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Home: Disease Management: Treatment
Drugs In Clinical Trials

Important Notice: The Forum does not endorse any medical product or therapy. ALL medications and supplements should be taken ONLY under the supervision of a physician, due to the possibility of side-effects, drug interactions, etc.

Name: AN 1792
Other Names: AIP 001
Development Status: investigational in U.S.
FDA Phase: Discontinued
Primary Medical Role: Potential treatment and prevention for Alzheimer's disease.
Role in Alzheimer's Disease: AN-1792 is a synthetic form of the 42 amino acid beta amyloid peptide. It is hypothesized that immunization with AN-1792 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.
Pharmacological Role: The precise mechanism of immune response from AN-1792 is not completely known. AN-1792 immunization results in the generation of anti-amyloid-beta antibodies. One possible mechanism could be that the antibodies trigger monocytic/microglial cells to clear amyloid-beta either before deposition, or after plaque formation.
Evidence pro its efficacy: Two studies performed on AD model (PDAPP) transgenic mice show remarkable results. One study, immunized a group of six- week old PDAPP mice with AN-1792. At age 13 months, virtually all of the mice treated with AN-1792 had no detectable amyloid deposits in their brains compared to controlled groups (treated with either saline or another plaque-associated protein), that had no reduction in the progressive deposition of plaques. Another study treated a group of 11 month old PDAPP mice with AN-1792 shows that the treated mice had significantly (>99%; p value=0.0002) less plaque and neuropathology than untreated mice. Recent studies also indicate that vaccination reverses or prevents cognitive deficits in transgenic mouse models engineered to deposit amyloid plaque.
Companies: American Home Products, Elan Pharmaceuticals, Inc.
Notes: Trial of this drug ended 1 March 2002. See press releases and ARF news story.

References

Morgan D, Gitter BD. Evidence supporting a role for anti- Abeta antibodies in the treatment of Alzheimer's disease. Neurobiol Aging. 2004 May-Jun ;25(5):605-8. Abstract


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