Wellcon Caniflam-S 2.5mg Tablets for Dogs & Cats | Meloxicam + Serratiopeptidase | COX-2 Preferential NSAID & Proteolytic Anti-Inflammatory | Pain, Arthritis & Post-Operative Relief

SCHEDULE H PRESCRIPTION VETERINARY MEDICINE — Not to be sold by retail without the prescription of a Registered Veterinary Practitioner. For veterinary use only. Not for human use. CRITICAL GI SAFETY WARNING: NSAIDs (including Meloxicam) can cause serious gastrointestinal adverse effects in dogs and cats including GI ulceration, haemorrhage, and perforation — do not administer on an empty stomach; always give with food; do not use concurrently with corticosteroids (glucocorticoids) or other NSAIDs (NSAID-NSAID or NSAID-corticosteroid combinations dramatically increase GI ulceration risk via additive COX-1 inhibition + glucocorticoid-mediated reduction of mucosal prostaglandin synthesis); a minimum 5–7 day washout period is required when switching between NSAIDs or from corticosteroids to NSAIDs. RENAL WARNING: NSAIDs can cause acute kidney injury (AKI) in dehydrated, hypotensive, or renally compromised animals — ensure adequate hydration before and during NSAID therapy; do not use in animals with pre-existing renal impairment, hypovolaemia, or cardiac failure (prostaglandin-dependent renal perfusion). CATS: Meloxicam in cats requires extreme care — cats have severely limited glucuronidation capacity (deficient UGT1A6 and UGT1A9 hepatic UDP-glucuronosyltransferase enzymes) causing markedly prolonged Meloxicam half-life and narrow therapeutic index; use strictly as directed and never exceed recommended dose or frequency. Perform baseline renal function assessment (creatinine, BUN, SDMA, urinalysis) before initiating NSAID therapy and monitor during long-term use. Keep out of reach of children. Store in a cool, dry place below 30°C.

Wellcon Caniflam-S 2.5mg Tablets for Dogs & Cats | Meloxicam + Serratiopeptidase | COX-2 Preferential NSAID & Proteolytic Anti-Inflammatory | Pain, Arthritis & Post-Operative Relief

Wellcon Caniflam-S 2.5mg is a Schedule H prescription veterinary combination anti-inflammatory tablet containing Meloxicam (a COX-2 preferential NSAID) and Serratiopeptidase (a bacterial-origin serine protease with fibrinolytic, anti-inflammatory, and analgesic properties) for dogs and cats. The combination synergistically addresses the two principal components of the inflammatory response: (1) Meloxicam targets the cyclooxygenase (COX) enzyme pathway to suppress prostaglandin synthesis — the primary mediator of inflammatory pain, pyrexia, and vasodilation; (2) Serratiopeptidase targets the proteinaceous debris and fibrin deposits of the inflammatory exudate, reducing oedema and swelling through enzymatic digestion of non-viable inflammatory substrates. The 2.5mg Meloxicam dose is appropriate for small dogs and cats as prescribed by the veterinarian. Administer strictly as directed under veterinary prescription and supervision.

