Therapeutics

Dayvigo

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Overview

Name: Dayvigo
Synonyms: Lemborexant, E2006
Chemical Name: (1R,2S)-2-{[(2,4-dimethylpyrimidin-5-yl)oxy]methyl}-2-(3-fluorophenyl)-N-(5-fluoropyridin-2-yl)cyclopropanecarboxamide)
Therapy Type: Small Molecule (timeline)
Target Type: Other (timeline)
Condition(s): Alzheimer's Disease
U.S. FDA Status: Alzheimer's Disease (Phase 2)
Company: Eisai Co., Ltd.
Approved for: Insomnia

Background

Dayvigo is the brand name of lemborexant, a brain-penetrant, small-molecule orexin/hypocretin receptor antagonist used to treat insomnia. The neuropeptide orexin regulates wakefulness; inhibiting orexin receptor signaling promotes sleep. Lemborexant has been reported to inhibit the orexin signaling pathway and promote both REM and non-REM sleep in mice and rats; preclinical pharmacological and pharmacokinetic data are formally published (Beuckmann et al., 2017Beuckmann et al., 2019Ueno et al., 2019).

The FDA approved lemborexant in December 2019 (press releaseScott, 2020). When tested in a large Phase 3 trial of people older than 55, lemborexant improved sleep in this population (Rosenberg et al., 2019).

People with AD experience poor sleep and disruption of circadian rhythms that lead to nighttime activity and daytime sleepiness (Harper et al., 2005). Changes in circadian rhythms also occur in preclinical AD, and are linked to increased amyloid deposition and risk of cognitive decline (Oct 2013 newsJu et al., 2013; Musiek et al., 2018). In preclinical work, lemborexant corrected abnormal sleep/wake rhythms in the SAMP8 mouse, which ages abnormally fast (Beuckmann et al., 2021).

Findings

In December 2016, Eisai began a Phase 2 trial to test the effect of lemborexant on multiple sleep parameters in 162 people with mild to moderate AD dementia and circadian rhythm sleep disorder. Participants had their activity recorded around the clock for two weeks with a motion-detecting wrist device. Sixty-two participants who met the criteria of excessive daytime sleep or nighttime wakefulness were randomized to placebo or 2.5, 5, 10, or 15 mg of lemborexant, taken by mouth five minutes before bedtime, for one month. Primary endpoints were change from baseline in 12 different parameters related to circadian rhythm, and daytime and nighttime sleep, during each week of treatment. 

Eisai announced results in an October 2018 press release and presented at the CTAD conference the same month. All participants completed the study, giving data for 12 or 13 people per dose arm. Doses of 2.5, 5, and 15 mg were associated with lower nighttime activity during the four weeks of treatment; 5 and 15 mg improved circadian rhythmicity as measured by an increased ratio of daytime to nighttime activity. Other endpoints showed no statistically significant changes, but trends toward less daytime sleepiness, and better, longer sleep at night.

Side effects were similar to those in the insomnia program for which this drug was originally developed. They included constipation, drowsiness, joint pain, headache, and nightmares, but no falls, confusion, or worsening cognition as measured by the MMSE or ADAS-Cog over the course of the study. For more details, see AAIC poster 2019. Results were published after peer review (Moline et al., 2021). An ongoing, 30-month, open-label extension of the trial was expected to end in April 2020.

A separate trial in 48 healthy volunteers was reported to not impair next-morning driving (Vermeeren et al., 2019). In a study of 60 healthy older adults that assessed middle-of-the-night safety, lemborexant did not impair participants' ability to wake in response to noise, but it did affect their balance and measures of memory and attention. Next-morning balance and cognition did not differ from placebo (Murphy et al., 2020).

Lemborexant is being studied in pain and alcohol use disorder. For details on lemborexant trials, see clinicaltrials.gov.

In Japan, lemborexant trials are ongoing in delirium, schizophrenia, depression and other conditions (see JPRN clinical trials register).

Last Updated: 17 Jan 2023

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Therapeutics

Troriluzole

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Overview

Name: Troriluzole
Synonyms: BHV-4157, trigriluzole, FC-4157
Chemical Name: Glycylglycyl-N2-methyl-N-[6-(trifluoromethoxy)-2-benzothiazolyl]-glycinamide
Therapy Type: Other
Target Type: Other Neurotransmitters (timeline)
Condition(s): Alzheimer's Disease
U.S. FDA Status: Alzheimer's Disease (Discontinued)
Company: Biohaven Pharmaceuticals

Background

Troriluzole is a prodrug formulation of riluzole, a medication used to treat amyotrophic lateral sclerosis. Following oral administration, aminopeptidases in the blood release riluzole from a tripeptide carrier. Unlike riluzole, which must be taken twice a day on an empty stomach, this prodrug requires only once-daily dosing and is unaffected by food.

