Therapeutics

LM11A-31-BHS

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Overview

Name: LM11A-31-BHS
Synonyms: LM11A-31
Chemical Name: (2S,3S)-2-amino-3-methyl-N-[2-(4-morpholinyl)ethyl]-pentanamide, dihydrochloride
Therapy Type: Small Molecule (timeline)
Target Type: Other (timeline)
Condition(s): Alzheimer's Disease
U.S. FDA Status: Alzheimer's Disease (Phase 2)
Company: PharmatrophiX

Background

LM11A-31 is an orally available, brain-penetrant, small-molecule ligand of the p75 neurotrophic receptor. P75NTF binds nerve growth factor, brain-derived growth factor, and other neurotrophins. Its signaling can promote either neuron survival or death by apoptosis, depending on its ligand and cellular context.

In AD models, P75NTF mediates neurotoxic effects of Aβ (Sotthibundhu et al., 2008; Knowles et al., 2009).

LM11A-31 selectively activates p75NTF survival pathways and inhibits apoptosis signaling (Massa et al., 2006). It blocks Aβ-induced neurodegeneration and synaptic impairment in neuronal and hippocampal slice cultures (Yang et al., 2008). Its neuroprotective actions are not specific for Aβ, as it also counteracts toxicity of anticancer drugs on neurons in culture (James et al., 2008).

LM11A-31 has been studied in multiple mouse models of AD, where it prevented tau phosphorylation and misfolding, microglia and astrocyte activation, loss of cholinergic neurites, and cognitive decline (Knowles et al., 2013; Nguyen et al., 2014). It reduced tau pathology in mice expressing amyloid precursor protein or the P301L tau mutant (Yang et al., 2020; Yang et al., 2020). In mouse models with cholinergic neuron deficits, treatment induced recovery of dendrites (Simmons et al., 2014).

In normal mice, LM11A-31 suppressed cholinergic loss during aging (Xie et al., 2019). LM11A-31 was reported to show efficacy in mouse models of Huntington’s disease (Simmons et al., 2016), traumatic brain or spinal cord injury (Haefeli et al., 2017; Shi et al., 2013; Tep et al., 2013), chemotherapy-induced peripheral neuropathy (Friesland et al., 2014), HIV-induced neurodegeneration (Xie et al., 2021, Killebrew et al., 2021), peripheral nerve injury (McGregor et al., 2021, Aby et al., 2021), and acute stroke (Nasoohi et al., 2023; Nguyen et al., 2022). In other rodent models, it reduced cognitive impairment caused by sepsis-induced neuroinflammation in mice (Ji et al., 2018), and reduced excessive alcohol intake in rats (Darcq et al., 2016). 

LM11A-31 has been evaluated in mouse models of strep meningitis and of erectile dysfunction, and in cats infected with feline immunodeficiency virus (Zhang et al., 2021, Yin et al., 2021Fogle et al., 2021).

Pharmatrophix advanced a modified version of LM11A-31, LM11A-31-BHS, to clinical trials.

Findings

No Phase 1 trial was registered for LM11A-31-BHS, but the company states that the compound is safe and well-tolerated based on a safety trial conducted in healthy young and elderly adults (Dec 2017 news). That trial was funded by the ADDF, the Alzheimer’s Association, and private investors. A second Phase 1 study ran in healthy adults in Spain (company website).

In February 2017, a Phase 1/2 trial of LM11A-31-BHS started enrolling 242 people with mild to moderate Alzheimer’s disease, confirmed with CSF Aβ biomarkers. Participants were randomized to receive 400 or 800 mg drug or placebo daily for six months. The primary outcome was safety on clinical, electrophysiological, and laboratory measures; secondary outcomes include CSF biomarkers of tau, phosphorylated tau, Aβ, and acetylcholinesterase activity. Also included as secondary outcomes were cognitive assessments of working memory, word fluency, processing speed, and executive function. The trial ran at 21 centers in Austria, Czechia, Germany, Spain, and Sweden, with funding from the U.S. National Institute on Aging and philanthropic support. It finished in June 2020.

At the November 2021 CTAD conference, safety and biomarker results were presented. Sixteen of the 242 participants discontinued dosing due to adverse events. These occurred more frequently on the high dose and included three serious adverse events. Dose-dependent increases in nasopharyngitis, gastrointestinal symptoms, and transient asymptomatic eosinophilia were seen. CSF biomarkers of Aβ, tau, synaptic function, and inflammation all moved in the direction of an expected benefit, with Aβ40 and 42, SNAP25, neurogranin, and YKL40 significantly changed in the treatment groups. Trend changes in hippocampal volume and cognition were not statistically significant but favored drug. A slowing of decline in FDG-PET in regions of interest did not reach significance, but a voxel-wise analysis found slower decline in most voxels in the treatment group compared to placebo. Trial results were published after peer review (Shanks et al., 2024). Additional exploratory biomarker results were presented at the October 2024 CTAD conference. In untreated patients, plasma pTau-217 increased by 29.1 percent per year, and LM11A-31-BHS significantly slowed this rise. Proteomics analysis confirmed significant changes in CSF YKL-40, neurogranin, and total tau, consistent with earlier results that used antibody-based detection methods. Treatment also slowed changes in proteomic networks related to AD progression.

For details, see clinicaltrials.gov

Last Updated: 15 Nov 2024

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Therapeutics

Ambroxol

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Overview

Name: Ambroxol
Synonyms: Ambrosan, Mucosolvan
Chemical Name: trans-4-(2-Amino-3,5-dibrombenzylamino)-cyclohexanol
Therapy Type: Small Molecule (timeline)
Target Type: alpha-synuclein, Other (timeline)
Condition(s): Parkinson's Disease, Parkinson's Disease Dementia, Dementia with Lewy Bodies
U.S. FDA Status: Parkinson's Disease (Phase 2), Parkinson's Disease Dementia (Phase 2), Dementia with Lewy Bodies (Phase 2)
Status in Select Countries: OTC for cough relief.

