Alembic Dexaflox Eye Drops for Dogs & Cats | Moxifloxacin 0.5% + Dexamethasone 0.1% Ophthalmic Solution | Antibiotic & Corticosteroid | Sterile Rx | 10ml

PRESCRIPTION VETERINARY MEDICINE — For veterinary (ophthalmic/external) 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. CRITICAL CONTRAINDICATION: DO NOT USE IN EYES WITH CORNEAL ULCERS, ACTIVE VIRAL OCULAR INFECTIONS (herpesvirus keratitis), OR FUNGAL OCULAR INFECTIONS — corticosteroid (Dexamethasone) immunosuppression markedly worsens corneal ulcers and viral/fungal infections, risking corneal perforation. A fluorescein stain test (Seidel test) must be performed by a veterinarian to confirm corneal integrity before prescribing. Do not touch the dropper tip to the eye, eyelid, or any surface. Keep out of reach of children. Store in a cool, dry place below 25°C. Protect from light. Do not freeze.

Alembic Dexaflox Eye Drops for Dogs & Cats | Moxifloxacin 0.5% + Dexamethasone 0.1% Ophthalmic Solution | Antibiotic & Corticosteroid | Sterile Rx | 10ml

Alembic Dexaflox is a prescription sterile veterinary ophthalmic solution for dogs and cats combining Moxifloxacin Hydrochloride 0.5% w/v (4th-generation fluoroquinolone bactericidal antibiotic) with Dexamethasone 0.1% w/v (synthetic halogenated glucocorticoid — the most potent topical ocular corticosteroid in standard clinical use). This combination provides simultaneous bactericidal elimination of ocular bacterial pathogens (Moxifloxacin) and broad upstream suppression of the entire prostaglandin, leukotriene, and cytokine-mediated ocular inflammatory cascade (Dexamethasone) — making Dexaflox appropriate for bacterial ocular infections with significant inflammatory component. Dexamethasone’s corticosteroid mechanism provides more comprehensive anti-inflammatory activity than ophthalmic NSAIDs (which only block the COX arm of the arachidonic acid cascade), but carries more significant risks: it is absolutely contraindicated in corneal ulceration and viral/fungal ocular infections. A thorough veterinary ophthalmic examination including fluorescein staining of the cornea is mandatory before initiating Dexaflox therapy. Administered as directed by a licensed veterinarian.