Riluzole inhibits voltage-dependent sodium channels and reduces synaptic glutamate by increasing its uptake and inhibiting its release. Glutamate dysfunction is a feature of Alzheimer’s disease. Studies in AD mouse models indicate protection from AD-related pathology and cognitive dysfunction by riluzole (Okamoto et al., 2018Hunsberger et al., 2015). In rats, riluzole was reported to prevent age-related changes in gene expression similar to those seen in AD (Pereira et al., 2016). No preclinical studies are published on troriluzole.

Findings

In July 2018, Biohaven began a Phase 2/3 trial enrolling 292 patients with mild to moderate AD at 44 sites across the U.S. This trial was in cooperation with the Alzheimer’s Disease Cooperative Study (ADCS). After an initial screening period of up to six weeks, participants were randomized to one 280 mg capsule of drug or placebo daily for 48 weeks, followed by four weeks of post-treatment observation. The primary outcome measure was to be change from baseline to 48 weeks on the ADAS-Cog11. Mid-trial, the CDR-SB was added as a co-primary outcome. According to a company press release, as of July 2019, around 400 patients had been screened and 180 randomized. The trial ended in November 2020 with a final enrollment of 350 and on January 18, 2021, Biohaven disclosed top-line results. The treatment group did not differ from placebo on either primary or on a key secondary endpoint of hippocampal volume measured by MRI (press release).

In 2021, the company removed troriluzole’s Alzheimer’s indication from its pipeline. Previously, Biohaven had terminated development for generalized anxiety disorder after a negative Phase 3 trial in 2020. In May 2022, Biohaven reported no effect on the primary outcome in a Phase 3 trial for spinal cerebellar ataxia (press release). Under the name of trigriluzole, the same drug was tested in Phase 1 as part of a combination therapy for various cancers (Silk et al., 2022); a Phase 2/3 study of troriluzole for glioblastoma is ongoing. Phase 3 development for obsessive-compulsive disorder continues.

For details on all troriluzole trials, see clinicaltrials.gov.

Last Updated: 07 Feb 2023

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Therapeutics

XPro1595

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Overview

Name: XPro1595
Synonyms: Pegipanermin, INB03, NeuLiv, XENP1595, DN-TNF, XENP345, XPro™ , LIVNate
Therapy Type: Other
Target Type: Inflammation (timeline)
Condition(s): Alzheimer's Disease, Mild Cognitive Impairment
U.S. FDA Status: Alzheimer's Disease (Phase 2), Mild Cognitive Impairment (Phase 2)
Company: INmune Bio Inc.

Background

This pegylated protein biologic targets and neutralizes the inflammatory cytokine TNFα. A non-receptor binding variant of TNFα, XPro1595 forms heterotrimers with native soluble TNFα and prevents its interaction with the type 1 TNFα receptor (Steed et al., 2003). 

Unlike etanercept and other widely used nonselective TNF inhibitor drugs, this second-generation TNF inhibitor does not block signaling by membrane-bound TNFα through the type 2 receptor. Thus, XPro1595 appears to selectively inhibit neuroinflammation mediated by type 1 receptors, but does not suppress innate immunity or myelination mediated by type 2 receptors (Zalevsky et al., 2007Brambilla et al., 2011). In adult mice, long-term treatment with etanercept, but not XPro1595, suppressed hippocampal neurogenesis, learning, and memory (Yli-Karjanmaa et al., 2019). 

XPro1595 is administered by subcutaneous injection and enters the brain.

TNFα is a central player in inflammatory responses. Its protein levels are low in healthy brain but chronically elevated in many neuroinflammatory diseases, including AD. In animal models of AD, TNFα promotes microglial activation, synaptic dysfunction, neuronal cell death, accumulation of plaques and tangles, and cognitive decline (Chang et al., 2017). 

