In patients with normal-type and inherited transthyretin amyloid cardiomyopathy (ATTR-CM), a study found that 61 mg of Bindamax (ingredient name tapamidis) improved long-term survival rate compared to 20 mg of tapamidismeglumine salt.
On November 13th, Pfizer Korea was published in the European Journal of Heart Failure.
As a result of an analysis of the ATTR-ACT study and the long-term extension study of the ATTR-ACT, the patient group who switched to Bindamax 61mg after treatment with Bindaquel 80mg was converted to Bindamax 61mg after 20mg treatment with tapamidismeglumine salt. The risk of death was reduced by 30% compared to one patient group.
Pfizer explains that this study demonstrates that the biological equivalent of Vindamax 61 mg to Vindakel 80 mg is the optimal dose for ATTR-CM patients.
When age, biomarker, and functional ability were corrected, the difference increased further, and the risk of death in the group converting tapamidismeglumine salt 80mg·Vindamax 61mg is 43 compared to the group converting tapamidismeglumine salt 20mg·Vindamax 61mg. % Was lower.
The safety profile was similar to placebo in both the tapamidismeglumine salt 80 mg/bindamax 61 mg conversion group and the tapamidismeglumine salt 20 mg/bindamax 61 mg conversion group.
Dr. Thibaud Damy, who served as president of the French Cardiology Association (FSC), said, “We reconfirmed that the biological equivalent of 80 mg of tapamidismeglumine salt and 61 mg of Vindamax is the optimal dose for the treatment of ATTR-CM.” “It will be a treatment that provides significant survival benefits for ATTR-CM, where options were limited.”
On the other hand, ATTR-CM is a rare progressive disease in which transthyretin (TTR), which is a transport protein in the blood, becomes unstable, separates into incorrectly folded units, and accumulates in the heart, causing restrictive cardiomyopathy. ATTR-CM is divided into inheritance caused by mutation of the TTR gene and normal type caused by aging.
Bindamax 61mg delays the accumulation of amyloid in the body by stabilizing and preventing division of the abnormal and unstable TTR protein. On August 19th, it was approved by the Ministry of Food and Drug Safety for the reduction of cardiovascular mortality and cardiovascular hospitalization in adult patients with normal and hereditary ATTR-CM.
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