Our proprietary pan-amyloid targeting agents are capable of diagnosing and treating all types of systemic amyloidosis.

Attralus is focused on targeting the underlying pathology in all systemic amyloid diseases, with the goal of developing potential treatments for many subtypes of amyloidosis.

Pioneering PAR Therapeutics

Attralus is advancing the amyloidosis treatment paradigm by developing first-in-class therapies using our proprietary pan-amyloid removal (PAR) technology. With our differentiated approach, Attralus designs novel biologics to target all types of toxic amyloid with high specificity and superb binding properties to stimulate the immune system to remove amyloid. Our PAR therapeutics are unique in their ability to target, engage and remove all types of toxic amyloid.

A new treatment paradigm with amyloid removal

Precursor protiens cause amyloid fibril formation

Precursor proteins cause amyloid fibril formation

Existing toxic amyloid fibril depositsEXISTING TOXIC
Most patients have significant accumulation of amyloid at time of diagnosis

Restrictive cardiomyopathy
Heart failure

Kidney failure

Loss of sensation
Loss of reflex
Muscle weakness



  • Pan-amyloid removal
  • All types of systemic amyloidosis
  • All stages of disease

PAR Therapeutics Target, Engage and Remove Amyloid

With our differentiated approach to pan-amyloid removal (PAR), Attralus designs novel biologics to target all types of toxic amyloid with high specificity and exquisite binding properties to stimulate the immune system to remove amyloid. The unique capabilities that enable us to develop novel PAR therapeutics include:

Our leading-edge capabilities for novel PAR therapeutics

icon image for Porprietary Amyloid Binding & Delivery of FcProprietary Amyloid Binding & Delivery of Fc


Our proprietary amyloid binding peptide has a unique structure providing highly specific binding to multiple accessible sites on disease-causing amyloid deposits. Exquisite binding characteristics enable the peptide to target amyloid throughout the body to deliver the Fc to stimulate removal of deposits.


Icon image for Fc-Medicated Phagoctosis
Fc-Medicated Phagoctosis

A bioactive IgG1 Fc-fusion region, a key component of PAR therapeutics, actively engages the innate immune system to signal macrophages to engulf and remove the amyloid through phagocytosis – following the therapeutic binding to the amyloid.

Modular Biologics Design

Modular protein design allows the combination of our proprietary amyloid binding peptide with a variety of different biomolecules, offering the potential for multiple diagnostic and therapeutic strategies for the detection, targeting and removal of amyloid.


Proprietary Pan-Amyloid Diagnostic: First Amyloidosis-Specific Imaging Agent

The same pan-amyloid targeting mechanism is used in AT-01, our imaging agent. AT-01 is a novel polybasic peptide radiotracer under clinical investigation for whole-body amyloid detection in diverse types of amyloidosis.

  • AT-01 is designed to be the first amyloidosis-specific imaging agent capable of detecting all amyloid types, in key organs, providing a complete picture of disease burden and enabling quantification, prediction and monitoring.
  • AT-01 has the potential to inform, de-risk and accelerate clinical development of our therapies.

It also provides the opportunity to expand the diagnosed patient population, even in asymptomatic patients.
There are no FDA-approved imaging agents as diagnostics for systemic amyloidosis. Patients typically undergo a multitude of diagnostic tests, none of which can visualize the extent and localization of amyloid deposition across the entire body.

Systemic amyloidosis patients imaged with AT-01

Examples of Images for Ph 1/2 trial of AT-01 in ATTR, AL and ALECT2 patients

Advancing the next generation of therapies for neurodegenerative diseases by
simultaneously targeting multiple forms of amyloid

Convergence of neurodegenerative diseases

AD – Alzheimer’s Disease (>30M people worldwide)
PD – Parkinson’s Disease (>10M people worldwide)
LB – Lewy Body Disease

Our preclinical neurodegenerative programs utilize our PAR-peptide fused to an antibody and will be optimized for the treatment of neurodegenerative disorders related to amyloid deposition. Our therapeutic candidates bind to multiple misfolded protein aggregates including amyloid beta (Ab), Tau, and α-Synuclein. These misfolded protein aggregates are often concomitantly present in Alzheimer’s, Parkinson’s, and Lewy Body diseases. We believe that by targeting multiple amyloid deposits rather than a single one, like currently approved therapies do, our approach has the potential to deliver additional clinical benefit. By adding a blood brain barrier (BBB) shuttle to our PAR-peptide and mAb fusion, we are exploring the potential to improve brain penetration, efficacy, dosing, and tolerability relative to the PAR-peptide-mAb fusion alone.