Preclinical XPro1595 evaluation has been reported in three mouse models of AD. In 5XFAD mice, twice-weekly subcutaneous dosing for two months reduced brain amyloid deposition and immune cell infiltration, and improved synaptic function (Mar 2015 conference news; MacPherson et al., 2017). One-month-old TgCRND8 mice received a one-month continuous subcutaneous infusion of XPro1595 and, by six months, had less amyloid deposition than untreated littermates, as well as normalized hippocampal neuron synaptic function (Cavanagh et al., 2016). Intracranial administration reduced pre-plaque amyloid pathology in 3xTg mice (McAlpine et al., 2009); up to six weeks of intracranial infusions in old rats reduced microglia activation and improved synaptic function and cognition (Sama et al., 2012). Blocking soluble TNFα with XPro1595 was also reported to ameliorate the AD risk that results from the effects of a high-fat, high-glucose diet on insulin metabolism, immune, and neural function (De Sousa Rodrigues et al., 2019MacPherson et al., 2023). 

XPro1595 reportedly improved outcomes in rodent models of Parkinson’s and Huntington’s diseases, but no clinical trials are ongoing (Barnum et al., 2014; McCoy et al., 2006; Hsiao et al., 2014). In a company-sponsored study of five rhesus monkeys with toxin-induced progressive parkinsonism, XPro1595 reduced some markers of inflammation, but did not prevent the degeneration of dopaminergic neurons (Joers et al., 2020).

Findings

In November 2019, INmune Bio began a Phase 1b open-label safety and target engagement trial in 20 patients with clinically diagnosed probable Alzheimer’s disease. Participants must have evidence of peripheral inflammation by way of elevated blood C-reactive protein, acetylated hemoglobin, or erythrocyte sedimentation rate, or carry at least one APOE4 allele. Participants received weekly injections of 0.3, 0.6, or 1.0 mg/kg XPro1595 for three months. The primary outcome was safety. Secondary outcomes included change from baseline in biomarkers of neuroinflammation, including blood and CSF C-reactive protein, TNFα, interleukin-1, and interleukin-6; an MRI measure of brain edema; and assessment of breath volatile organic compounds. Investigators also measured CSF Aβ and tau, and cognitive and psychiatric endpoints (Nov 2018 news). 

In October 2020, INmune started a 366-patient trial in the United States to evaluate this drug's ability to treat pulmonary complications of COVID-19. The study was terminated for futility in October 2021, after enrolling 76 patients.

In January 2021, the company announced results on six patients treated with the 1 mg/kg dose. The drug was safe, with injection site reactions being the main adverse event. After three months, white-matter free water, an exploratory imaging marker of neuroinflammation, was decreased by 5 percent. Participants also registered decreases in multiple inflammatory proteins in the CSF, detected by cytokine assays and proteomics analysis. The changes were sustained in three patients who continued on the drug for a year (press release/webinar). The study was completed in September 2021.

IIn February 2022, the company began the Phase 2 MINDFuL trial in people with mild AD and signs of inflammation. As in the Phase 1b, participants must have some combination of elevated C-reactive protein, hemoglobin A1c, or erythrocyte sedimentation rate, and at least one APOE4 allele. The trial plans to randomize 201 participants in a 2:1 ratio to weekly subcutaneous injections of 1 mg/kg XPro1595 or placebo for six months. The sole primary outcome is the six-month change in the Early and Mild Alzheimer’s Cognitive Composite. Secondary outcomes include the Clinical Dementia Rating and other measures of cognition and daily function, MRI measures of axonal and gray matter integrity and brain structure, biomarkers of amyloid, tau, and inflammation, and adverse events. The study is anticipated to run until July 2025 in Australia, Canada, and the United States, and offers an optional open label extension of up to 18 months for all participants.

In April 2022, INmune registered a Phase 2 in 60 participants with mild cognitive impairment who were also positive for amyloid and APOE4. Dosing and primary outcome were the same as the MINDFuL design. The company withdrew this trial before enrollment began, because they plan to enroll MCI patients in MINDFuL.

In May 2022, the FDA placed a clinical hold on XPro1595 trials in the United States, and requested additional information on the manufacturing of the drug (company press release). The trial is active in Australia, where the first patient began treatment in April (press release). As of October 2023, the MINDFul trial is active in Australia and Canada.

INmune is developing XPro1595 for treatment-resistant depression (company pipeline). It is also undergoing trials for cancer, under the name INB03 (see Australian/New Zealand Clinical Trials Registry and Aug 2019 press release). A third indication for hepatitis, under the name of NeuLiv (company press release) or LIVNate, no longer appears in the pipeline.

For trials on XPro1595 in Alzheimer’s disease, see clinicaltrials.gov.