Background

Ambroxol is a mucolytic compound and the main ingredient of over-the-counter cough medicines sold in many countries. Syrup, tablet, and other forms are used at doses of 30 to 120 mg per day to reduce or thin mucous secretions and ease sore throat pain. The most common side effects are gastrointestinal. Ambroxol is unavailable in North America.

Interest in repurposing ambroxol to treat Parkinson’s disease stems from its activity as a molecular chaperone for the lysosomal enzyme glucocerebrosidase (GCase) (Maegawa et al., 2009). Loss-of-function mutations in the GCase gene, GBA1, are the leading genetic risk factor for the synucleinopathies Parkinson’s disease and dementia with Lewy bodies (DLB).

GCase activity and α-synuclein are linked: GCase deficiency causes pathologic accumulation of α-synuclein (Cullen et al., 2011), while GCase overexpression in brain reduces pathology and memory deficits in a synucleinopathy mouse model (Sardi et al., 2011). GCase activity is also diminished in cases of idiopathic PD and DLB without GBA1 mutations, and lower GCase correlates with earlier disease onset and worse cognitive and non-motor symptoms (Gegg et al., 2012; Chiasserini et al., 2015). GBA1 mutations were originally identified as the cause of parkinsonism in Gaucher’s disease, a lysosomal storage disorder characterized by the buildup of sphingolipids, and, in some cases, α-synuclein pathology (Lwin et al, 2004Mazzulli et al., 2011).

In cells derived from patients with Gaucher’s or PD, ambroxol stabilized mutant GCase and facilitated its movement from the endoplasmic reticulum to lysosomes, increasing protein levels, enzyme activity, and lysosome function (Bendikov-Bar et al., 2013; McNeill et al., 2014). In flies with GCH1 mutations, ambroxol increased GCase activity, decreased ER stress, and protected motor function (Sanchez-Martinez et al., 2016).

In wild-type and GCH1-mutation-bearing mice, ambroxol induced brain GCase activity, and in mice overexpressing human α-synuclein, it decreased total and phosphorylated α-synuclein (Migdalska-Richards et al., 2016). In a mouse model of amyotrophic lateral sclerosis, ambroxol improved motor function and extended survival (Bouscary et al., 2019).

In healthy, non-human primates, daily ambroxol increased brain GCase activity (Migdalska-Richards et al., 2017).

Findings

In December 2016, an open-label pilot study in Parkinson’s disease, called AIM-PD, began at University College London. It enrolled 23 patients, half with a GBA1 mutation and half without, to assess safety, tolerability, CNS penetration and target engagement of ambroxol. After a one-month dose escalation, participants received 1,260 mg per day for five months—a dose 10 times higher than used to treat cough. Primary endpoints were ambroxol levels and GCase activity in CSF. Secondary outcomes included safety, GCase protein and activity, α-synuclein and tau in CSF and blood, and measures of cognitive and motor function.

Results were presented at a 2018 AD/PD conference and later formally published (Apr 2018 conference newsMullin et al., 2020). Eighteen patients completed the study, five withdrew due to problems related to lumbar-puncture, but no serious adverse events were reported. The study met its primary endpoints: Ambroxol crossed the blood-brain barrier and in the CSF achieved a concentration of 11 percent of blood levels. CSF GCase activity decreased by 19 percent, consistent with ambroxol’s ability to inhibit the enzyme at neutral pH. Other findings included a 35 percent increase in CSF GCase protein levels, and a significant increase in CSF α-synuclein, with no change in tau or glucosyl ceramide. Participants improved on the Unified Parkinson’s Disease Rating Scale, mainly due to gains in motor function. Drug effects were detected in patients with or without GBA mutations.

In November 2015, a Phase 2 trial at the Parkwood Institute, Ontario, Canada, began recruiting 75 people with Parkinson’s and mild to moderate dementia (Silveira et al., 2019). Participants were to receive 525 or 1,050 mg daily ambroxol or placebo for one year. Primary outcomes are changes on ADAS-Cog and ADCS-CGIC; secondary outcomes include additional cognitive measures, movement testing, CSF biomarkers of α-synuclein, tau, phospho-tau, and Aβ, MRI measures of ventricular volume and hippocampal atrophy. The trial also assesses GCase activity in lymphocytes and plasma ambroxol levels. As of July 2018, the trial had enrolled 25 patients, with 10 completing one year of treatment (see AAIC abstract). Blood levels of ambroxol were sufficient to increase GCase activity in peripheral lymphocytes. The drug was well tolerated. The trial is slated to end in December 2021. Sometime after this report, the lower-dose group was discontinued and the enrollment target reduced to 58. Enrollment is expected to be complete in the summer of 2021.

In May 2020, the same investigators registered an additional Phase 2 trial to test a higher dose of 1,350 mg/day. The study will treat 15 people with PDD for one year, with primary outcomes of MMSE, safety, pharmacokinetics, and GCase activity in blood and CSF.

In March 2019, an open-label Phase 2 began in Israel for 60 participants with Gaucher’s disease who responded poorly to enzyme replacement therapy.

Japanese researchers published a pilot study on five people with neurological symptoms due to Gaucher’s, in whom open-label ambroxol ameliorated muscle spasms (Narita et al., 2016). In September 2019, this group registered a larger, open-label trial in 25 patients in Japan.

In spring 2021, a Phase 2 trial will begin testing ambroxol in people with dementia or mild cognitive impairment with Lewy Bodies. The study, at seven centers in Norway, will enroll 172 participants for 18 months treatment with 1,320 mg daily or placebo. Treatment groups will be stratified based on ApoE4 and CSF Aβ42 concentrations. Primary outcomes are adverse events, treatment discontinuations, and other safety signs, plus measures of cognition, functional decline, and neuropsychiatric symptoms. Secondary outcomes will assess sleep, cognitive fluctuations, motor symptoms, and falls. The trial offers a one-year, open label extension.

