ACP-204 for Alzheimer's Disease
Recruiting in Palo Alto (17 mi)
+111 other locations
Age: 18+
Sex: Any
Travel: May Be Covered
Time Reimbursement: Varies
Trial Phase: Phase 2 & 3
Recruiting
Sponsor: ACADIA Pharmaceuticals Inc.
Must be taking: Cholinesterase inhibitors, Memantine
Must not be taking: Anti-tau therapy, Donanemab
Disqualifiers: Hospice care, Atrial fibrillation, others
Prior Safety Data
Trial Summary
What is the purpose of this trial?This is a master protocol for 3 independent, seamlessly enrolling, multicenter, randomized, double-blind, placebo-controlled, parallel-group studies in patients with ADP
* Substudy 1 (Phase 2) will evaluate efficacy and dose response of ACP-204 30 and 60 mg vs placebo. This substudy will be initiated first.
* Substudies 2A and 2B (both: Phase 3) will be confirmatory studies of either both doses (ACP-204 30 and 60 mg, respectively) or a single dose from Part 1 vs placebo. Substudies 2A and 2B will be performed independently of each other and will commence after enrollment of Part 1.
All 3 substudies will be analyzed independently of each other.
Each substudy individually will consist of a screening period (up to 49 days); a double-blind treatment period (6 weeks); a safety follow-up period (30 days) for patients not rolling over into an open-label extension study; and vital status follow-up (for patients who terminated their substudy early).
Do I have to stop taking my current medications for the trial?
The trial requires that you stay on a stable dose of a cholinesterase inhibitor or memantine, if applicable. However, you cannot take certain medications prohibited by the protocol, such as anti-tau therapy or donanemab within 2 months prior to screening.
How is the drug ACP-204 different from other Alzheimer's treatments?
ACP-204 is unique because it may involve a novel approach to targeting Alzheimer's disease, potentially focusing on mechanisms related to amyloid-beta (a protein associated with Alzheimer's) and its effects on memory, which is different from existing treatments that primarily focus on symptom management.
12345Eligibility Criteria
This trial is for adults aged 55 to 95 with Alzheimer's Disease Psychosis (ADP), living at home or in a facility, who have a caregiver and are stable on certain dementia medications. They must meet specific criteria for ADP diagnosis, including evidence of amyloid plaque deposition. Excluded are those needing prohibited meds, receiving end-of-life care, having conditions that explain their psychosis other than dementia, or with certain medical exclusions like atrial fibrillation.Inclusion Criteria
I am between 55 and 95 years old and live at home or in a care facility.
I have been diagnosed with psychosis in a cognitive disorder as per IPA guidelines.
I have experienced symptoms like hallucinations or delusions for at least 2 months.
+8 more
Exclusion Criteria
On a stable dose of medication?
Have been diagnosed with Alzheimer's Disease?
Are you a male or female and ≥55 and ≤95 years old?
+9 more
Trial Timeline
Screening
Participants are screened for eligibility to participate in the trial
7 weeks
Treatment
Participants receive ACP-204 30 mg, 60 mg, or placebo once daily for 6 weeks
6 weeks
Safety Follow-up
Participants are monitored for safety after treatment if not entering the open-label extension
4 weeks
Vital Status Follow-up
Monitoring of vital status for participants who terminated their substudy early
Open-label Extension (optional)
Participants may opt into continuation of treatment long-term
Participant Groups
The study tests ACP-204 at two doses (30 mg and 60 mg) against a placebo in three parts: an initial phase to assess efficacy and dose response followed by two confirmatory phases for the chosen doses. Each participant undergoes screening, six weeks of treatment, safety follow-up unless entering an extension study, and vital status updates if leaving early.
3Treatment groups
Experimental Treatment
Placebo Group
Group I: ACP-204 60 mgExperimental Treatment1 Intervention
Administration once daily at approximately the same time of day, with or without food
Group II: ACP-204 30 mgExperimental Treatment1 Intervention
Administration once daily at approximately the same time of day, with or without food
Group III: PlaceboPlacebo Group1 Intervention
Administration once daily at approximately the same time of day, with or without food
Find a Clinic Near You
Research Locations NearbySelect from list below to view details:
R & H Clinical Research Inc.Stafford, TX
Reliable Clinical Research LLC.Hialeah, FL
Floridian Neuroscience InstitutueMiami Lakes, FL
Central Miami Medical InstituteMiami, FL
More Trial Locations
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Who Is Running the Clinical Trial?