Last Updated: 16 Oct 2023

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Research Models

APPswe/PSEN1dE9 (C57BL6)

Synonyms: APP/PS1, C57BL/6J APPswePsen1de9, B6.APBTg

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Species: Mouse
Genes: APP, PSEN1
Mutations: PSEN1: deltaE9
Modification: APP: Transgenic; PSEN1: Transgenic
Disease Relevance: Alzheimer's Disease
Strain Name: B6.Cg-Tg(APPswe,PSEN1dE9)85Dbo/Mmjax

Summary

Phenotype Characterization

When visualized, these models will distributed over a 18 month timeline demarcated at the following intervals: 1mo, 3mo, 6mo, 9mo, 12mo, 15mo, 18mo+.

Absent

  • Tangles
  • Neuronal Loss

No Data

  • Changes in LTP/LTD

Plaques

Amyloid plaques begin to emerge in the cortex at about 4 months of age and in the hippocampus at about 6 months.

Tangles

Not observed.

Synaptic Loss

Synapse loss in the hippocampus occurs by 4 months.

Neuronal Loss

Neuron loss has not been observed in mice up to 12 months of age.

Gliosis

Plaque-associated astrogliosis and microgliosis are evident by 4 and 8 months, respectively.

Changes in LTP/LTD

No data.

Cognitive Impairment

Deficits in the Morris water maze emerge between 6 and 10 months and worsen with age.

Last Updated: 07 Oct 2019

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Therapeutics

Simufilam

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Overview

Name: Simufilam
Synonyms: PTI-125, sumifilam
Chemical Name: 4-benzyl-8-methyl-1,4,8-triazaspiro[4.5]decan-3-one
Therapy Type: Small Molecule (timeline)
Target Type: Amyloid-Related (timeline)
Condition(s): Alzheimer's Disease
U.S. FDA Status: Alzheimer's Disease (Discontinued)
Company: Cassava Sciences

Background

Simufilam binds to filamin, a ubiquitous scaffolding protein and regulator of the actin cytoskeleton. Filamin has been claimed to stabilize the high-affinity interaction of soluble Aβ42 and the α7 nicotinic acetylcholine receptor (α7nAChR), which has been reported to trigger tau phosphorylation and synaptic dysfunction in some experimental systems (Wang et al., 2000; Wang et al., 2003Snyder et al., 2005).

Preclinical studies suggest that PTI-125 prevents and reverses the binding of Aβ42 to α7nAChR. In one, daily infusions of human synthetic Aβ42 into mouse cerebral ventricles resulted in association of Aβ42 and filamin with α7 receptors in the hippocampus and prefrontal cortex. Concomitant intraperitoneal PTI-125 injections prevented this association, reduced tau phosphorylation and amyloid deposition, and normalized signaling through the α7, NDMA, and insulin receptors. PTI-125 reportedly tamped down Aβ-induced inflammatory cytokine release by blocking filamin recruitment to toll-like receptor 4. When applied to human AD postmortem brain tissue, PTI-125 was reported to cause filamin and Aβ42 to dissociate from the α7 receptor (Jul 2012 news). Subsequently, the same group reported that simufilam could inhibit Aβ42-induced filamin A interactions with multiple inflammatory receptors (Wang et al., 2023). These studies used immunoprecipitation and western blotting to quantitate protein-protein interactions. One study using fluorescence resonance energy transfer in intact cells reported that simufilam reduced Aβ42 binding to α7 with picomolar potency (Wang et al., 2023).

Two months of oral PTI-125 in 3xTg AD mice reportedly reduced tau hyperphosphorylation, amyloid and tau deposition, and neuroinflammation, and restored synaptic function, nesting behavior, and spatial and working memory relative to untreated mice. The study claimed that Aβ42 induces a conformational change in filamin, which would promote its association with the α7 and toll-like receptors, enabling Aβ42 toxicity and inflammation. PTI-125 was said to preferentially bind altered filamin and normalize its conformation (Wang et al., 2017). Most research on filamin, Aβ42 and Alzheimer's comes from the same laboratory, although several independent studies have implicated filamin in AD and progressive supranuclear palsy (Levert et al., 2023; Aumont et al., 2022; Tsujikawa et al., 2022).

Findings

In 2017, Cassava Sciences started with a Phase 1 safety study of 50, 100, or 200 mg of PTI-125 in 24 healthy adults.