In May 2020, an investigator-initiated global registry of ambroxol use in 300 patients with Gaucher's or GBA-Parkinson's disease was listed as an observational study of real-world evidence on clinicaltrials.gov. In March 2021, it published data from the first 41 participants, reporting no severe adverse effects related to ambroxol, and clinical benefit in 25 of them (Istaiti et al., 2021). 

For details on ambroxol trials, see clinicaltrials.gov.

Last Updated: 22 Apr 2021

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Research Models

Bace1 conditional knockout (Tesco)

Synonyms: Bace1 cKO, BACE1flox/flox;RosaCreERT2+/WT

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Species: Mouse
Genes: Bace1
Modification: Bace1: Conditional Knock-out
Disease Relevance: Alzheimer's Disease
Strain Name: C57BL/6-Bace1tm1.1mrl

Summary

This is the second of two similar models designed to mimic BACE1 inhibition, in which researchers can control the timing of BACE1 deficiency. These conditional knockouts avoid the developmental effects of BACE1 deficiency that are seen in germline knockouts, and, if crossed with mouse models of amyloidosis, allow the investigation of the effect of timing of BACE1 reduction on the progression of pathology.

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

  • Cognitive Impairment

No Data

  • Plaques
  • Tangles
  • Neuronal Loss
  • Gliosis
  • Synaptic Loss

Plaques

No data.

Tangles

No data.

Synaptic Loss

No data.

Neuronal Loss

No data.

Gliosis

No data.

Changes in LTP/LTD

Deficit in long-term potentiation at Schaffer collateral–CA1 synapses in slices from 14-month-old animals that had received tamoxifen between 8 and 12 weeks of age.

Cognitive Impairment

Animals that had received tamoxifen between 8 and 12 weeks of age were tested at 4–5 or 12–14 months. Tamoxifen-treated mice performed similarly to vehicle-treated controls in the Y-maze, contextual fear conditioning, pre-pulse inhibition, open field, and light-dark transition tests.

Last Updated: 17 Jan 2020

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Therapeutics

Fosgonimeton

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Overview

Name: Fosgonimeton
Synonyms: ATH-1017, NDX-1017
Therapy Type: Small Molecule (timeline)
Target Type: Other (timeline)
Condition(s): Alzheimer's Disease, Dementia with Lewy Bodies, Parkinson's Disease Dementia
U.S. FDA Status: Alzheimer's Disease (Discontinued), Dementia with Lewy Bodies (Discontinued), Parkinson's Disease Dementia (Discontinued)
Company: Athira Pharma

Background

NDX-1017 is a brain-penetrant small molecule that activates signaling via the hepatocyte growth factor (HGF)/MET receptor system (Moebius and Church, 2023). HGF promotes proliferation and survival of neurons, enhances hippocampal synaptic plasticity, and boosts learning and memory (Akimoto et al., 2004; Kato et al., 2012). NDX-1017 is being developed as a subcutaneous once-daily injection.

Hippocampal expression of MET receptors is diminished in Alzheimer’s disease (Hamasaki et al., 2014). Conversely, expression of HGF by gene transfer improved Aβ-induced cognitive deficits in mice, and prevented motor symptoms and neuron loss in a rat model of parkinsonism (Takeuchi et al., 2008; Koike et al., 2006).

Direct, intrathecal administration of hepatocyte growth factor itself has been studied in a rat model of ALS and a marmoset model of traumatic brain injury, and is being investigated clinically for ALS in Japan (Aoki et al., 2019). 

Fosgonimeton is a prodrug formulation of a small molecule originally identified in a screen for positive modulators of HGF/MET signaling (Johnston et al., 2023). The small molecule, fosgonimeton-active metabolite (fosgo-AM), was reported to be neurotrophic and neuroprotective in primary rat neurons, and to reverse scopolamine-induced learning deficits in rats. To improve its pharmacokinetics, the company developed the prodrug formulation, which generated higher blood and brain levels of fosgo-AM than were possible with direct delivery of the metabolite. In a mouse model of cognitive impairment due to acute inflammation, fosgonimeton partly reversed cognitive deficits. It was also reported to prevent Aβ42 toxicity and protect dopamine neurons against 6-OHDA (2023 AD/PD conference poster, Reda et al., 2024).

This drug may be related to N-hexanoic-Tyr-Ile-(6) aminohexanoic amide, aka DihexaU.S. Patent 8598118B2. This small-molecule, brain-penetrant angiotensin IV analog was invented by researchers at Washington State University, Pullman. Dihexa activates HGF/MET signaling to stimulate dendritic arborization and synaptogenesis, and improves learning/memory in aged rats, and in rats with scopolamine-induced amnesia (ScienceDaily news storyMcCoy et al., 2013; Benoist et al., 2014; reviewed in Wright and Harding, 2015). 

M3 Biotechnology was founded to commercialize Dihexa (see WSU article). The company told Alzforum that further development led to NDX-1017. M3 Biotechnology in 2019 was renamed Athira Pharma, and NDX-107 in 2020 was renamed ATH-1017 and, in March 2022, fosgonimeton.

Findings

In October 2017, the company began a first-in-human, Phase 1 safety study of single- and multiple-ascending doses in 88 healthy people and AD patients. Funded by ADDF and others, the placebo-controlled trial tested doses from 2 to 90 mg, injected subcutaneously. Outcomes were drug-related adverse events and pharmacokinetics.

Results were presented at the 2019 CTAD conference (Dec 2019 conference news). In the single-ascending-dose portion, 48 healthy men received up to 90 mg and no drug-related adverse events were seen. Likewise, multiple dosing of 29 healthy elderly and 11 AD patients with up to 80 or 40 mg/day, respectively, for nine days raised no safety issues, with dose-proportional pharmacokinetics in all groups.

