Alembic Mectin Ivermectin 10mg Tablet for Dogs & Cats | Broad-Spectrum Macrocyclic Lactone Antiparasitic | GI Worms, Mange, Microfilaria & Ectoparasites | 1 Strip (10 Tablets)

PRESCRIPTION VETERINARY MEDICINE — For veterinary use only. Must be prescribed and dispensed by or under the supervision of a licensed veterinarian. CRITICAL SAFETY WARNING: IVERMECTIN IS CONTRAINDICATED IN MDR1/ABCB1 GENE MUTATION-POSITIVE HERDING BREEDS (Rough/Smooth Collie, Shetland Sheepdog — Sheltie, Australian Shepherd, Border Collie, Old English Sheepdog, German Shepherd — partial) — P-glycoprotein deficiency allows Ivermectin to cross the blood-brain barrier causing potentially fatal neurotoxicity. CATS ARE EXQUISITELY SENSITIVE TO IVERMECTIN — do not use in cats without confirmed veterinary weight-based dosing; overdose causes severe neurological toxicity. Do not use in puppies under 6 weeks of age. Do not use in breeding, pregnant, or lactating animals without veterinary confirmation. Keep out of reach of children. Store in a cool, dry place away from direct sunlight.

Alembic Mectin Ivermectin 10mg Tablet for Dogs & Cats | Broad-Spectrum Macrocyclic Lactone Antiparasitic | GI Worms, Mange, Microfilaria & Ectoparasites | 1 Strip (10 Tablets)

Alembic Mectin contains Ivermectin 10mg per tablet — a broad-spectrum macrocyclic lactone endectocide (active against both endo- and ectoparasites) for dogs and cats. Ivermectin is a semisynthetic derivative of Avermectin B1a/B1b — a 16-membered macrocyclic lactone produced by fermentation of Streptomyces avermitilis — that acts by selectively activating glutamate-gated chloride ion channels (GluCl channels) present exclusively in invertebrate nerve and muscle cells, causing irreversible paralysis and death of susceptible parasites. Use strictly as directed by a licensed veterinarian — confirm breed MDR1/ABCB1 mutation status and weight before dosing.

Active Ingredient & Mechanism of Action

• Ivermectin 10mg per tablet — Macrocyclic lactone endectocide (GluCl channel positive allosteric modulator/irreversible agonist): Ivermectin is a semisynthetic mixture of Avermectin B1a (~80%) and B1b (~20%), 22,23-dihydro derivatives of the Avermectin B1 macrocyclic lactones; mechanism: Ivermectin selectively binds to glutamate-gated chloride ion channels (GluCl channels — invertebrate-specific ligand-gated anion channels of the Cys-loop receptor superfamily, homologous to vertebrate glycine receptors and GABA-A receptors; GluCl channels are present in the nervous system and body wall/pharyngeal musculature of nematodes and arthropods but are absent from vertebrate nervous systems as vertebrates lack GluCl channel subunits); Ivermectin acts as a potent positive allosteric modulator (PAM) and at higher concentrations an irreversible agonist at GluCl channels: it binds at the transmembrane interface between adjacent α-subunits of the GluCl homopentameric channel complex (a Cys-loop receptor with an extracellular ligand-binding domain and a transmembrane domain comprising M1–M4 helices per subunit; the ion-conducting pore is formed by the five M2 helices) — specifically at a transmembrane allosteric site distinct from the glutamate orthosteric site; Ivermectin binding → conformational change in the channel → irreversible (at high concentrations) or sustained (at low concentrations) opening of the GluCl channel pore → massive, unregulated Cl− influx into the invertebrate nerve and muscle cell → membrane hyperpolarisation (the membrane potential becomes more negative, moving away from the action potential threshold) → inhibition of action potential generation and propagation → pharyngeal muscle paralysis in nematodes (preventing feeding → starvation) and body wall muscle flaccid paralysis → paralysis and death of adult worms and larval stages; additionally, Ivermectin potentiates GABA-gated chloride channel (GABA-Cl) activity in invertebrate neuromuscular junctions (NMJs) by acting as a PAM at invertebrate GABA-A-like receptors — augmenting the inhibitory GABAergic tone at nematode and arthropod NMJs → further muscle paralysis; vertebrate safety margin: (1) GluCl channels are absent from vertebrate CNS — vertebrates lack the GluCl channel subunit genes; (2) Ivermectin has very low affinity for vertebrate GABA-A receptors at therapeutic antiparasitic plasma concentrations; (3) the blood-brain barrier (BBB) normally excludes Ivermectin from the vertebrate CNS via P-glycoprotein (Pgp/ABCB1 — the multidrug resistance efflux transporter expressed on the luminal surface of brain capillary endothelial cells that actively extrudes Ivermectin from the CNS back into the blood); CRITICAL MDR1/ABCB1 mutation risk: the ABCB1 gene (encoding P-glycoprotein) has a common loss-of-function 4-base pair deletion mutation (nt230del4 — a frame-shift mutation causing premature stop codon) that is highly prevalent in herding dog breeds due to a founder effect (a single MDR1-mutant dog ancestor in the herding breed lineage); homozygous MDR1(-/-) dogs completely lack functional P-glycoprotein → Ivermectin freely crosses the BBB → accumulates in the CNS → potentiates GABAergic inhibition at vertebrate CNS GABA-A receptors at concentrations sufficient to cause neurological toxicity: ivermectin toxicosis signs in MDR1(-/-) dogs: mydriasis (fixed dilated pupils — from ciliary muscle paralysis), hypersalivation, ataxia (incoordination), muscle tremors, disorientation/confusion, blindness, recumbency, coma, respiratory depression, and death; MDR1 mutation prevalence: Rough/Smooth Collie (~75% homozygous MDR1-/-), Shetland Sheepdog/Sheltie (~15%), Australian Shepherd (~50%), Border Collie (~5%), Old English Sheepdog (variable), McNab Shepherd (~30%), Longhaired Whippet (~65%); heterozygous MDR1(+/-) dogs have intermediate P-gp activity and intermediate sensitivity; breed screening with the MDR1 gene mutation test (ABCB1 genetic PCR test) is available before Ivermectin administration; CATS: cats have functional P-glycoprotein but are approximately 8–10-fold more sensitive to Ivermectin than dogs due to differences in hepatic CYP3A-mediated Ivermectin metabolism (cats have reduced CYP3A activity) and reduced biliary excretion capacity; the therapeutic index for Ivermectin in cats is narrow — doses must be precisely weight-calculated; at overdose in cats: the same neurotoxicity signs as MDR1(-/-) dogs occur; treatment of Ivermectin toxicosis: supportive care — there is no specific antidote; physostigmine (an acetylcholinesterase inhibitor) has been used experimentally but is not standard; intravenous lipid emulsion (ILE) therapy has been used as a lipid sink to redistribute lipophilic Ivermectin from the CNS; management is primarily supportive (mechanical ventilation if respiratory depression, IV fluids, thermoregulation, prevention of aspiration)