In early 2019, the company ran an NIH-funded Phase 2a trial in people with mild to moderate AD. This open-label, multicenter safety, pharmacokinetics, and biomarker study enrolled 13 participants with MMSE scores between 16 and 24 and a CSF total tau/Aβ42 ratio of 0.30 or higher. They took 100 mg PTI-125 capsules twice daily for 28 days. Primary outcomes were pharmacokinetic measures; secondary ones were CSF biomarkers of Alzheimer’s pathology, neurodegeneration, and neuroinflammation. The study measured levels of PTI-125DX, an experimental diagnostic biomarker to indicate altered filamin in blood.

In a September 2019 press release, Cassava claimed that drug treatment significantly decreased CSF total and phosphorylated tauT181, neurofilament light, neurogranin, YKL-40, Il-6, Il-1β, and TNFα, consistent with drug effects countering neurodegeneration and -inflammation. P-tauT181 and neurogranin reportedly fell by about a third with treatment, while the inflammatory markers decreased from 5 to 14 percent. Every participant showed changes on most markers with treatment. The ratio of phosphorylated tau to Aβ42 apparently improved. This trial did not measure cognition. At CTAD, the company presented data claiming reduction in plasma levels of neurogranin, total tau, neurofilament light, and YLK-40 after treatment. Multiple forms of modified tau declined in plasma, including p-tauT181, p-tauT202, and p-tauT231, as did a nitrated form of tau, n-tauY29 (Dec 2019 conference news). The data were published after peer review (Wang et al., 2020). In a subsequent analysis, the company claimed that simufilam treatment had normalized suboptimal insulin responses in patients’ blood cells by modulating filamin A interaction with the mTOR protein (Wang et al., 2023).

From September 2019 to March 2020, the company ran an NIH-funded Phase 2b study at 10 sites across the U.S. It compared 100 or 50 mg PTI-125 with placebo, dosed twice daily for 28 days, in 64 participants with a clinical diagnosis of mild to moderate AD, confirmed by CSF biomarkers. The primary endpoint was change in CSF phosphorylated tau, neurofilament light chain, neurogranin, total tau, YKL-40, and Aβ42; secondary outcomes include cognition and plasma biomarkers. The randomized period of this trial was followed by an open-label extension for participants who completed previous Phase 2 trials, plus new enrollees to bring its participant number up to 100. This study aimed to gather one-year treatment data on the 100 mg twice-daily dose.

In top-line results announced in May 2020, the 28-day dosing phase missed its primary outcome of improving CSF disease biomarkers (press release). In November 2020 at CTAD, data on reanalyzed CSF samples were presented, whereby both doses reportedly led to improvements in all CSF biomarkers tested, compared to placebo, with 10 to 40 percent decreases in total tau, p-tau181, neurogranin, NfL, HMGB1, YKL40, IL-6, sTREM2, albumin, and immunoglobulin G. CSF Aβ42 was reported to have risen by about 10 percent. Scores on episodic memory and spatial working memory tests were reported as having improved in treated groups, with effect sizes between 17 and 46 percent. No safety issues were reported (press release). In a poster at the July 2021 AAIC, the company claimed to see a significant reduction in plasma p-tau181 in both treated groups compared to placebo. 

The study confirmed target engagement as defined by reduced association of filamin-A with the α7 and TLR4 receptor in lymphocytes.

In November 2020, the drug's name was changed to simufilam, due to a potential trademark conflict with the previous name (press release).

In February 2021, the company announced interim data from the open-label extension, claiming that 50 patients who had completed six months of dosing improved by 1.6 points on the ADAS-Cog and 1.3 points on the NPI (press release). Adverse events were said to be mild and transient. At the July 2021 AAIC, the company reported on CSF biomarkers measured in 25 people after six months treatment. Aβ42 significantly increased, while total tau, p-tau181, NfL, neurogranin, sTrem2, YKL40, and HMGB1 all significantly decreased between 18 and 72 percent. At the same conference, the company claimed a continued improvement on ADAS-COG11 by 3 points in the first 50 patients who completed nine months of the open-label treatment. 

In mid-2021, Cassava expanded the open-label study from 100 to 200 patients, and added a new extension. Patients who completed one year of open-label simufilam were randomized to further treatment or placebo for six months to assess effects of withdrawal, followed by another six months of open-label treatment. The open-label portion of the study finished in December 2022. Dosing for the placebo-controlled extension was completed in May 2023.

In May 2021, a pharmacokinetic study of formulation and food effects was completed in 24 healthy volunteers.