Quantitative electroencephalography (qEEG) and event-related potential (ERP) measures were evaluated as noninvasive markers of brain penetration and target engagement by NDX-1017. EEG gamma power is associated with learning, memory, and executive functions, while ERP P300 latency is a marker of cognitive processing speed. In people with AD, gamma power is reduced, and P300 latency is lengthened. In the trial, NDX-1017 was reported to cause a dose-related increase in gamma power in healthy people; in the AD group, multiple dosing led to improvements in gamma power and p300 latency. The trial included no cognitive assessments. Trial results were published after peer review (Hua et al., 2022NeurologyLive).

In September 2020, the company began a Phase 2 trial called LIFT-AD. It planned to enroll 300 participants with clinically diagnosed mild to moderate AD, and compare two doses of drug to placebo, given once daily using prefilled syringes, for six months. The primary outcome will be the Global Statistical Test, a combination of scores from the ADAS-Cog11 and the ADCS-Clinical Global Impression of Change. Secondary endpoints will include ADAS-Cog11, ADCS CGIC, and ADCS-ADL. In early 2022, the company increased enrollment to 420, and reclassified the trial to Phase 3. In 2023, enrollment was further increased to 475, with completion expected in January 2024.

In November 2021, another Phase 2 study called ACT-AD began to assess the relationship between ERP changes and cognition in 77 people with mild to moderate AD. Participants received 40 or 70 mg ATH-1017 or placebo daily for six months, with an optional six-month open-label extension. The primary outcome was ERP P300 latency; secondary outcomes included ADAS-Cog11, global clinical change, ADCS-ADL, and drug pharmacokinetics. The trial was completed in May 2022. In June, the company announced the trial had failed to meet its primary endpoint (press release). A prespecified subgroup analysis suggested that use of cholinesterase inhibitors by 60 percent of participants may have diminished the effects of fosgonimeton. A post hoc analysis of people taking only fosgonimeton indicated improvements in ERP P300 latency and ADAS-Cog11 endpoints, the company reported. There were no serious adverse events or deaths in the study. The most common adverse event was injection site reaction. Results were presented at meetings in 2022 (e.g. see AAIC slides). The company presented additional post hoc analyses at the April 2023 American Academy of Neurology conference (slides). They reported that fosgonimeton, in the absence of acetylcholinesterase inhibitors, improved MMSE scores by 1.6 points from baseline; however, the change compared to placebo was not statistically significant. Decreases in biomarkers NfL and GFAP correlated with clinical outcomes in people taking only fosgonimeton. The company presented data suggesting that acetylcholinesterase inhibitors antagonize the effect of fosgonimeton on HGF/MET signaling.

Both ACT-AD and LIFT-AD offer a two-year, open-label safety extension.

In June 2021, the company placed CEO Leen Kawas on temporary leave amid questions about research integrity related to her doctoral dissertation, which laid the foundations for work on ATH-1017 (Seattle Times news story). According to news reports, Washington State University is conducting an investigation of multiple papers from her time as a researcher there, after comments on PubPeer noted irregularities in figures and data (Puget Sound Business Journal newsSTAT news). Kawas resigned in October 2021, after an independent investigation found altered images in her dissertation and at least four publications related to her graduate work (company release).

In January 2022, Athira began a Phase 2 trial testing 26 weeks of fosgonimeton on cognition in people with Parkinson’s disease dementia or dementia with Lewy bodies (DLB). Seventy-five participants were to be randomized to 40 or 70 mg fosgonimeton or placebo, injected daily, against a primary outcome of a combined score of the ADAS-Cog 13 and P300 latency. By December 2022, the trial had stopped recruiting at 28 participants, and was expected to finish in May 2023. In a December 2023 press release, the company announced that this trial had failed on the primary endpoint. Results were presented at the March 2024 AD/PD conference (poster). An apparent improvement in the ADAS-Cog13 with 40 mg fosgonimeton compared to placebo was difficult to interpret due to baseline differences between the groups. The treatment appeared safe, but four of 10 participants in the higher dose arm dropped out because of adverse events. The most common side effect was injection site reaction.

From July to October 2022, a study of absorption, metabolism, and excretion of a single dose of [14C]-fosgonimeton was conducted in eight male volunteers.

Athira is developing additional small-molecule modulators of HGF/MET signaling that, unlike fosgonimeton, are orally available (Taylor et al., 2022).

In April 2024, the company completed a Phase 1 trial in 32 healthy adults of ATH-1020 (Berthiaume et al., 2022, poster).

In February 2024, company scientists reported beneficial effects of ATH-1105 in cell culture and in animal models of ALS (Berthiaume et al., 2024). In April 2024, the company began Phase 1 trial to test single and multiple daily doses of ATH-1105 in healthy volunteers in Dallas.

On September 3, 2024, Athira announced that the Phase 2/3 LIFT-AD trial had failed to meet its primary endpoint of improvement in the Global Statistical Test after 26 weeks treatment (press release, slides). Treatment also missed the key secondary endpoints of the ADAS-Cog11 or ADCS-ADL23. The company reported numerical improvements on cognitive and biomarker endpoints, but none were statistically significant. The trial had enrolled 549 participants, but the efficacy analysis covered only 287. Participants who took acetylcholinesterase inhibitors were excluded from the analysis, after results of the ACT-AD study (above) suggested that these drugs blocked the effects of fosgonimeton on HGF/MET signaling. In addition, the higher-dose arm had been discontinued mid-trial because of injection site reactions. Plans for an additional study have been canceled, the company told news sources (Endpoints News). Results presented at the October 2024 CTAD conference reiterated the negative results. Trial participants had milder dementia than intended, and the placebo group did not decline as expected. Both treated and placebo groups improved on the ADAS-Cog11 in the first six weeks, and neither group returned to baseline by the end of the trial. In a subgroup analysis, patients with more severe cognitive impairment had larger numerical improvements on the ADAS-Cog11. Plasma biomarkers NfL, GFAP, pTau181, and pTau217 all stayed stable in the placebo group, and improved on treatment. The change in pTau217 reached statistical significance. Twenty-two percent of enrollees dropped out of the trial due to bothersome injection site reactions. Besides these and brief eosinophilia, other adverse events were mainly mild and similar in placebo and treatment groups.

