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.
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Attach
VYNDAMAX attaches to the TTR protein.

Stabilize
VYNDAMAX stabilizes TTR, helping it stay together.
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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.
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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Hear from Stan, a real patient taking VYNDAMAX
“Once I learned that VYNDAMAX can help to slow the progression of ATTR-CM, I was eager to begin the treatment journey.”