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NAME: ACC-001

FDA PHASE: Phase II/IIa/IIb

ROLE IN ALZHEIMER'S DISEASE: ACC-001 is a short amino-terminal Aβ(1-6) fragment that is derived from the N-terminal B cell epitope of Aβ while avoiding T cell activation (reviewed in Lemere and Masliah 2010). This vaccine aims to avoid the safety concerns associated with AN1792 vaccine (Aβ1-42) that implicated residues Aβ15-42, the most common T cell epitope, as the cause of Th1 lymphocyte activation and predominantly responsible for autoimmune meningoencephalitis. Elan research indicates that antibodies specific for Aβ peptide can cross the blood-brain barrier and act directly in the central nervous system to induce plaque clearance. These findings suggest that this novel method may clear plaques in human patients.

NAME: AN1792

OTHER NAMES: AIP 001

FDA PHASE: Discontinued

MECHANISMS: Active immunotherapy

ROLE IN ALZHEIMER'S DISEASE: AN1792 is a synthetic form of the 42 amino acid beta amyloid peptide. Extensive preclinical evidence shows that immunization with Aβ1-42 peptide can prevent or reverse the development of the neuropathological hallmarks of Alzheimer's diseases, including extensive amyloid plaque formation, neuritic dystrophy, synaptic loss and gliosis (Schenk et al 1999). The history of AN1792 has been extensively chronicled in Alzforum News: See Vaccinating Against Plaques and Live Discussion: Alzheimer Immunotherapy Trial Grounded Phase II clinical trial NCT00021723 was initiated in 2001 and abruptly terminated in January 2002 due to the development of aseptic meningoencephalitis and leukoencephalopathy in 6% Aβ1-42 vaccinated patients (Orgogozo et al 2003; Gilman et al 2005). Despite this trial termination, follow up studies of the Phase IIa trial participants have shown that AN1792 immunization-induced plaque clearance improved neurite abnormalities induced by plaque (Serrano-Pozo et al 2010), although positive anti-amyloid effects did not prevent severity of end-stage dementia nor improved survival (Holmes et al 2008).

NAME: ELND005

OTHER NAMES: AZD-103, cyclohexane-1,2,3,4,5,6-hexol, myo-inositol, Scyllo-inositol

FDA PHASE: Phase II/III

MECHANISMS: Block accumulation of Aβ oligomers; prevent Aβ oligomer formation

ROLE IN ALZHEIMER'S DISEASE: Phase II testing of ELND005 was completed in August 2010. Primary outcome measures included cognition and function. Safety and tolerability were also tested. See related Alzforum News August 13, 2010 and Alzforum News Dec 16, 2009. Scyllo-inositol is a specific stereoisomer of the cyclic sugar alcohol inositol, occurring naturally in coconut palm, dogwood flowers and oak bark. McLaurin et al 2006 showed that scyllo-inositol can inhibit aggregation of Aβ in transgenic mice, improves many AD-like phenotypes and protects from cognitive decline. The Phase II trial completed the treatment of patients receiving 250 mg twice daily dosing. Elan has reported the study's cognitive (NTB) and functional (ADCS-ADL) co-primary endpoints did not achieve statistical significance. However, Elan reported that 250mg bid dose “demonstrated a biological effect” on Aβ in the cerebrospinal fluid (CSF), although no details have been provided. (See Elan press release). Twenty subjects total volunteered to provide CSF samples at beginning and end of trial. CSF analysis provided evidence that the 250 mg bid dose “achieved targeted drug levels in the CSF, and showed some effects on clinical endpoints in an exploratory analysis”.

NAME: MABT5102A

FDA PHASE: Phase II/IIa/IIb

MECHANISMS: Designed to bind and remove the Aβ peptide that accumulates in the brain.

ROLE IN ALZHEIMER'S DISEASE: MABT5102A (crenezumab)is a humanized monoclonal antibody, which binds to Aβ. Aβ is the main constituent of amyloid plaque in the brains of patients with Alzheimer's disease and is proposed to be causative in the development of the disease.

1 to 4 of 4 results