In September 2024, the company announced it would focus on development of the oral HGF/MET modulator ATH-1105 for ALS (press release).

For details on NDX-1017/ATH-1017, ATH-1020, and ATH-1105 trials, see clinicaltrials.gov.

Clinical Trial Timeline

  • Phase 2
  • Study completed / Planned end date
  • Planned end date unavailable
  • Study aborted
Sponsor Clinical Trial 2018 2019 2020 2021 2022 2023 2024 2025 2026 2027 2028 2029 2030 2031 2032 2033 2034 2035
Athira Pharma NCT04488419
N=300
Athira Pharma NCT04491006
N=75
Athira Pharma NCT04886063
N=300
Athira Pharma NCT04831281
N=75

Last Updated: 09 Nov 2024

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Therapeutics

Relyvrio

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Overview

Name: Relyvrio
Synonyms: Albrioza, AMX0035
Therapy Type: Combination, Small Molecule (timeline)
Target Type: Other (timeline)
Condition(s): Amyotrophic Lateral Sclerosis, Alzheimer's Disease
U.S. FDA Status: Amyotrophic Lateral Sclerosis (Approved), Alzheimer's Disease (Phase 2)
Company: Amylyx Pharmaceuticals Inc
Approved for: ALS

Background

AMX0035 is a proprietary, oral combination of two drugs already in use, sodium phenylbutyrate (PB) and tauroursodeoxycholic acid (TUDCA). PB is prescribed under the brand name Buphenyl to treat urea cycle disorders. It acts as a scavenger to facilitate the excretion of excess nitrogen. Interest in repurposing PB to treat neurodegenerative diseases stems from its action as a chemical chaperone, which inhibits endoplasmic reticulum stress responses and neuronal cell death induced by accumulation of misfolded or mutant proteins (Kubota et al., 2006). PB also epigenetically regulates gene expression by inhibiting histone deacetylase.

TUDCA is a naturally occurring bile acid with anti-apoptotic and neuroprotective effects. TUDCA has been used for centuries in Asian medicine, and is widely available over the counter as a nutritional supplement. It is used clinically to help dissolve gallstones, and treat some forms of liver disease. TUDCA inhibits mitochondria-mediated apoptosis and the formation of reactive oxygen species, and blocks apoptosis caused by ER stress (reviewed in Daruich et al., 2019).

The only preclinical data comparing AMX0035 to PB and TUDCA individually describes gene expression and metabolomic changes in ALS patient-derived primary skin cells (Fels et al., 2022). The combination changed more genes and different genes than did PB or TUDCA alone. Both compounds show activity in mouse models of neurodegeneration. PB resulted in fewer plaques and better performance in a spatial memory task in APPswePS1delta9 (Wiley et al., 2011). PB prolonged survival in an ALS mouse model, both when given alone and together with riluzole (Ryu et al., 2005Del Signore et al., 2009). PB was also reported to protect against neurodegeneration in models of α-synuclein toxicity and Parkinson’s disease (Sturm et al., 2016; Ono et al., 2009). TUDCA reduced amyloid deposition and improved cognition in APP/PS1 mice (Nunes et al., 2012). It also improved pathology and behavior in mouse models of Parkinson’s disease, HD, and ALS (reviewed by Ackerman and Gerhard, 2016).

In a clinical study conducted 10 years ago in Milan, Italy, TUDCA alone reportedly had a treatment benefit in ALS. In a Phase 2 trial in 34 ALS patients, treatment with 2 g per day for one year slowed deterioration on the ALS Functional Rating Scale (ALSFRS-R) compared with placebo (Elia et al., 2015). Post hoc analysis suggested a reduced risk of death during the trial (Reggiardo et al., 2023). Following those results, investigators in February 2019 began a Phase 3 trial of TUDCA (Albanese et al., 2022). It has enrolled 337 ALS patients at 25 sites in seven European Union countries, for an 18-month course of 2 g daily plus riluzole. The primary outcome will be change on the ALSFRS-R; the trial was set to end in December 2023.

In another trial, PB was judged safe and well-tolerated after open-label dose escalation in 40 ALS patients (Cudkowicz et al., 2009). No efficacy measures were included, but PB at 9 g/day was sufficient to induce changes in histone acetylation in patients’ blood cells. PB was also evaluated in Huntington’s (PHEN-HD trial) and Parkinson’s diseases; results are not published.

Findings

In June 2017, Amylyx began CENTAUR, a Phase 2 safety and efficacy study of AMX0035 in people with ALS. Funded by foundations and conducted at 25 academic centers in the U.S., the trial enrolled 137 patients aged 18-80 who had been symptomatic for 18 months or less. Participants were randomized 2 to 1 to take either 3 grams PB plus 1 g TUDCA twice daily, or placebo for six months. They could also take edaravone or riluzole. Primary outcomes were disease progression, measured as change on the ALSFRS-R compared with placebo, adverse events, and number of people who stayed on AMX0035. Secondary outcomes included measures of muscle strength, vital lung capacity, survival, need for tracheostomy, and hospitalizations. Other secondary endpoints were plasma phosphorylated neurofilament H and unspecified imaging biomarkers. The study was completed in September 2019.

