Alavnbio Ketop Eye Drop for Dogs & Cats | Moxifloxacin 0.5% + Ketorolac Tromethamine 0.5% Ophthalmic Solution | Antibiotic & Anti-inflammatory | Sterile Rx | 10ml

PRESCRIPTION VETERINARY MEDICINE — For veterinary (external/ophthalmic) use only. Not for human use. Must be prescribed and dispensed by or under the supervision of a licensed veterinarian. FOR OPHTHALMIC USE ONLY — Do not inject or ingest. Do not use if the solution is cloudy or discoloured. Do not touch the dropper tip to the eye, eyelid, or any surface — contamination of the dropper tip will contaminate the entire bottle. Keep out of reach of children. Store in a cool, dry place below 25°C. Protect from light. Do not freeze.

Alavnbio Ketop® Eye Drop for Dogs & Cats | Moxifloxacin 0.5% + Ketorolac Tromethamine 0.5% Ophthalmic Solution | Antibiotic & Anti-inflammatory | Sterile Rx | 10ml

Alavnbio Ketop is a prescription sterile veterinary ophthalmic solution for dogs and cats combining two complementary active ingredients: Moxifloxacin Hydrochloride IP 0.5% w/v (4th-generation fluoroquinolone broad-spectrum bactericidal antibiotic) and Ketorolac Tromethamine IP 0.5% w/v (NSAID — non-selective COX-1 and COX-2 inhibitor). This dual-action combination addresses two of the three key pathophysiological components of ocular disease simultaneously — bacterial infection (Moxifloxacin) and prostaglandin-mediated ocular inflammation and pain (Ketorolac) — making Ketop particularly suitable for bacterial conjunctivitis with significant conjunctival hyperaemia and chemosis, post-surgical ocular inflammation, and infectious keratitis with associated anterior uveitis. Administered as directed by a licensed veterinarian.

Active Ingredients & Mechanisms of Action

• Moxifloxacin Hydrochloride IP 0.5% w/v — 4th-generation fluoroquinolone bactericidal antibiotic (DNA gyrase & topoisomerase IV dual inhibitor): Moxifloxacin is an 8-methoxy-fluoroquinolone (the 8-methoxy substitution on the quinolone scaffold is the key structural feature distinguishing 4th-generation from 3rd-generation fluoroquinolones — it enhances activity against anaerobes and Gram-positive organisms by reducing single-step resistance mutation frequency at GyrA/GyrB and ParC/ParE); mechanism: fluoroquinolones target two essential bacterial type II topoisomerases — DNA gyrase (topoisomerase II — a tetrameric GyrA2/GyrB2 enzyme) and topoisomerase IV (a tetrameric ParC2/ParE2 enzyme); both enzymes are essential for bacterial DNA replication and cell division: DNA gyrase introduces negative supercoils ahead of the replication fork (removing positive torsional stress generated by replication fork progression) via a transient double-strand break (DSB) → strand passage → religation mechanism (ATP-dependent); topoisomerase IV decatenates interlinked daughter chromosomes at the completion of replication, allowing chromosome segregation into daughter cells; Moxifloxacin intercalates into the ternary complex of enzyme–DNA–Moxifloxacin (the “cleavage complex”) formed when the topoisomerase creates the transient DSB intermediate, stabilising the cleavage complex and preventing enzyme-mediated DSB religation → accumulation of lethal DSBs in bacterial chromosomal DNA → SOS stress response activation → RecA-mediated filamentation and cell elongation → bactericidal DNA fragmentation and cell death (distinct from the bacteriostatic mechanism of most other antibiotic classes); in Gram-positive bacteria (Staphylococcus, Streptococcus), topoisomerase IV (ParC/ParE) is the primary Moxifloxacin target; in Gram-negative bacteria (Pseudomonas, Haemophilus, Enterobacteriaceae), DNA gyrase (GyrA/GyrB) is the primary target; the 4th-generation structural features of Moxifloxacin (8-methoxy group + C7 diazabicyclononyl substituent) provide: (a) dual-target inhibition with lower frequency of single-step resistance (requires simultaneous mutations in both GyrA/ParC to achieve high-level resistance); (b) enhanced Gram-positive activity (including MRSA for systemic Moxifloxacin — clinical relevance for topical ophthalmic use may be limited); (c) enhanced anaerobic activity (8-methoxy substitution reduces oxygen requirement for bactericidal activity); (d) excellent ocular bioavailability — 0.5% Moxifloxacin ophthalmic solution achieves aqueous humour concentrations well above the MIC90 for common ocular pathogens (Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus pneumoniae, Haemophilus influenzae, Pseudomonas aeruginosa) following topical application; ocular bacterial spectrum: excellent Gram-positive coverage (Staphylococcus aureus including many MRSA strains, Staphylococcus epidermidis, Streptococcus pneumoniae, Streptococcus pyogenes, Corynebacterium spp.), Gram-negative coverage (Haemophilus influenzae, Pseudomonas aeruginosa, Moraxella catarrhalis, Haemophilus aegyptius — Koch-Weeks bacillus causing acute contagious conjunctivitis), atypical organisms (Chlamydia spp. — important in feline chlamydial conjunctivitis); self-preserved: Moxifloxacin 0.5% ophthalmic solution is inherently self-preserved (the acidic pH of the formulation provides preservative activity), eliminating the need for benzalkonium chloride (BAK) preservative — avoiding BAK-related corneal epithelial and goblet cell toxicity that is a recognised adverse effect of BAK-preserved ophthalmic solutions (BAK disrupts corneal epithelial tight junctions, causes apoptosis of superficial corneal epithelial cells, and reduces goblet cell density with chronic use)
• Ketorolac Tromethamine IP 0.5% w/v — Non-selective COX-1 and COX-2 inhibitor (NSAID — ophthalmic): Ketorolac is a pyrrolo-pyrrole class non-selective NSAID that inhibits both COX-1 (prostaglandin H synthase-1 — PGHS-1) and COX-2 (PGHS-2) by competing with arachidonic acid (AA) for the substrate-binding channel (cyclooxygenase channel) of the COX active site, preventing the bis-dioxygenase reaction that converts AA to prostaglandin G2 (PGG2) → PGH2 (prostaglandin H2 — the unstable common PG precursor); COX pathway in ocular inflammation: tissue injury, infection, or surgical trauma → phospholipase A2 (PLA2 — specifically cytosolic cPLA2α activated by Ca2+/MAP kinase signalling) releases AA from membrane phosphatidylcholine and phosphatidylethanolamine → COX-1 (constitutive, present in most tissues — maintains physiological PG production) and COX-2 (inducible by inflammatory cytokines: IL-1β, TNF-α, LPS → NF-κB → COX-2 gene transcription) convert AA to PGH2 → cell-specific prostaglandin synthases convert PGH2 to: PGE2 (prostaglandin E2 — major pro-inflammatory ocular prostaglandin — binds EP1/EP2/EP3/EP4 GPCRs on uveal blood vessels, ciliary body, and iris sphincter → vasodilation and increased vascular permeability of uveal and conjunctival vasculature → conjunctival hyperaemia, chemosis, and aqueous humour protein exudation — the “flare” of uveitis; EP2/EP4 on ciliary body → increased aqueous humour production and trabecular meshwork relaxation → transient IOP changes; EP3 on iris sphincter smooth muscle → miosis; PGE2 also sensitises corneal and uveal sensory C-fibre nociceptors → ocular pain, photophobia, blepharospasm), PGI2 (prostacyclin — IP receptor-mediated vasodilation and platelet anti-aggregation in uveal vasculature), and TXA2 (thromboxane A2 — TP receptor-mediated platelet aggregation and vasoconstriction); COX-1-derived PGE2 and TXA2 also drive intraoperative miosis during cataract and corneal surgery — a major problem in ophthalmic surgery as intraoperative miosis limits surgical access to the lens and anterior segment; topical Ketorolac 0.5% inhibits COX-1 and COX-2 in the conjunctiva, corneal stroma, uveal tract, and aqueous humour, reducing: (a) conjunctival hyperaemia, chemosis, and ocular pain — symptomatic relief in conjunctivitis and anterior uveitis; (b) miosis in peri-operative ophthalmic procedures; (c) cystoid macular oedema (CMO) post-cataract surgery in dogs — an uncommon but recognised post-operative complication; complementarity with Moxifloxacin: bacterial infection and inflammatory response are co-occurring processes in infectious keratitis and bacterial conjunctivitis — Moxifloxacin eliminates the causative bacteria while Ketorolac reduces the prostaglandin-mediated inflammatory sequelae (conjunctival hyperaemia, chemosis, anterior chamber flare, miosis, ocular pain) simultaneously; single-bottle combination simplifies the treatment regimen and improves owner compliance vs separate antibiotic + NSAID ophthalmic bottles

