tafamidis: clinical use

Prescribing considerations

• Confirm ATTR-CM and exclude light-chain amyloidosis before treatment using appropriate imaging, blood or urine testing and, where needed, biopsy.
• Use TTR genotyping to distinguish hereditary from wild-type disease.
• Initiate under an amyloidosis- or cardiomyopathy-experienced physician and continue appropriate standard care.
• Clinical evidence is limited in very advanced cardiac disease; initiation or continuation requires specialist judgement.
• Review the need for other treatment, including transplantation. Tafamidis should be stopped in patients undergoing organ transplantation because use in that setting has not been studied.
• Data are limited in severe renal impairment, and severe hepatic impairment has not been studied.

Contraindications and cautions

• Hypersensitivity to tafamidis or any excipient.

Monitoring

• Follow cardiac status and disease progression as part of standard ATTR-CM care.
• Monitor for adverse effects from concomitant BCRP substrates.
• Be aware that liver-function tests may increase.
• Tafamidis may lower measured total thyroxine without changing free thyroxine or TSH; corresponding clinical thyroid dysfunction was not observed.

Clinical pharmacology

Tafamidis selectively occupies transthyretin thyroxine-binding sites and stabilises the native tetramer, slowing the rate-limiting dissociation step in amyloid formation. It is highly plasma-protein bound and has a prolonged elimination half-life.

Formulation and product differences

• The selected product contains tafamidis in a soft capsule.
• Tafamidis and tafamidis meglumine formulations are not interchangeable on a milligram-for-milligram basis.
• The capsule contains gelatine and sorbitol and must be swallowed whole.

Capsule

Route: Oral

Strengths: 61 mg