According to published trial results, AMX0035 slowed decline on the ALSFRS-R. The treated group lost 1.24 points per month compared to 1.66 for placebo (Sep 2020 news on Paganoni et al., 2020). The benefit appeared over and above any effects of riluzole and edaravarone. No significant differences between AMX0035 and placebo were noted in secondary outcomes. The most common side effects were diarrhea and abdominal pain, which occurred in 5 percent of participants and lessened with time. Ninety-eight out of 137 participants completed the trial. A post hoc analysis comparing long-term survival of the active drug participants to matched external controls found a 10-month survival advantage with treatment (Paganoni et al., 2023).

Between March 2018 and September 2019, 95 CENTAUR completers went on to an open-label extension study, whose primary outcome was adverse events. An analysis of survival in this phase concluded that people who originally had been randomized to drug lived 6.5 months longer than those originally in the placebo group. The participants from the active drug group survived a median of 24 months after randomization, compared to 18.5 months for the placebo group, a statistically significant difference (Paganoni et al., 2021Paganoni et al., 2022). 

In this trial, AMX0035 treatment were reported to have reduced levels of inflammatory biomarkers YKL-40 and CRP in plasma by 20 and 30 percent, respectively (Bowser et al., 2023).

From August 2018 to April 2021, Amylyx ran PEGASUS, a Phase 2 trial in Alzheimer’s disease. Conducted at 10 sites in the U.S., the study enrolled 95 participants with a biomarker-confirmed diagnosis of probable Alzheimer’s disease or mild cognitive impairment due to AD, and randomized them to an undisclosed dose of AMX0035 or placebo for 24 weeks. The primary outcome was safety; secondary outcomes include volumetric and functional MRI, cognition, and psychiatric symptoms, as well as unspecified CSF and plasma biomarkers. The company reported topline results at the November 2021 CTAD conference (press release). AMX0035 met safety and tolerability endpoints, with gastrointestinal side effects in line with previous clinical trials. The trial was not powered to detect efficacy and clinical endpoints revealed none. Treatment led to a significant reduction in CSF AD biomarkers Tau and pTau181, and an increased Aβ42/40 ratio. A marker of DNA damage, 8-hydroxy-2'-deoxyguanosine, was higher in the treated group. At the December 2022 CTAD conference, the company reported changes favoring drug in CSF biomarkers neurogranin, fABP3, and YKL40, but not in NfL, GFAP, an inflammation composite, soluble insulin receptor, or 24S-OH-cholesterol.

From November 2020 to January 2023, Amylyx sponsored a compassionate-use program for 28 people with ALS. In August 2021, the company started a Phase 1/2 drug exposure/pharmacodynamic study in 14 people with ALS.

In October 2021, Amylyx began PHOENIX, a 664-participant, international Phase 3 trial in ALS, comparing a 48-week course of an undisclosed dose of AMX0035 to placebo. The drug is to be delivered by mouth or feeding tube once daily for three weeks, then twice daily for the rest of the study. Primary outcomes are slope change on the ALS-FRS and survival, adverse events, and number of people able to complete the trial; secondary outcomes include various functional and quality-of-life measures but not biomarkers such as neurofilament light or others. Ongoing at around 70 sites in the U.S. and Europe, the trial is expected to run until November 2023, with topline results expected in 2024. An open-label extension began in December 2022; an expanded access program exists, as well.

On March 30, 2022, after a day-long meeting, the FDA's Peripheral and Central Nervous System Drugs Advisory Committee voted 6 to 4 against approving AMX0035 for the treatment of ALS based on the data submitted to the agency. In its briefing document issued prior to this AdComs meeting, the FDA had registered concerns with the statistical analysis method chosen for the primary endpoint, with the accounting of deaths that occurred during the study, center effects, group imbalances in incident concomitant medications, and other weaknesses in the data. For the purposes of the AdComs meeting, the briefing document concluded that the available evidence did not amount to substantial evidence of effectiveness. A decision was initially expected in June 2022, but the FDA pushed it back to September, citing a need for more time to evaluate the data.

In May 2022, company scientists published data claiming that AMX0035 treatment lengthened tracheostomy/ventilation-free survival and delayed first hospitalization in the CENTAUR trial (Paganoni et al., 2022). 

On June 10, AMX0035, brand name Albrioza, received conditional marketing approval from Health Canada, the country's drug regulatory agency. The approval is contingent on the outcome of the ongoing PHOENIX trial (see Notice of Compliance).

On July 5, 2022, Amylyx announced the U.S. FDA would reconvene the advisory committee to discuss a "major amendment" to the AMX0035 application (press release). In this rare second meeting, the committee voted in favor of the drug. The decision came after new analysis of data from the CENTAUR Phase 2 trial and long-term extension, and a pledge from Amylyx to voluntarily withdraw the drug if it fails to show efficacy in its ongoing Phase 3 trial (Endpoints News). On September 29, the FDA approved Albrioza, which is marketed in the U.S. as Relyvrio (Oct 2022 news). For review and commentary, see Sun et al., 2023; and Flynn et al., 2023.

In March 2023, the company began a 12-patient pilot study of AMX0035 in adults with Wolfram Syndrome, a genetic disorder characterized by diabetes, optic nerve atrophy, and deafness. The company began a 600-patient Phase 3 trial in progressive supranuclear palsy in December 2023.

On June 22, 2023, the European Medicines Agency rejected this drug, citing unconvincing data on its efficacy at slowing progression or prolonging survival (EMA statement). The company appealed, seeking conditional approval, but was rejected again in October (Endpoints News; company press release).

On March 8, 2024, Amylyx announced that the 664-patient PHOENIX trial had failed to meet its endpoints (press release; Mar 2024 news). Relyvrio did not change disease progression on the ALSFRS-R compared to placebo (p=0.667), nor did it change any secondary outcomes. The company said it would take eight weeks to decide the drug’s fate, and would continue to provide it to current users for that time. The open-label extension to PEGASUS will continue in Europe, as will the studies in Wolfram syndrome and Progressive Supranuclear Palsy. The trial result may reverse Relyvrio’s conditional approval in Canada.