Indications

• Bacterial conjunctivitis in dogs and cats — Staphylococcal, Streptococcal, Pseudomonal, and Moraxella ocular bacterial infections with associated conjunctival inflammation
• Feline chlamydial conjunctivitis (Chlamydophila felis) — Moxifloxacin provides antichlamydial activity; for systemic chlamydial infections, concurrent oral Doxycycline is recommended
• Bacterial keratitis — corneal ulcer with secondary bacterial infection and associated anterior uveitis
• Post-operative ocular inflammation — following cataract surgery, corneal grafting, or anterior segment surgery in dogs and cats
• Anterior uveitis — adjunctive anti-inflammatory ophthalmic therapy for prostaglandin-mediated uveal inflammation (use under veterinary supervision — uveitis has multiple causes including infectious, immune-mediated, and neoplastic that require specific systemic treatment)
• Ocular surface disease with secondary bacterial involvement and inflammatory component

Administration

• Instil as directed by veterinarian — typically 1–2 drops into the affected eye(s) as prescribed
• Wash hands before handling; do not touch the dropper tip to the eye, eyelid, or any surface — replace cap immediately after use
• If using multiple ophthalmic preparations, allow at least 5 minutes between instillations to prevent dilution and washout of the first drop
• In cats, gently restrain and instil from behind to reduce blink reflex; apply gentle digital pressure on the nasolacrimal duct (medial canthus) after instillation to reduce systemic absorption via nasolacrimal drainage
• Complete the full prescribed course even if ocular signs resolve

Contraindications & Safety

• For ophthalmic (external) use only — not for injection or oral use; not for human use
• Do not use if the cornea has a full-thickness (perforated) ulcer — topical NSAIDs (Ketorolac) may impair corneal epithelial healing and are contraindicated on perforated corneas; confirm corneal integrity before use
• Use with caution in animals with known bleeding disorders or those receiving systemic anticoagulant therapy — COX-1 inhibition reduces TXA2-mediated platelet aggregation; systemic absorption of topical Ketorolac is low but should be considered in small-bodied cats
• Do not use concurrently with topical corticosteroid eye drops without veterinary guidance — combined NSAID + corticosteroid topical ophthalmic use increases the risk of corneal melting (keratomalacia) by dual inhibition of corneal protective mechanisms
• Store below 25°C; protect from light; do not freeze; discard opened bottle as directed on label (typically within 4 weeks of opening)