity — Geraniin (ellagitannin) inhibits TGF-β/Smad hepatic stellate cell activation; (4) Antiviral hepatoprotection — Phyllanthus niruri lignans inhibit hepatitis B virus (HBV) DNA polymerase and surface antigen (HBsAg) production — relevant for hepatitis-associated liver disease context
Indications
- Drug-induced liver injury (DILI) — hepatic support during or after prolonged antibiotic therapy (tetracyclines, fluoroquinolones), NSAID use (Carprofen, Meloxicam — hepatic glucuronidation and CYP metabolism), antifungal therapy (Ketoconazole, Itraconazole — azole hepatotoxicity), chemotherapy, or anticonvulsant use (Phenobarbitone — CYP induction → hepatic enzyme elevation)
- Hepatic lipidosis (fatty liver disease) — particularly in obese cats with anorexia-triggered hepatic lipid accumulation (hepatic lipidosis is the most common severe liver disease in cats)
- Chronic hepatitis and liver disease — adjunctive hepatoprotective support in dogs and cats with chronic active hepatitis, copper-associated hepatopathy (Bedlington Terrier, Labrador, Dalmatian), or idiopathic hepatic fibrosis
- Post-illness hepatic recovery — liver support following systemic infections (leptospirosis, ehrlichiosis, parvoviral enteritis with hepatic involvement), pancreatitis-associated hepatic injury
- Anorexia and hepatic encephalopathy support — improving appetite and reducing hepatic toxin load (ammonia) in dogs and cats with reduced hepatic function
- Routine hepatic maintenance — prophylactic liver support in dogs and cats on long-term medications or with breed-specific hepatic predispositions
Dosage & Administration
- Shake well before each use
- Administer orally by syringe directly into the mouth or mix into food
- Dose based on body weight, species, and clinical indication as directed by a veterinarian
- Can be used short-term (acute hepatic support) or long-term (chronic liver disease maintenance) as directed by veterinarian
Safety Information
- For veterinary use — use under veterinary supervision
- Very well tolerated; herbal hepatoprotective ingredients have a favourable safety profile at recommended doses
- Confirm from Bionex Livfit product label whether specific herbal ingredients or concentrations differ from the above — formulation may vary
- Use with caution in animals with confirmed bile duct obstruction — choleretic herbs (Picrorhiza kurroa) increase bile flow and may be contraindicated in complete biliary obstruction
- Shake well before use; store in a cool, dry place away from direct sunlight; keep tightly capped after use