On April 4, the company announced it would withdraw Relyvrio from the market in the U.S. and Canada (press release). No new patients will be able to start therapy. Patients already taking the drug are eligible to transition to the PHOENIX open-label extension for free. Development for Wolfram syndrome and PSP will continue.

For details on AMX0035 trials, see clinicaltrials.gov.

Clinical Trial Timeline

  • Phase 2
  • Study completed / Planned end date
  • Planned end date unavailable
  • Study aborted
Sponsor Clinical Trial 2016 2017 2018 2019 2020 2021 2022 2023 2024 2025 2026 2027 2028 2029 2030 2031 2032 2033 2034 2035
Amylyx Pharmaceuticals Inc NCT03533257
N=100

Last Updated: 20 May 2024

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External Resources

  1. The FDA almost never pulls fully-approved drugs. Amylyx's ALS treatment might be the exception
  2. A.L.S. Drug Relyvrio Fails Clinical Trial and May Be Withdrawn From the Market

Therapeutics

PU-AD

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Overview

Name: PU-AD
Synonyms: PU-HZ151, icapamespib
Therapy Type: Small Molecule (timeline)
Target Type: Other (timeline)
Condition(s): Alzheimer's Disease
U.S. FDA Status: Alzheimer's Disease (Phase 2)
Company: Samus Therapeutics

Background

A member of a new class of drugs called epichaperome inhibitors, PU-AD is an oral, brain-permeable inhibitor of the molecular chaperone heat shock protein 90. HSP90 stabilizes mutant or aberrantly modified proteins associated with cancer and multiple neurodegenerative diseases. 

HSP90 inhibitors enhance degradation of pathogenic proteins and promote cell survival in animal models of tau pathology, and of Parkinson’s disease, dementia with Lewy bodies, amyotrophic lateral sclerosis/frontotemporal dementia, Huntington’s disease, and spinal and bulbar muscular atrophy (reviewed in Carman et al., 2013). Brain-penetrant HSP90 inhibitors were reported to enhance the degradation of mutated or hyperphosphorylated tau in mouse models (May 2007 news). Another brain-penetrant inhibitor enhanced working memory and spatial learning/memory in Tg2576 AD mice, and improved conditioned fear memory after infusion of Aβ into the brain (Wang et al., 2016).

Although all cells express HSP90 at high levels, PU-AD and some other HSP90 inhibitors bind with high affinity to HSP90 from cancer cells and AD tissue, but not from normal tissue, suggesting the possibility of selective inhibition in disease states (Moulick et al., 2011; Dickey et al., 2007).

Affinity purification using PU-AD, and proteomic analyses, have identified HSP90-centered, stable chaperone complexes that emerge in cells under stress, including in cancer, Parkinson’s, and Alzheimer’s diseases (Rodina et al., 2016; Kishinevsky et al., 2018; Joshi et al., 2018). In AD tissues and mouse models, these complexes, dubbed epichaperomes, incorporate cell proteins not normally associated with HSP90, including some involved in synaptic function, learning, and memory. PU-AD treatment dissociates the epichaperome, and restores HSP90’s normal protein associations (Inda et al., 2020).

PU-AD has been tested in the PS19 tau mouse and the 3xTg mouse. After 6 to 12 weeks of thrice-weekly dosing, 3-month-old or 8- to 9-month-old PS19 mice performed better on learning and memory trials in a Barnes maze, compared to untreated animals (Inda et al., 2020). Treatment also normalized deficits in synaptic long-term potentiation, extended life span, and decreased phospho-tau and tau oligomers in multiple brain regions. PU-AD had similar effects on tau and on memory and learning in 3XTg mice.

Findings

Between June and December 2019, Samus Therapeutics ran a Phase 1 study of PU-AD in 40 healthy volunteers, who received single or multiple doses of an oral solution of drug or placebo. At the CTAD 2019 conference, the company reported that single doses of 10, 20, or 30 mg were well-tolerated, with mild adverse events and linear pharmacokinetics. Healthy elderly volunteers completed one week of 20 mg per day doses, with no events resulting in interruption of dosing (see Dec 2019 press release). 

A second Phase 1 study, at Memorial Sloan Kettering Cancer Center, New York, evaluated a radioactively labeled form of PU-AD (1241-PU-AD) as a diagnostic reagent in five people with cancer and/or AD. Participants received a low dose of 1241-PU-AD, followed by PET-CT. This study was completed in June 2019. The investigators reported low binding of the PET ligand in the brain of a cognitively normal 58-year-old, but elevated retention in a 71-year-old person with AD (Inda et al., 2020). Accumulation of the tracer in peripheral tumors in cancer patients was also reported (Pillarsetty et al., 2019). 1241-PU-AD was shown to cross the blood-brain barrier and accumulate in glioblastoma tumors in humans (Bolaender et al., 2021).

In June 2020, a Phase 2 trial began recruiting 150 people with mild Alzheimer’s dementia and a positive tau-PET scan to evaluate safety and pharmacological effects of PU-AD. Participants receive 30 mg PU-AD daily or placebo for six months. Primary outcomes are changes in brain glucose uptake by FDG-PET, and the incidence and severity of adverse events. Secondary outcomes include tau-PET, CSF tau, and p-tau, multiple measures of cognition and function, and pharmacokinetics. The trial is slated to end in December 2022.

A Phase 2 trial in people with amyotrophic lateral sclerosis is registered to start in December 2021. It will enroll 30 participants for six months of PU-AD 30 mg daily or placebo, against conventional primary outcomes of function, breathing capacity, and strength. Blood and CSF biomarkers are secondary measures. The study is planned to run through December 2022.

A Phase 1 trial in people with recurrent glioblastoma is slated to begin in November 2021.