Active Ingredients & Mechanisms of Action

• Meloxicam — COX-2 preferential NSAID (non-selective cyclooxygenase inhibitor with relative selectivity for COX-2 over COX-1 at therapeutic doses): Meloxicam is an oxicam-class NSAID (4-hydroxy-2-methyl-N-(5-methyl-2-thiazolyl)-2H-1,2-benzothiazine-3-carboxamide-1,1-dioxide — the thiazolyl oxicam) that inhibits cyclooxygenase (COX — prostaglandin H2 synthase — PGHS) enzymes, blocking the committed step in prostanoid biosynthesis: arachidonic acid (AA — 20:4n-6) → PGG2 (via COX reaction — cyclisation and peroxidation) → PGH2 (via hydroperoxidase reaction) → tissue-specific prostanoid products (PGE2, PGI2, TXA2, PGD2, PGF2α); COX enzyme isoforms and their distinct physiological roles:
  • COX-1 (PGHS-1 — constitutively expressed): the homeostatic COX isoform expressed constitutively in most tissues; key physiological COX-1-derived prostanoids: (a) gastric mucosal PGE2 and PGI2 — stimulate mucus (MUC5AC glycoprotein) and bicarbonate (via cAMP/PKA-activated CFTR Cl− channel and apical HCO3− secretion) secretion by surface mucous cells, increase mucosal blood flow (submucosal arteriolar vasodilation), and stimulate mucosal cell proliferation — collectively maintaining the gastric mucosal barrier against luminal HCl; COX-1 inhibition removes this gastroprotective PGE2/PGI2 → increased mucosal vulnerability to acid-peptic injury → the primary mechanism of NSAID-induced GI ulceration; (b) renal afferent arteriolar PGE2 and PGI2 — vasodilatory prostaglandins that maintain renal cortical blood flow and GFR under conditions of reduced effective circulating volume (dehydration, cardiac failure, hypovolaemia) by counteracting angiotensin II and sympathetic nervous system-mediated afferent arteriolar vasoconstriction; COX-1 (and COX-2, which is also constitutively expressed in the kidney) inhibition in volume-depleted animals removes this compensatory vasodilation → unopposed afferent arteriolar constriction → reduced RBF and GFR → NSAID-induced AKI; (c) platelet TXA2 (thromboxane A2) — synthesised by COX-1 in platelets (platelets are anucleate and cannot synthesise new COX-1 — aspirin’s irreversible COX-1 acetylation produces permanent platelet inactivation for the platelet lifespan — 7–10 days; reversible NSAIDs like Meloxicam have a shorter antiplatelet effect lasting only for the drug’s plasma half-life); TXA2 is a potent platelet aggregation agonist and vasoconstrictor — COX-1 inhibition reduces TXA2 and impairs primary haemostasis
  • COX-2 (PGHS-2 — inducible): the inflammatory COX isoform; COX-2 expression is low or absent in most tissues at baseline but is rapidly and powerfully induced (within 1–6 hours) by pro-inflammatory stimuli: IL-1β, TNF-α, LPS (lipopolysaccharide), phorbol esters, and growth factors; induction is mediated primarily by NF-κB (RelA/p65 homodimer and RelA/p50 heterodimer — liberated from IκBα inhibitor by IKKβ-mediated IκBα phosphorylation and proteasomal degradation → NF-κB nuclear translocation → binding to κB response elements in the COX-2 promoter → transcriptional activation) and AP-1 (activator protein 1 — c-Fos/c-Jun heterodimer activated by MAP kinases ERK1/2, p38 MAPK, and JNK); COX-2-derived PGE2 at the site of tissue injury: (a) directly sensitises nociceptor peripheral terminals (Aδ and C fibres) by activating EP1 and EP4 PGE2 receptors (Gq-coupled → IP3/DAG/PKC → TRPV1 potentiation; Gs-coupled → cAMP/PKA → phosphorylation of Nav1.8 and TRPV1 lowering activation threshold) → peripheral sensitisation and hyperalgesia; (b) acts centrally in the spinal dorsal horn (COX-2 is also induced in spinal cord microglia and astrocytes by peripheral inflammation → spinal PGE2 → EP2 receptor activation on inhibitory interneurons → reduced glycine and GABA inhibitory tone → central sensitisation and allodynia); (c) acts on the hypothalamic pre-optic area (OVLT/MnPO → COX-2-derived PGE2 → EP3 receptor on thermosensitive neurones → raised thermoregulatory setpoint → fever); COX-2-derived PGI2 (prostacyclin) from endothelial cells: vasodilation and increased vascular permeability → oedema formation at inflammatory site; Meloxicam’s COX-2 preferential selectivity (COX-2/COX-1 IC50 ratio ~0.08 — i.e., Meloxicam is approximately 10–25× more potent at COX-2 than COX-1 in canine whole blood assays) provides better GI and platelet safety vs non-selective NSAIDs (aspirin, phenylbutazone) while maintaining effective anti-inflammatory and analgesic efficacy; note: ‘preferential’ (not ‘selective’) — Meloxicam is NOT fully COX-2 selective like Celecoxib or Coxibs — it retains clinically relevant COX-1 inhibitory activity at higher doses and the GI/renal risks described above apply; Meloxicam pharmacokinetics in dogs: oral bioavailability ~97%; Tmax ~7.5h; half-life ~24h (allows once-daily dosing); highly protein-bound (~97% to albumin); hepatic metabolism via CYP2C9-equivalent enzymes to pharmacologically inactive 5’-hydroxymethyl and 5’-carboxymethyl metabolites; biliary and renal excretion; Meloxicam in cats: oral bioavailability ~90%; Tmax ~1.3h; half-life significantly longer (~15–24h in cats vs dogs) due to severely limited feline glucuronidation (UGT1A6/UGT1A9 enzyme deficiency in cats — cats also rely on CYP-mediated oxidative metabolism but with lower capacity); narrow therapeutic index in cats requires strict dose adherence
• Serratiopeptidase (Serrapeptase — Serratia peptidase) — bacterial serine metalloprotease with fibrinolytic, anti-oedematous, and analgesic properties: Serratiopeptidase is a zinc-dependent serine endoprotease originally isolated from the non-pathogenic gram-negative enterobacterium Serratia marcescens E-15 (isolated from the intestine of the Japanese silkworm Bombyx mori where it dissolves the cocoon walls; the enzyme is now produced by fermentation of Serratia sp. or Bacillus licheniformis for pharmaceutical use); mechanism of action in inflammation: (a) fibrinolysis — Serratiopeptidase selectively hydrolyses fibrin and fibrinogen (cleaving at hydrophobic amino acid residues — particularly leucyl and valyl peptide bonds) in the inflammatory exudate; fibrin deposition in the post-injury inflammatory exudate is the primary structural component of oedema (fibrin gel traps fluid and cells ’locking’ them in the interstitial space); by digesting fibrin, Serratiopeptidase reduces oedema volume and allows resorption of exudate fluid into the lymphatic and venous capillaries → reduces post-operative and post-traumatic swelling (this is distinct from Meloxicam’s anti-inflammatory mechanism which reduces new oedema formation by suppressing PGI2/PGE2-driven vascular permeability — Serratiopeptidase addresses established fibrin-bound oedema while Meloxicam prevents further oedema); (b) bradykinin degradation — Serratiopeptidase cleaves the nonapeptide bradykinin (Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg — B2 receptor agonist; kallikrein cleaves kininogen → bradykinin → B2 receptor on nociceptors → Gq → IP3 → Ca2+ release → BK-mediated nociceptor sensitisation; also acts on vascular endothelium → NO/PGI2 release → vasodilation and pain); bradykinin is one of the most potent endogenous pain-producing molecules; Serratiopeptidase’s bradykinin degradation provides complementary analgesic activity alongside Meloxicam’s COX-2/PGE2 inhibition; (c) inhibition of pro-inflammatory cytokine release — Serratiopeptidase reduces IL-1β, TNF-α, and IL-6 release from activated macrophages by partially inhibiting NF-κB activation (mechanism not fully elucidated); (d) mucus thinning — Serratiopeptidase cleaves mucus glycoproteins reducing viscosity, which may improve resolution of mucopurulent exudates in respiratory and sinus conditions; (e) biofilm disruption — emerging evidence suggests Serratiopeptidase can disrupt bacterial biofilm matrices (by hydrolysing biofilm structural proteins) enhancing antibiotic penetration — potentially relevant in chronic infected wound and periodontal contexts in veterinary medicine; pharmacokinetics: Serratiopeptidase is an oral enzyme preparation that relies on enteric coating to survive gastric acid pH and reach the duodenum for absorption; absorbed via intestinal transcytosis across enterocytes (the intact protease is transported into the circulation where it binds to plasma α2-macroglobulin which acts as an enzyme carrier and protects Serratiopeptidase from protease inhibitors, allowing the enzyme to reach inflammatory sites)

