OT: AC Immune
This is text from the AC Immune page of PCNS 2010.
<<ACI-24/Alzheimer’s: AC Immune’s basic vaccine principle is to stimulate an immune system response to misfolded proteins by introducing a peptide antigen similar enough to the misfolded protein that, when recognized as ‘other’, both the antigen and the target protein will be reduced via an antibody response. The peptide antigens are attached to liposomes, eliminating the need for an adjuvant. ACI-24 went into Phase I in 2009. AC Immune is utilizing a Bayer Schering imaging technology, the AB plaque tracer florbetaben, as part of this development program.
MAb/Alzheimer’s: This antibody program is was partnered with Genentech in 2006, which put them under Genentech’s control and timeframe. The lead therapeutic antibody, MABT5102A, went into Phase Ib in August 2008.
ACI-91/Alzheimer’s: This is a small-molecule tactic aimed at an AB sheet-breaking effect via linking to the misfolded, AB aggregate. This premise presumes that a reinstated balance between aggregated beta-amyloid sheets and soluble AB is therapeutic. They believe that rendering AB soluble will be less prone to triggering inflammation than spurring macrophage removal. AB plaques have been reduced in animal models, and functional memory improvement appeared correlated. The lead compound is in Phase II, and is not expected to report data until 2012.
ACI-636/Alzheimer’s: This is the lead oligomer-disaggregation small molecule candidate from AC Immune, now in full preclinical testing.
ACI-518/Alzheimer’s: Inlicensed in January 2010 from the State University of Moscow (from the same inventor who came up with Dimebon), this is an AMPA receptor upmodulator, intended as a memory enhancer. It is preclinical.
Oncology/Vaccine: MDR1, which targets P-170, is an active vaccine approach to multi-drug resistance in cancer, being developed in collaboration with the University of Reims.
Partner: Genentech
This is a sophisticated scientific platform which has two AB disaggregation strategies, one passive vaccine, and a newly inlicensed AMPAkine. There is a fundamental question attached to disaggregation approaches: they assume that soluble beta-amyloid is either not harmful, or that it will be processed and eliminated. But this remains a principle yet to be proven.
AC Immune raised enough money in 2009 to take them to 2013, which means that they do not have to partner the AC-91 or ACI-24 programs. But given the enormous burden of taking them ahead alone, one would think they would be responsive to partnering inquiries.>>
NeuroInvestment