VetSheet

Dichlorphenamide

Carbonic Anhydrase InhibitorPODogsCats

Also known as: Daranide · Antidrasi · Fenamide · Glaucol · Glauconide · Glaumid · Oralcon · Oratrol · Tensodilen · Diclofenamidum

Reviewed by the VetSheet Veterinary TeamUpdated Apr 5, 2026Evidence-based veterinary reference

Audited v13 dosing evidence

Structured calculator evidence

Adjunctive glaucoma treatment (extra-label)

2–5 mg/kgPO
  • q8-12h

NA

Governing clinical context (2)
  • ■ Give this medicine as directed by your veterinarian. If your animal vomits or acts sick after receiving the medicine on an empty stomach, try giving the next dose with food or a small treat. If vomiting continues, contact your veterinarian.
  • Store tablets in well-closed containers and at room temperature (20°C-25°C [68°F-77° F]).
formularyProtocol 2023Audit dose-audit-plumb-v13

Doses are a clinical reference for licensed veterinary professionals. Always confirm against the current label and the individual patient.

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Overview

Dichlorphenamide is a systemic ​carbonic anhydrase inhibitor (CAI)​ traditionally used in veterinary ophthalmology for the medical management of glaucoma.

  • Clinical Pearl: Due to significant systemic side effects (such as metabolic acidosis and hypokalemia) and widespread commercial unavailability, systemic CAIs have largely been superseded by topical alternatives such as dorzolamide and brinzolamide.
  • When prescribed today, it is typically sourced through a compounding pharmacy.
  • It possesses mild anticonvulsant and diuretic properties, though it is rarely used for these indications in modern veterinary medicine.

Mechanism of action

Dichlorphenamide exerts its effects via noncompetitive, reversible inhibition of the enzyme ​carbonic anhydrase (CA)​.

  • In the ciliary body: Inhibition of CA-II → decreased formation of bicarbonate (HCO3-) and hydrogen (H+) ions from carbon dioxide and water → reduced active transport of sodium into the posterior chamber → decreased aqueous humor production → ​lowered intraocular pressure (IOP)​.
  • In the kidneys: Inhibits CA in the proximal convoluted tubule → increased renal tubular secretion of Na+, K+, and HCO3- → alkaline diuresis and potential metabolic acidosis.
  • In the CNS: Exhibits mild anticonvulsant activity, likely secondary to localized metabolic acidosis or direct CA inhibition in the brain.

Safety & warnings

Contraindications

  • Significant hepatic disease (may precipitate hepatic coma)
  • Renal or adrenocortical insufficiency
  • Hyponatremia
  • Hypokalemia
  • Hyperchloremic acidosis
  • Electrolyte imbalance
  • Severe pulmonary obstruction (unable to increase alveolar ventilation)
  • Hypersensitivity to carbonic anhydrase inhibitors
  • Chronic, noncongestive, angle-closure glaucoma (long-term use)

Adverse effects

  • Panting
  • GI disturbances (inappetence, vomiting, diarrhea)
  • CNS effects (sedation, depression, excitement)
  • Hematologic effects (bone marrow depression)
  • Renal effects (crystalluria, dysuria, renal colic, polyuria)
  • Metabolic acidosis
  • Hypokalemia
  • Hyperglycemia
  • Hyponatremia
  • Hyperuricemia
  • Hepatic insufficiency
  • Dermatologic effects (rash)
  • Hypersensitivity reactions

Precautions

Warning: Long-term use is contraindicated in patients with chronic, noncongestive, angle-closure glaucoma as it may mask the condition by lowering IOP while angle closure progresses.