Active Ingredients & Mechanisms of Action

• Moxifloxacin Hydrochloride 0.5% w/v — 4th-generation fluoroquinolone bactericidal antibiotic (DNA gyrase & topoisomerase IV dual inhibitor): Moxifloxacin is an 8-methoxyfluoroquinolone that inhibits two essential bacterial type II topoisomerases: DNA gyrase (GyrA2/GyrB2 tetramer — introduces negative supercoils ahead of the replication fork via transient double-strand break/strand passage/religation) and topoisomerase IV (ParC2/ParE2 tetramer — decatenates interlinked daughter chromosomes post-replication); Moxifloxacin intercalates into the ternary cleavage complex (enzyme–DNA–drug) formed when the topoisomerase creates the transient double-strand break intermediate, stabilising the cleavage complex and preventing religation → accumulation of lethal irreparable chromosomal double-strand breaks → SOS response → RecA-mediated filamentation → bactericidal cell death; the 8-methoxy substitution of 4th-generation fluoroquinolones confers: (a) dual-target simultaneous inhibition of gyrase + TopoIV → lower single-step resistance mutation frequency (requires simultaneous mutations at GyrA Ser83 and ParC Ser80 for high-level resistance); (b) enhanced Gram-positive activity (Staphylococcus aureus, Streptococcus pneumoniae, Staphylococcus epidermidis); (c) enhanced anaerobic activity; broad ocular bacterial spectrum: Gram-positive (Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus pneumoniae, Streptococcus pyogenes, Corynebacterium spp.), Gram-negative (Haemophilus influenzae, Pseudomonas aeruginosa, Moraxella catarrhalis), atypical (Chlamydophila felis — important cause of feline conjunctivitis); achieves aqueous humour concentrations above MIC90 for common ocular pathogens following topical instillation
• Dexamethasone 0.1% w/v — Synthetic halogenated glucocorticoid (GR agonist — upstream PLA2 inhibitor via Annexin A1/Lipocortin-1 induction and direct NF-κB/AP-1 transcriptional repression): Dexamethasone is a synthetic fluorinated glucocorticoid (9α-fluoro-16α-methyl prednisolone derivative — the 9α-fluoro and 16α-methyl substitutions markedly increase glucocorticoid receptor (GR) binding affinity and anti-inflammatory potency while reducing mineralocorticoid activity vs hydrocortisone); as the most potent standard topical ophthalmic corticosteroid, Dexamethasone provides broader and more powerful anti-inflammatory activity than Ketorolac (NSAID) by acting upstream of both the COX (prostaglandin) and 5-LOX (leukotriene) branches of the arachidonic acid (AA) inflammatory cascade; mechanism: (1) Genomic/transactivation mechanism (slow onset, hours): Dexamethasone diffuses passively across the hydrophobic plasma membrane → binds the cytosolic glucocorticoid receptor (GRα — a 777-amino acid member of the nuclear receptor superfamily with N-terminal transactivation domain AF-1, central C4-type zinc finger DNA-binding domain — DBD, and C-terminal ligand-binding domain — LBD); unliganded GRα is maintained in the cytoplasm in an inactive chaperone complex with Hsp90 (heat shock protein 90 — maintains GR in a high-affinity ligand-binding conformation), Hsp70, Hsp40, and the co-chaperones FKBP51 and p23; Dexamethasone binding to the GR LBD → conformational change → dissociation of Hsp90/chaperone complex → GR homodimerisation via the DBD P-box zinc finger → nuclear translocation via importin-α/β-mediated nuclear import → binding of GR homodimer to palindromic Glucocorticoid Response Elements (GREs — consensus 5’-GGTACAnnnTGTTCT-3’) in the promoter regions of anti-inflammatory target genes → transcriptional upregulation of: Annexin A1 (Lipocortin-1 — an endogenous phospholipase A2 inhibitor that binds and sequesters membrane phospholipids, blocking cPLA2α-mediated release of arachidonic acid — the shared precursor of all pro-inflammatory prostanoids and leukotrienes → upstream simultaneous suppression of both COX/prostaglandin AND 5-LOX/leukotriene inflammatory arms), MAPK phosphatase-1 (MKP-1/DUSP1 — dephosphorylates and inactivates pro-inflammatory MAPKs: p38 MAPK and JNK → reduced AP-1-mediated COX-2 and cytokine gene transcription), and IκBα (IkappaB alpha — the endogenous NF-κB inhibitor that sequesters NF-κB p65/p50 in the cytoplasm → reduced NF-κB-mediated transcription of TNF-α, IL-1β, IL-6, COX-2, iNOS, and VCAM-1); (2) Non-genomic/transrepression mechanism (faster onset, minutes): liganded GR directly interacts with and inhibits the transcription factors NF-κB (p65 subunit) and AP-1 (c-Fos/c-Jun heterodimer) via protein–protein interaction (tethering mechanism) — this transrepression inhibits NF-κB- and AP-1-driven transcription of COX-2, TNF-α, IL-1β, IL-6, IL-8, and MMP genes without requiring GR–GRE DNA binding; ocular Dexamethasone effects: suppression of conjunctival and corneal stromal oedema (reduced VEGF-A and vascular permeability), reduced conjunctival hyperaemia and chemosis, suppression of anterior chamber flare and cells (uveitis), inhibition of fibrin formation in the anterior chamber, reduced cystoid macular oedema post-cataract surgery, suppression of corneal stromal vascularisation (neovascularisation) in chronic keratitis; why Dexamethasone > NSAID for ocular use: topical NSAIDs (Ketorolac) only inhibit COX enzymes → blocking prostaglandin synthesis only; Dexamethasone blocks AA release via Annexin A1/Lipocortin-1 upstream of both COX and 5-LOX → simultaneously suppresses prostaglandins (PGE2, PGI2, TXA2) AND leukotrienes (LTB4 — neutrophil chemotaxis; LTC4/D4/E4 — smooth muscle constriction, vascular permeability) AND inflammatory cytokines via transrepression; this broader suppression is more powerful but at the cost of more significant immunosuppressive adverse effects; critical adverse effects and risks of topical Dexamethasone: (a) Corneal ulcer worsening — Dexamethasone inhibits corneal epithelial proliferation and migration (suppresses keratinocyte growth factor — KGF/FGF-7 and EGF receptor signalling → impaired corneal epithelial wound healing), inhibits stromal fibroblast collagen synthesis, and reduces matrix metalloproteinase inhibitors (TIMPs) → stromal collagen degradation; concurrent bacterial superinfection of a corticosteroid-immunosuppressed ulcerated cornea by proteolytic Gram-negative bacteria (Pseudomonas, Proteus) produces rapid stromal keratolysis (“melting ulcer” — corneal melting) → corneal perforation and vision loss; this is the most serious risk of inappropriately using a corticosteroid eye drop in a dog or cat with a pre-existing corneal ulcer; (b) Viral keratitis exacerbation — Dexamethasone suppresses antiviral T-cell-mediated immunity → reactivation and exacerbation of latent feline herpesvirus-1 (FHV-1) stromal keratitis in cats; FHV-1 is the most common cause of feline keratitis and corticosteroid ophthalmic preparations are contraindicated in active or suspected FHV-1 keratitis; (c) Fungal keratitis exacerbation — similarly contraindicated in fungal ocular infections; (d) Elevated intraocular pressure (IOP) / ocular hypertension — topical glucocorticoids increase IOP in susceptible individuals via upregulation of MYOC (myocilin) gene expression in trabecular meshwork cells → increased aqueous humour outflow resistance → glaucoma; dogs with pre-existing primary or secondary glaucoma require IOP monitoring during corticosteroid ophthalmic therapy

