how-vyndamax-works

VYNDAMAX works by slowing the break down and build up of dangerous TTR deposits

Transthyretin cardiac amyloidosis (ATTR-CM) occurs when a protein called transthyretin (TTR) weakens and becomes unstable.

The TTR protein is mostly made in the liver and in smaller amounts in the outer lining of the brain and retina.

VYNDAMAX attaches to the TTR protein.

Attach

VYNDAMAX attaches to the TTR protein.

VYNDAMAX stabilizes TTR, helping it stay together.

Stabilize

VYNDAMAX stabilizes TTR, helping it stay together.

Maintain

Maintain

By stabilizing TTR, VYNDAMAX slows the break down and build up of dangerous deposits, which can help to slow the progression of ATTR-CM.

VYNDAMAX delivers near complete stabilization of TTR

VYNDAMAX works by binding to the TTR protein, stabilizing it and preventing it from breaking down.

A model using data from the ATTR-ACT clinical trial, which studied VYNDAMAX, predicted how much of the TTR protein in human plasma is occupied by VYNDAMAX. It showed that VYNDAMAX can stabilize more than 90% of the TTR protein.

CARDIOLOGIST RECOMMENDED

VYNDAMAX is the only treatment with a Class 1* recommendation for ATTR-CM in guidelines from:

  • American College of Cardiology

  • American Heart Association

  • Heart Failure Society of America

*Class 1 guidelines are given when there’s strong evidence or general agreement that a treatment is beneficial, useful, and effective. The above recommendation is from the 2022 guidelines. As of September 2024, VYNDAMAX is the only treatment approved for ATTR cardiac amyloidosis.

Questions to ask your doctor

  • What causes ATTR-CM to develop?
  • Could my heart failure diagnosis and other symptoms be ATTR-CM?
  • If so, what are the next steps we should take to determine if I have ATTR-CM?
  • If I have ATTR-CM, could VYNDAMAX be right for me?

Create a discussion guide to help you log your symptoms and talk to your doctor about ATTR-CM

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