Neurimmune enrols patient in NI006 trial for ATTR cadiomyopathy

27th February 2020 (Last Updated February 27th, 2020 15:01)

Zurich-based biopharmaceutical firm Neurimmune has enrolled the first patient in a Phase I clinical trial to analyse NI006 in transthyretin amyloid cardiomyopathy (ATTR cardiomyopathy).

Neurimmune enrols patient in NI006 trial for ATTR cadiomyopathy
The company intends to analyse the safety, tolerability of NI006 in patients with ATTR. Credit: Pexels from Pixabay.

Zurich-based biopharmaceutical firm Neurimmune has enrolled the first patient in a Phase I clinical trial to analyse NI006 in transthyretin amyloid cardiomyopathy (ATTR cardiomyopathy).

A human antibody targeted against transthyretin amyloid (TTR amyloid) consisting of misfolded and aggregated forms of transthyretin, NI006 was discovered by Neurimmune by translating genetic information of human memory B cells through its Reverse Translational Medicine technology.

In this first-in-human, placebo-controlled, multicentre Phase I clinical trial, the company intends to analyse the safety, tolerability, pharmacokinetics and exploratory efficacy of the drug in patients suffering from wild-type and hereditary types of ATTR cardiomyopathy.

Neurimmune CEO Roger Nitsch said: “This is the fifth of our recombinant human antibody programmes tested in clinical trials in human diseases linked to protein aggregation and misfolding.

“Leveraging our expertise in antibodies for Alzheimer’s and Parkinson’s diseases enabled the discovery of evolutionarily optimised antibodies that selectively bind and remove TTR amyloid fibrils in vivo.”

Serving as a human monoclonal antibody, NI006 binds with high affinity to TTR amyloid, but not to the physiological forms of transthyretin.

Up to four monthly infusions of NI006 will be analysed in patients suffering from ATTR cardiomyopathy at clinical centres in Europe in the single and multiple ascending dose study recently initiated.

Neurimmune CMO Christoph Hock said: “ATTR cardiomyopathy is characterised by the intramyocardial deposition of TTR amyloid fibrils that increase heart wall thickness and cause heart muscle stiffness leading to ventricular dysfunction.

“Our goal is to develop NI006 as a novel treatment option for patients with ATTR cardiomyopathy and to improve their heart function by clearing cardiac amyloid.”