Those of us holding almost 2 billion shares of Actinogen have enough cognition to recognize that despite slow (but steady) progress, we have one of the highest probabilities in the world that we can bring to market a drug that can improve cognition and delay regression associated with numerous conditions. While our short term stock price is stomach churning, we are smart enough to recognize, without the aid of Xanamem, that we have been through this before and will again have to wait a bit for trial results to catch up with the cortisol hypothesis. Other significant trials with alternative modes of action have failed to achieve endpoints, causing medicine to heighten their consideration of cortisol.
A few days ago, a bold attempt to interrupt alzheimer's cognition decline in people with a strong genetic predispostion to early onset alzheimer's was judged a failure, as have multiple other approaches targeting amyloid. With prevention being a major focus of current research and development, Actinogen is uniquely well positioned to offer both prevention (for both "healthy" and mild cognition affected populations) and treatment across multiple conditions.
Here is an excerpt from a June 16, 2022 New York Times article:
A closely watched clinical trial of a potential Alzheimer’s drug failed to prevent or slow cognitive decline, another disappointment in the long and challenging effort to find solutions for the disease.The decade-long trial was the first time people who were genetically destined to develop the disease — but who did not yet have any symptoms — were given a drug intended to stop or delay decline. The participants were members of an extended family of 6,000 people in Colombia, about 1,200 of whom have a genetic mutation that virtually guarantees they will develop Alzheimer’s in their mid-40s to mid-50s.For many members of the family, who live in Medellín and remote mountain villages, the disease has quickly stolen their ability to work, communicate and carry out basic functions. Many die in their 60s. In the trial, 169 people with the mutation received either a placebo or the drug, crenezumab, produced by Genentech, part of the Roche Group. Another 83 people without the mutation received the placebo as a way to protect the identities of people likely to develop the disease, which is highly stigmatized in their communities.The trial investigators had hoped that intervening with a drug years before memory and thinking problems were expected to emerge might hold the disease at bay and provide important insights for addressing the more common type of Alzheimer’s that is not driven by a single genetic mutation.“We’re disappointed that crenezumab did not show a significant clinical benefit,” Dr. Eric Reiman, the executive director of Banner Alzheimer’s Institute, a research and treatment center in Phoenix, and a leader of the research team, said at a news conference about the results. “Our hearts go out to the families in Colombia and to everyone else who would benefit from an effective Alzheimer’s prevention therapy as soon as possible. At the same time, we take heart in the knowledge that this study launched and continues to help shape a new era in Alzheimer’s prevention research.”The results are also another setback for drugs that target a key protein in Alzheimer’s: amyloid, which forms sticky plaques in the brains of patients with the disease. Years of studies with various drugs that attack amyloid in different stages of the disease have fallen flat. In 2019, Roche halted two other trials of crenezumab, a monoclonal antibody, in people in the early stages of the more typical Alzheimer’s disease, saying the studies were unlikely to show benefit. Last year, in a highly controversial decision, the Food and Drug Administration granted its first approval of an anti-amyloid drug, Aduhelm. The F.D.A. acknowledged that it was unclear if Aduhelm could help patients, but greenlighted it under a program that allows authorization of drugs with uncertain benefit if they are for serious diseases with few treatments and if the drugs affect a biological mechanism that is reasonably likely to help patients. The F.D.A. said that biological mechanism was Aduhelm’s ability to attack amyloid, but many Alzheimer’s experts criticized the decision because of the poor track record of anti-amyloid therapies. The trial results on Thursday only added to the disappointing evidence.“Wish there were something more positive to say,” said Dr. Sam Gandy, the director of Mount Sinai’s Center for Cognitive Health, who was not involved in the Colombia research.“The pathogenic mutation in the Colombian family is known to be involved in amyloid metabolism,” Dr. Gandy said, adding, “The thinking was that these were the patients most likely to respond to anti-amyloid antibodies.”
Good Health To All! I remain convinced that our medical leadership is dedicated, determined and destined to prove out a breakthrough treatment.
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