Acoramidis goes deeper into the TTR protein to better stabilize it. The covalent bond of the hydrogen atoms are less likely to be disrupted for those with either wtATTR or hATTR. It is the hydrogen atoms that hold the 4 Thyretin proteins together to form the TTR protein. When that bond is broken, the tetramer cloverleaf shaped complex protein comes apart into 4 monomeric separate Thyretin proteins. Those then misfold, clump, and aggregate extracellurally around nerves , in the heart and possibly in other internal organs. Acoramidis is more effective in its stabilization.

Acoramidis may be superior to Vyndamax but it may be priced out of the market. The FDA may not see any reason to approve a 2nd TTR stabilizer given the wide acceptance of Vyndamax by doctors who see no advantages in Acoramidis.

On your question if anyone has noticed and improvement or stabalization of the treatment?
I want to know also. I have only been diagnosed for a year and am on Vyndamax for a year. Jim 4

Beverly, you're welcome as always.

Thank you Sheldon. No one has ever explained to me so effectively how the TTR proteins are formed and potentially broken. I can better see why they multiply so rapidly. Thanks again.