In November 2021, the company began two Phase 3 trials. The ReThink-ALZ study was to randomize 750 participants with AD and a clinical dementia rating of 0.5, 1, or 2 to placebo or 100 mg simufilam twice a day for one year, with co-primary outcomes of the ADAS-Cog12 and ADCS-ADL. This trial will run through October 2023. The parallel ReFocus-ALZ trial was to enroll 1,083 similar patients to be randomized to placebo, 50, or 100 mg simufilam twice a day for 18 months, with the same primary outcomes, and run until June 2024. The company announced an agreement with the FDA on special protocol assessments for these trials of simufilam (corporate presentation).

In August 2021, an anonymous citizen petition was filed with the FDA, requesting the agency halt ongoing simufilam trials. The complaint alleged instances of research misconduct involving the clinical trial biomarker data and previous, foundational research on the drug (Endpoint news, FDA website). Soon after, several independent scientists reported instances of apparent data manipulation in several published studies (see PubPeer and Retraction Watch) and in the blood biomarker data on the 2021 AAIC poster (Science Integrity Digest blog). On September 3, the company denied wrongdoing, admitting errors in a figure on the poster but standing by the underlying data analysis and conclusions (see statement, corrected figure). Quanterix, the biomarker testing CRO that analyzed the blood, denied any role in the disputed analysis beyond assaying blinded samples and reporting raw values to Cassava (press release). In January 2022, a New Yorker article on whistleblowers detailed the circumstances surrounding this citizen petition. In February 2022, the FDA rejected the petition on procedural grounds (FDA letter).

In September 2021, a securities fraud class action lawsuit was filed against Cassava Sciences (Yahoo Finance news). In November 2021, the company disclosed that it is the target of an SEC investigation into claims that it manipulated research results on simufilam (WSJ article).

In February, 2022, the journal Neuroscience published an editorial note to a 2005 paper, finding no evidence of data manipulation. In March 2022, the journal PlosOne retracted five papers by Cassava academic collaborator Hoau-Yan Wang at CUNY; although none were related to the AD work, two had been co-authored with a Cassava employee (Wang et al., 2008Wang and Burns, 2009Bakshi et al., 2011Bakshi et al., 2014Stucky et al., 2016). In 2021 and 2022, journals re-examined three of Wang’s papers related to simufilam; none found convincing evidence of data manipulation, according to a Cassava press release.

On 18 April 2022, the New York Times featured simufilam in a news article. On May 5, the company announced that the phase 3 program had thus far enrolled about 120 participants. On July 7, a securities class action case was opened. On July 27, Reuters news agency reported that the U.S. Department of Justice had opened a criminal investigation into whether Cassava Sciences manipulated research results (Reuters news). 

In their August 2022 earnings report, Cassava released additional results on the open-label trial. The first 100 patients to complete at least 12 months treatment reportedly improved their ADAS-COG scores by an average of 1.5 points from baseline. The company also reported that their Phase 3 trials had enrolled more than 500 patients out of an intended 1,750, evenly split between the two studies (press release; September 13 corporate presentation). A 2023 publication is under investigation for image irregularities (Wang et al., 2023Frontiers Editorial Office, Aug 2023).

In October 2022, a person unaffiliated with Cassava asked the FDA to grant breakthrough therapy designation to simufilam. The agency rejected the request, on the grounds that only the drug sponsor can apply for this designation (FDA letter).

Also in October 2022, the company added an optional, one-year, open-label extension to their Phase 3 trials (press release).

In November 2022, Cassava announced it had filed a defamation lawsuit against the whistleblowers who originated the citizen’s complaint with the FDA, and others (press release).

In January 2023, Cassava announced final results of their open label study (press release). In 200 patients treated for one year or more, ADAS-Cog scores declined by an average of 0.5 points. This was in contrast to previous findings on the first 100 patients, where the company reported an improvement of 1.5 points after one year. The drug remained safe, with no serious adverse events reported. 

In February 2023, the company said 953 patients were enrolled in the Phase 3 trials, just over half the target (press release). In July 2023, the company reported topline results of the six-month withdrawal study involving 157 patients (press release). The primary outcome of change in the ADAS-Cog was not statistically significantly different between drug continuation and withdrawal groups.

In October 2023, Science magazine reported that the City University of New York had accused Wang of research misconduct involving 20 research papers, including work that formed the basis for simufilam’s clinical development (Science articleWSJ story). The news story was based on a confidential draft report. The leak of the report and other questions about the integrity of the investigation led the University to pause its inquiry (statement; NYT article). In a press release, Cassava denied wrongdoing. 

