AN1792

AN1792

A synthetic form of the 42-residue A beta protein seen in Alzheimer’s disease (AD) brains. It prevents appearance of amyloid plaques and the neuropathology characteristic of autosomal dominant AD in young PDAPP mice; immunisation of older mice with established AD-like pathology resulted in a marked reduction or stopped disease progression.
AN-792 made it to early trials as an immune therapy for AD; some patients developed CNS inflammation; trials were halted in 2002.
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Previously, Dr Callaway led the Alzheimer's immunotherapy programme at Elan Pharmaceuticals, which became the first company to introduce disease-modifying biologics (AN1792, bapinuzumab, ACC001) into clinical studies.
In 2002, the first active AD vaccine (AN1792) developed by ELAN in Ireland and Wyeth in USA went through a phase IIa clinical trial.
Bapineuzumab was the first antibody to be tested in clinical trials after the termination of the AN1792 clinical study.
The vaccine, known as EB101, was patented in 2010 in the United States but, when scientists tried to compare it with AN1792, a vaccine currently approved by the US Food and Drug Administration (FDA), they discovered side effects that resulted in the analysis being dropped.
The first clinical trial involving a vaccine against AD was carried out in 2000 with the aggregated human [A[beta].sub.1-42] peptide combined with a saponin-based adjuvant (AN1792) (39).
Most infamously, a clinical trial of AN1792, utilizing an A[beta] peptide vaccine to induce immune responses to aggregates, was halted due to aseptic meningoencephalitis and leukoencephalopathy in a number of the vaccinated patients, emphasizing the importance of antigen and adjuvant selection [145].
Translation of these therapeutic approaches to human patients resulted in drastically different results, leading to the early termination of the AN1792 phase II clinical study.
The first active immunization clinical trial, which tested AN1792 in AD patients, was halted when a subset of patients developed meningoencephalitis.
Effects of Abeta immunization (AN1792) on MRI measures of cerebral volume in Alzheimer disease.
Plc and Wyeth (Madison NJ) known as AN1792 may have removed signature plaques from patients' brains, but they all developed severe dementia anyway.
all Irish pharmaceutical company, recently began testing AN1792. This experimental vaccine had garnered high praise from scientists and patient advocates after experiments on mice indicated that it might be able to halt the progression of Alzheimer's disease progression and cure it.
Delphine Boche, Ph.D., of the University of Southampton (England), studied the tau effects of another Abeta immunotherapy agent called AN1792, which was pulled from development in 2002 after 6% of the patients who received it developed serious brain inflammation and subsequent brain atrophy.