ACADIA Pharmaceuticals Inc.Lead Sponsor
References
Anti-amnesic effect of ESP-102 on Aβ(1-42)-induced memory impairment in mice. [2010]The aim of this study was to characterize the effects of ESP-102 on the memory impairments and pathological changes induced by amyloid-β (Aβ)(1-42) peptide in mice. The ameliorating effect of ESP-102 on memory impairment was investigated using the passive avoidance and the Morris water maze tasks, and the pathological changes were identified by immunohistochemistry and western blotting. Aβ(1-42) peptide (3μg/3μl) was administered by intracerebroventricular injection. By the single administration of ESP-102 (100mg/kg, p.o), the memory impairment induced by Aβ(1-42) peptide was significantly attenuated (P
Some Candidate Drugs for Pharmacotherapy of Alzheimer's Disease. [2021]Alzheimer's disease (AD; progressive neurodegenerative disorder) is associated with cognitive and functional impairment with accompanying neuropsychiatric symptoms. The available pharmacological treatment is of a symptomatic nature and, as such, it does not modify the cause of AD. The currently used drugs to enhance cognition include an N-methyl-d-aspartate receptor antagonist (memantine) and cholinesterase inhibitors. The PUBMED, Medical Subject Heading and Clinical Trials databases were used for searching relevant data. Novel treatments are focused on already approved drugs for other conditions and also searching for innovative drugs encompassing investigational compounds. Among the approved drugs, we investigated, are intranasal insulin (and other antidiabetic drugs: liraglitude, pioglitazone and metformin), bexarotene (an anti-cancer drug and a retinoid X receptor agonist) or antidepressant drugs (citalopram, escitalopram, sertraline, mirtazapine). The latter, especially when combined with antipsychotics (for instance quetiapine or risperidone), were shown to reduce neuropsychiatric symptoms in AD patients. The former enhanced cognition. Procognitive effects may be also expected with dietary antioxidative and anti-inflammatory supplements-curcumin, myricetin, and resveratrol. Considering a close relationship between brain ischemia and AD, they may also reduce post-brain ischemia neurodegeneration. An investigational compound, CN-105 (a lipoprotein E agonist), has a very good profile in AD preclinical studies, and its clinical trial for postoperative dementia is starting soon.
Beta-amyloidbased immunotherapy as a treatment of Alzheimers disease. [2017]The pathology of Alzheimer's disease shows a significant correlation between beta-amyloid peptide conformation and the clinical severity of dementia. For many years efforts have been focused on the development of inhibitors of beta-amyloid formation and its related neurotoxic effects. A new concept has been developed which shows that site-directed antibodies may modulate formation of beta-amyloid. The performance of anti-beta-amyloid antibodies in transgenic mice models of Alzheimer's disease showed that they are delivered to the central nervous system, preventing in vivo formation of beta-amyloid. Moreover, those antibodies dissolve beta-amyloid plaques and protect the mice from learning and age-related memory deficits. Experimental active immunization with beta-amyloid (1-42) in humans was stopped in phase II of their clinical trials. However, several new preparations, able to provide antibodies against beta-amyloid by either active or passive routes, have been formulated and have reached clinical testing. The data presented support the hypothesis that beta-amyloid peptide plays a central role in Alzheimer's disease, and antibodies which modulate beta-amyloid conformation may lead to immunotherapy of the disease.
Amyloid-P-component-like immunoreactivity in beta/A4-immunoreactive deposits in Alzheimer-type dementia brains. [2019]An immunohistochemical study using the mirror-image technique was performed in order to establish whether amyloid P component is involved in the mechanism of deposition of amyloid fibrils in senile plaques (SPs) in Alzheimer-type dementia (ATD). Ninety percent of beta/A4 protein-immunoreactive SPs were also stained by the anti-amyloid P component immunohistochemistry, and this applied to all of the diffuse, primitive and classical types of beta/A4 deposits. These findings may suggest an involvement of amyloid P component in the formation of amyloid fibrils in senile plaques in ATD brains.
Serum amyloid P component level in Alzheimer's disease. [2019]Serum amyloid P component (AP) is a normal plasma constituent that is observed in senile plaques and neurofibrillary tangles in brains of Alzheimer's disease (AD) patients. In this study we have evaluated the AP levels in sera of 16 patients with AD and in 16 control subjects by enzyme-linked immunosorbent assay. The AP level was 22.4 +/- (SD) 7.0 micrograms/ml in the AD group and 34.4 +/- (SD) 6.6 micrograms/ml in the control group. The AP level in the AD group was significantly lower than that of the control group (p