In November 2023, the company announced that enrollment was complete in both Phase 3 trials (press release).

On June 28 2024, a federal grand jury indicted Wang for fraud, charging he falsified data, including measurements of clinical samples, to obtain NIH grants for himself and Cassava (DOJ press release).

On July 1, Cassava disclosed in an SEC filing that the DOJ and SEC were investigating two senior employees. According to the filing, an internal inquiry prompted by information shared by the SEC found the possibility of unblinding and inaccuracies in the Phase 2b data reported in 2020 (SEC Form 8-K). On July 17, Cassava’s CEO and its chief scientist both resigned (press release). On July 27, Reuters reported the DOJ criminal probe of Cassava relating to Simufilam development (Reuters story). On September 26, the SEC announced that Cassava would pay a $40 million penalty to settle charges of securities fraud and reporting violations related to misrepresentations of the Phase 2 trial data (SEC press release). Former Cassava employees Remi Barbier and Lindsay Burns paid smaller fines for fraud, and were barred from taking officer or director positions for three and five years, respectively. Wang was also fined. The Phase 3 trials continued.

On November 25, 2024, Cassava announced negative results for the Phase 3 ReThink-ALZ trial (press release). One year of treatment did not change any of the co-primary, secondary, or exploratory endpoints in patients with mild to moderate AD. A planned subgroup analysis of mild or moderate patients likewise found no treatment effects. The company said it will stop the ongoing ReFocus-ALZ Phase 3 trial, and the open-label extension.

For details of registered trials, see clinicaltrials.gov.

Clinical Trial Timeline

  • Phase 2
  • Study completed / Planned end date
  • Planned end date unavailable
  • Study aborted
Sponsor Clinical Trial 2017 2018 2019 2020 2021 2022 2023 2024 2025 2026 2027 2028 2029 2030 2031 2032 2033 2034 2035
Cassava Sciences NCT04079803
N=60

Last Updated: 25 Nov 2024

Further Reading

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Research Models

PWK.APP/PS1

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Species: Mouse
Genes: APP, PSEN1
Mutations: PSEN1: deltaE9
Modification: APP: Transgenic; PSEN1: Transgenic
Disease Relevance: Alzheimer's Disease
Strain Name: PWK.Cg-Tg(APPswe,PSEN1dE9)85Dbo/How

Summary

Phenotype Characterization

When visualized, these models will distributed over a 18 month timeline demarcated at the following intervals: 1mo, 3mo, 6mo, 9mo, 12mo, 15mo, 18mo+.

Absent

  • Tangles
  • Neuronal Loss
  • Cognitive Impairment

No Data

  • Synaptic Loss
  • Changes in LTP/LTD

Plaques

Thioflavin S-positive amyloid plaques are present in the cortex and CA1 region of the hippocampus by 8 months of age, with females having more plaques in the cortex than males.

Tangles

Not observed.

Synaptic Loss

No data.

Neuronal Loss

Not observed.

Gliosis

Plaque-associated microgliosis observed by 8 months.

Changes in LTP/LTD

No data.

Cognitive Impairment

Working memory and short-term memory were intact at 7 to 8 months, as assessed by tests in the Y-maze.

Last Updated: 01 Oct 2019

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Further Reading

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Research Models

WSB.APP/PS1

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Species: Mouse
Genes: APP, PSEN1
Mutations: PSEN1: deltaE9
Modification: APP: Transgenic; PSEN1: Transgenic
Disease Relevance: Alzheimer's Disease
Strain Name: WSB.Cg-Tg(APPswe,PSEN1dE9)85Dbo/How

Summary

Phenotype Characterization

When visualized, these models will distributed over a 18 month timeline demarcated at the following intervals: 1mo, 3mo, 6mo, 9mo, 12mo, 15mo, 18mo+.

Absent

  • Tangles

No Data

  • Synaptic Loss
  • Changes in LTP/LTD

Plaques

Thioflavin S-positive amyloid plaques are present in the cortex and CA1 region of the hippocampus by 8 months of age, with females having more plaques in the cortex than males.

Tangles

Not observed.

Synaptic Loss

No data.

Neuronal Loss

Compared with their non-transgenic littermates, female WSB.APP/PS1 mice have fewer neurons in the cortex and in CA1. Neuron numbers in male mice do not differ between the genotypes.

Gliosis

Plaque-associated microgliosis observed by 8 months.

Changes in LTP/LTD

No data.

Cognitive Impairment

Deficits in short-term memory by 8 months in females (data from males unavailable).