Indications

• Osteoarthritis (OA) and degenerative joint disease (DJD) in dogs and cats — chronic synovial joint inflammation with cartilage degradation, subchondral bone remodelling, and periarticular osteophyte formation
• Post-operative pain and swelling management — following orthopaedic surgery (cruciate repair, fracture fixation, TPLO), soft tissue surgery, and dental extractions
• Soft tissue injuries — sprains, strains, traumatic myositis, bruising, and haematomas
• Musculoskeletal inflammatory conditions — spondylosis, intervertebral disc disease (IVDD) pain management
• Perioperative analgesia — as part of multimodal pain management protocols alongside opioids and local anaesthetics

Dosage & Administration

• As directed by a Registered Veterinary Practitioner based on body weight, species, and clinical indication
• Always administer with food to reduce GI adverse effects
• Do not exceed prescribed dose or frequency; do not use for longer than prescribed without veterinary re-evaluation
• Perform baseline renal and hepatic function assessment before initiation; monitor during long-term use

Safety & Contraindications

• Do not use with corticosteroids or other NSAIDs (washout 5–7 days required when switching)
• Do not use in dehydrated, hypotensive, or hypovolaemic animals
• Do not use in animals with pre-existing renal impairment, hepatic disease, GI ulceration, or coagulopathy
• Do not use in pregnant, lactating, or breeding animals without veterinary assessment
• Cats: do not use without strict veterinary prescription and dose calculation — markedly narrow therapeutic index due to UGT enzyme deficiency
• Store below 30°C in a cool, dry place; keep out of reach of children