Indications (confirmed cornea integrity required before use)

• Bacterial conjunctivitis with significant inflammatory component — Staphylococcal, Streptococcal, Pseudomonal, and Moraxella infections with conjunctival hyperaemia, chemosis, and discharge
• Bacterial keratitis WITHOUT corneal ulceration — superficial bacterial keratitis with stromal oedema and vascularisation in the absence of corneal epithelial defect (confirmed by fluorescein stain)
• Blepharitis — bacterial eyelid margin infection with significant periocular inflammatory response
• Post-operative anterior segment surgery — cataract surgery, corneal grafting, anterior chamber paracentesis — controlling post-surgical uveitis and anterior chamber flare
• Anterior uveitis with confirmed bacterial aetiology — adjunctive topical corticosteroid therapy under veterinary supervision with systemic treatment of the underlying infectious cause

Critical Contraindications

• CONTRAINDICATED in corneal ulcers (any depth — superficial epithelial erosions to deep stromal ulcers) — fluorescein staining mandatory before use
• CONTRAINDICATED in active or suspected feline herpesvirus-1 (FHV-1) keratitis or conjunctivitis in cats
• CONTRAINDICATED in fungal ocular infections (keratomycosis)
• CONTRAINDICATED in eyes with suspected or confirmed glaucoma without IOP monitoring
• Do not use concurrently with topical NSAIDs without veterinary guidance — combination may increase corneal melting risk

Administration

• Instil as directed by veterinarian — typically 1–2 drops into the affected eye(s) as prescribed; frequency as directed
• Perform fluorescein staining to confirm corneal integrity before initiating therapy — veterinarian responsibility
• 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
• Complete the full prescribed course; do not discontinue abruptly with chronic use — taper as directed by veterinarian
• Store below 25°C; protect from light; do not freeze; discard opened bottle as directed on label