  • Use with extreme caution in patients with pre-existing electrolyte imbalances (especially hypokalemia or hyponatremia).
  • May precipitate hepatic coma in patients with severe liver disease.
  • Avoid in patients with severe pulmonary obstruction who cannot increase alveolar ventilation to compensate for metabolic acidosis.
  • Pregnancy Category C: Teratogenic effects observed in animal studies; use only if benefits outweigh risks.
  • Laboratory Interference: May cause false-positive results for urine protein using certain test methods (e.g., bromphenol blue, sulfosalicylic acid) due to urine alkalinization. May also decrease iodine uptake by the thyroid gland.

Drug interactions

Antidepressants, Tricyclic

Alkaline urine caused by dichlorphenamide may decrease excretion of tricyclic antidepressants.

Aspirin (or other salicylates)

Increased risk of dichlorphenamide accumulation and toxicity; increased risk for metabolic acidosis; dichlorphenamide increases salicylate excretion.

Digoxin

Dichlorphenamide may cause hypokalemia, leading to an increased risk for digoxin toxicity.

Insulin

Rarely, carbonic anhydrase inhibitors interfere with the hypoglycemic effects of insulin.

Methenamine compounds

Dichlorphenamide may negate the effects of methenamine in the urine due to alkalinization.

Potassium-depleting drugs (corticosteroids, amphotericin B, corticotropin, diuretics)

Concomitant use may exacerbate potassium depletion.

Phenobarbital

Increased urinary excretion, which may reduce phenobarbital levels.

Primidone

Decreased primidone concentrations.

Quinidine

Alkaline urine caused by dichlorphenamide may decrease quinidine excretion.

Monitoring

  • Intraocular pressure (IOP) / tonometry
  • Serum electrolytes (may need to supplement potassium)
  • Baseline CBC with differential and periodic retests if using chronically
  • Clinical signs of adverse effects (GI upset, panting, CNS changes)

Pharmacokinetics

Absorption

Onset of action in small animals is approximately 30 minutes, with maximal effect occurring in 2-4 hours.

Distribution

Not well studied in domestic animals.

Metabolism

Not well studied in domestic animals.

Elimination

Duration of action in small animals is 8-12 hours.

Overdose

Information regarding acute toxicity of dichlorphenamide is limited.

  • Clinical Signs: Likely extensions of adverse effects, including severe electrolyte derangements (hypokalemia, hyponatremia), profound metabolic acidosis, CNS depression, and dehydration.
  • Treatment:
    • Monitor serum electrolytes, blood gases, volume status, and CNS status.
    • Provide aggressive supportive care, including IV fluid therapy to correct dehydration and acid-base/electrolyte imbalances (e.g., potassium supplementation). Treat symptomatically.

Available products

Formulations

  • Tablets (historically)
  • Compounded oral formulations

Veterinary

  • None commercially available (requires compounding)

Human-labeled

  • None commercially available (requires compounding)

Regulatory status

No regulatory data for: 🇺🇸 US · 🇪🇺 EU · 🇬🇧 UK · 🇭🇰 HK · 🇹🇼 TW · 🇯🇵 JP · 🇰🇷 KR · 🇦🇺 AU

Storage & stability

Store tablets in well-closed containers and at room temperature. An expiration date of 5 years after the date of manufacture is assigned to the commercially available tablets (when available).

Client information

  • Administration: Give this medication exactly as prescribed. If your pet experiences stomach upset (vomiting or loss of appetite), try giving the dose with a small meal or treat.
  • What to Watch For: Contact your veterinarian immediately if you notice:
    • Unusual bleeding or bruising (could indicate bone marrow suppression).
    • Muscle tremors, weakness, or severe lethargy (signs of low potassium).
    • Skin rashes or excessive panting.
  • Follow-up: Regular check-ups are crucial to monitor your pet's eye pressure (glaucoma) and blood work (electrolytes and blood cell counts).

Note: This medication is often custom-made (compounded) since commercial tablets are rarely available. Ensure you get refills well in advance.

VetSheet drug reference is intended for licensed veterinary professionals as a clinical decision-support aid, not a substitute for professional judgement or the manufacturer’s current label.