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Two main types of transthyretin amyloidosis are hereditary transthyretin amyloidosis and wild type transthyretin amyloidosis. Hereditary transthyretin amyloidosis (hATTR) is further classified into familial amyloid polyneuropathy (FAP), and familial amyloid cardiomyopathy (FAC). Whereas, wild type variant (ATTRwt) predominantly affects the heart.

Transthyretin amyloidosis results from transthyretin produced by the liver, which forms dimers and then monomers. These monomers aggregate to form amyloid fibrils, which get deposited in multiple organs such as heart, nervous system, gastrointestinal tract, and kidneys. Familial amyloid polyneuropathy (FAP) is a subtype of hereditary transthyretin amyloidosis (hATTR), and the most common type of FAP is caused by the Val30Met variant of TTR.

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In familial amyloid polyneuropathy, the symptoms are first detected after the patient crosses 30 years of age, however, it can also be detected as early as 20 years or as late as 80 years of age. Symptoms are divided depending on the location such as peripheral neuropathy and autonomic neuropathy. Symptoms may worsen in case excess amyloid protein starts to collect in the nerves.

Introduction of novel therapies is expected to boost growth of the U.S. transthyretin amyloidosis treatment market

Hereditary transthyretin amyloidosis occurs due to genetic mutations in the genes responsible for manufacturing transthyretin.

Available therapies for treatment of transthyretin amyloidosis such as Tafamidis (not approved in the U.S.), Diflunisal (off-label indication), and other therapies are supportive treatment options and only treat symptoms of the disease.

Liver transplant is the only curative option in case of familial transthyretin polyneuropathy, and is generally not used in case of familial transthyretin cardiomyopathy or wild type TTR. New therapies that are expected to receive approval (Patisiran and Inotersen) have a novel therapeutic action known as gene silencing and work by either interfering with the abnormal transthyretin formation or by silencing the gene (antisense) responsible for production of transthyretin protein.

These novel therapies are expected to treat the underlying cause of the disease and are thus, expected to gain significant traction over the forecast period.

The U.S. transthyretin amyloidosis treatment market size is expected to be valued at US$ 36.9 million in 2018 and is expected to witness a robust CAGR of 52.4% over the forecast period (2018–2026).

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This release was published on openPR.