Last Updated: 01 Oct 2019

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Further Reading

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Research Models

CAST.APP/PS1

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Species: Mouse
Genes: APP, PSEN1
Mutations: PSEN1: deltaE9
Modification: APP: Transgenic; PSEN1: Transgenic
Disease Relevance: Alzheimer's Disease
Strain Name: CAST.Cg-Tg(APPswe,PSEN1dE9)85Dbo/How

Summary

Phenotype Characterization

When visualized, these models will distributed over a 18 month timeline demarcated at the following intervals: 1mo, 3mo, 6mo, 9mo, 12mo, 15mo, 18mo+.

Absent

  • Tangles

No Data

  • Synaptic Loss
  • Changes in LTP/LTD

Plaques

Thioflavin S-positive amyloid plaques are present in the cortex and hippocampus by 8 months of age, with more severe plaque pathology in females than in males.

Tangles

Not observed.

Synaptic Loss

No data.

Neuronal Loss

Compared with their non-transgenic littermates, CAST.APP/PS1 mice have fewer neurons in area CA1 of the hippocampus. Cortical neuron numbers do not differ between the genotypes.

Gliosis

Plaque-associated microgliosis observed by 8 months.

Changes in LTP/LTD

No data.

Cognitive Impairment

Deficits in short-term memory by 8 months in males (data from females unavailable).

Last Updated: 08 Oct 2019

COMMENTS / QUESTIONS

No Available Comments

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Further Reading

No Available Further Reading

Research Models

AD-BXD

Synonyms: 5xFAD BxD

Tools

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Species: Mouse
Genes: APP, PSEN1
Modification: APP: Transgenic; PSEN1: Transgenic
Disease Relevance: Alzheimer's Disease
Strain Name: (B6.Cg-Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/Mmjax x BXD[strain number]

“AD-BXD” refers to a panel of transgenic mouse strains, created to model the genetic diversity seen in human populations. These mice represent a unique resource for scientists seeking to identify genetic factors that influence resilience or vulnerability to AD, examining the interactions between genetic and environment factors, or wishing to conduct preclinical studies in an animal population that incorporates genetic heterogeneity that better reflects human populations.

Phenotype Characterization

When visualized, these models will distributed over a 18 month timeline demarcated at the following intervals: 1mo, 3mo, 6mo, 9mo, 12mo, 15mo, 18mo+.

Absent

No Data

  • Tangles
  • Neuronal Loss
  • Synaptic Loss
  • Changes in LTP/LTD

Plaques

Transgenic AD-BXD mice develop amyloid plaques by 6 months of age, the earliest age examined. The extent of plaque deposition is strain-dependent.

Tangles

No data.

Synaptic Loss

No data.

Neuronal Loss

No data.

Gliosis

Strain-dependent gliosis by 6 months. 

Changes in LTP/LTD

No data.

Cognitive Impairment

In the AD-BXD population as a whole, transgenic mice performed similarly to non-transgenic littermates in a contextual fear-conditioning test at 6 months, but were impaired at 14 months. The age of onset and severity of impairment are strain-dependent.

Last Updated: 30 Jan 2025

COMMENTS / QUESTIONS

No Available Comments

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Further Reading

No Available Further Reading

Research Models

AppNL-G-F/MAPT double knock-in

Synonyms: AppNL-G-F/MAPT double knock-in, AppNL-G-F/MAPT dKI

Tools

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Species: Mouse
Genes: App, MAPT
Modification: App: Knock-In; MAPT: Knock-In
Disease Relevance: Alzheimer's Disease
Strain Name: N/A

Summary

Phenotype Characterization

When visualized, these models will distributed over a 18 month timeline demarcated at the following intervals: 1mo, 3mo, 6mo, 9mo, 12mo, 15mo, 18mo+.

Absent

  • Tangles
  • Neuronal Loss

No Data

  • Synaptic Loss
  • Changes in LTP/LTD

Plaques

Plaques observed at 2 months.

Tangles

No neurofibrillary tangles observed up to 24 months of age.

Synaptic Loss

No data.

Neuronal Loss

No neurodegeneration observed up to 24 months of age.

Gliosis

Astrogliosis and microgliosis observed by 4 months.

Changes in LTP/LTD

No data.

Cognitive Impairment

Deficits in the Y-maze test of working memory at 12 months of age.

Last Updated: 13 Aug 2019

COMMENTS / QUESTIONS

No Available Comments

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Further Reading

No Available Further Reading

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