Parasite Spectrum

• Gastrointestinal nematodes (roundworms): Toxocara canis, Toxocara cati, Toxascaris leonina (adult and larval stages); Ancylostoma caninum, Ancylostoma tubaeforme (hookworms — adult stages)
• Microfilariae (larval heartworm): Dirofilaria immitis (heartworm) microfilariae suppression — Ivermectin at monthly preventative doses (6–12mcg/kg) kills Dirofilaria microfilariae and L3/L4 larvae; NOT effective against adult D. immitis — adulticide treatment (Melarsomine) required for patent heartworm infection; WARNING: administering Ivermectin to dogs with high microfilarial burdens (patent D. immitis infection) can cause anaphylactoid shock from rapid microfilarial kill — antigen test mandatory before first Ivermectin dose in endemic areas
• Sarcoptic mange (Sarcoptes scabiei var. canis): Ivermectin is highly effective against Sarcoptes mites at higher doses (0.2–0.4mg/kg SC or PO repeated doses)
• Demodectic mange (Demodex canis): Ivermectin at higher daily doses (0.3–0.6mg/kg/day) can suppress Demodex populations (off-label; newer isoxazolines — Fluralaner, Afoxolaner — are now preferred for Demodex due to superior efficacy and safety profile)
• Ear mites (Otodectes cynotis): Effective at standard antiparasitic doses
• Capillaria spp. (whipworms — partial), Strongyloides spp., Trichuris vulpis (partial)

Dosage & Administration

• Administer orally with food as directed by a licensed veterinarian
• Dose is strictly weight-based — confirm body weight before dosing; 10mg tablet is a large dose suitable for large breed dogs (approximately 25–50kg at standard antiparasitic doses)
• Confirm MDR1/ABCB1 mutation status in herding breeds before administration — genetic testing recommended
• In cats: use only under strict veterinary supervision with precise weight-based dosing; the therapeutic index is narrow
• Heartworm endemic areas: perform Dirofilaria antigen test before first dose to rule out patent heartworm infection

Critical Contraindications

• CONTRAINDICATED in MDR1/ABCB1 homozygous mutant herding breeds without MDR1 testing — Collie, Sheltie, Australian Shepherd, Border Collie (list not exhaustive)
• CONTRAINDICATED in cats at dog dosing levels — confirm veterinary feline-specific dosing
• CONTRAINDICATED at standard antiparasitic doses in dogs with patent Dirofilaria immitis infection (positive heartworm antigen test) without pre-treatment microfilarial management protocol
• Do not use in puppies under 6 weeks of age
• Do not use concurrently with other P-glycoprotein substrate drugs in MDR1-sensitive breeds (spinosad, certain macrolide antibiotics)

Safety Information

• Prescription veterinary medicine — veterinary prescription mandatory
• Monitor dogs for signs of neurological adverse effects for 8–12 hours after first dose, especially in herding breeds and cats
• Store in a cool, dry place away from direct sunlight; keep in original packaging; keep out of reach of children