Samus is testing another epichaperome inhibitor, PU-H71, in Phase 1 for multiple forms of cancer. PU-H71 does not cross the blood brain barrier.

For details on PU-AD trials, see clinicaltrials.gov.

Last Updated: 07 Oct 2021

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Therapeutics

Citalopram

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Overview

Name: Citalopram
Synonyms: escitalopram, Celexa, Lexapro , Cipralex
Chemical Name: (RS)-1-[3-(Dimethylamino)propyl]-1-(4-fluorophenyl)-1,3-dihydroisobenzofuran-5-carbonitrile
Therapy Type: Small Molecule (timeline)
Target Type: Other Neurotransmitters (timeline)
Condition(s): Alzheimer's Disease, Preclinical Alzheimer's Disease
U.S. FDA Status: Alzheimer's Disease (Phase 3), Preclinical Alzheimer's Disease (Inactive)
Approved for: Depression, generalized anxiety disorder

Background

Citalopram is a selective serotonin reuptake inhibitor used to treat depression and anxiety. It is a chiral molecule that exists as two enantiomers. Citalopram consists of a 1:1 mixture of (R)- and (S)-stereoisomers. A purified (S)-isomer formulation, marketed as Escitalopram, is approved to treat depression and generalized anxiety disorder. Both are available as generics. Both work by increasing serotonin activity in the brain. Escitalopram is considered superior at treating depression, with faster onset at lower doses than citalopram (Lepola et al., 2004Gartlehner et al., 2011). Side effects in older adults include abnormal heart rhythm, loss of coordination, and bleeding.

Many people with Alzheimer’s disease have noncognitive symptoms, which add to their and caregivers’ burdens. Agitation, including disruptive or aggressive behaviors, may stem from degeneration of serotonin systems. No treatments are approved for agitation in people with Alzheimer’s disease, but based on existing clinical evidence, citalopram and escitalopram are sometimes used (Aga 2019Kales et al., 2019).

Some research has suggested anti-amyloid actions for SSRIs. Activation of certain serotonin receptors reduces Aβ production by increasing non-amyloidogenic α-secretase processing of APP (Nitsch et al., 1996; Fisher et al., 2016). Citalopram was reported to lower Aβ production and amyloid plaque load in mice and people (Cirrito et al., 2011; Sheline et al., 2014; Zhang et al., 2018). However, in one study, escitalopram did not reduce brain Aβ in mice (von Linstow et al., 2017). More recently, escitalopram was found to increase hippocampal α-secretase activity by 50 percent, and reduce brain interstitial Aβ42 in mice (Cirrito et al., 2020). The same study showed chronic escitalopram halted plaque growth, but did not remove established plaques. In cognitively normal older people, two or eight weeks of treatment with escitalopram led to a 6 percent reduction in CSF Aβ42 concentrations, compared to a slight increase in placebo-treated volunteers (Sheline et al., 2020).

In ADNI participants with a history of depression, long-term use of SSRIs was linked to a three-year delay in progression to dementia (Bartels et al., 2018). Another study linked SSRI use in people with depression and MCI or AD to slowed cognitive decline, reduced progression of gray-matter atrophy, and a trend toward slower amyloid deposition (Brendel et al., 2018). A retrospective review of medical records of 14,269 people with MCI in New York found that use of citalopram or escitalopram was associated with a significant slowing of progression to dementia (Xu et al., 2023).

Findings

In the first placebo-controlled trial of citalopram for behavioral disturbances in people with AD, four weeks of citalopram led to decreased confusion, anxiety, and irritability (Nyth and Gottfries, 1990). A second randomized trial, in dementia patients hospitalized for agitation or psychosis symptoms, found citalopram taken for 17 days lessened agitation and aggression (Pollock et al., 2002). Citalopram or escitalopram improved agitation and psychosis as effectively as the typical antipsychotic risperidone, but with fewer side effects (Pollock et al., 2007Barak et al., 2011).

In July 2009, a group of academic investigators started a randomized study of citalopram. Called CitAD, it enrolled 186 participants with probable AD and agitation, and compared a nine-week course of psychosocial intervention plus 30 mg/day citalopram to psychosocial intervention plus placebo. Citalopram reduced agitation and caregiver distress compared with placebo, but caused cardiac side effects and cognitive worsening (Feb 2014 news; Dec 2014 conference news; Porsteinsson et al., 2014). Subsequent to this trial, the FDA established a safe limit for citalopram of 20 mg/day for people over 60 (Marcum et al., 2012).

An analysis of the blood concentrations of citalopram isomers associated cognitive worsening with the (R) isomer and clinical improvements with the (S) form (Ho et al., 2016). In January 2018, the same investigators began an NIA-funded Phase 3 trial of escitalopram, called S-CitAD (Ehrhardt et al., 2019). In the run-in phase, participants with AD and agitation received a psychosocial intervention for three weeks. Those who did not improve were randomized to receive up to 15 mg/day escitalopram or placebo for three months, with continuing psychosocial intervention. The planned primary outcome in this pragmatic trial was the proportion of patients showing marked improvement on a modified form of the ADCS-Clinical Global Impression of Change scale after 12 weeks. The trial spanned the COVID-19 pandemic, and was completed in November 2023. According to results presented at the August 2024 AAIC in Philadelphia, the trial failed to meet its primary endpoint. It intended to enroll 392 patients, but just 205 started the psychosocial intervention, and 173 went on to randomization. Adverse events included falls, anxiety, constipation and diarrhea, and cardiac rhythm changes. Compared to citalopram, fewer patients showed marked or moderate improvement in agitation, but escitalopram did not cause cognitive worsening.

A trial in South Korea evaluated 20 mg/day escitalopram for one year on AD progression in 74 people with probable AD, and found no difference in hippocampal or whole-brain volumes, and no benefit on cognitive, neuropsychiatric, or depression scores, compared with placebo (Choe et al., 2015). Another trial in South Korea, of a 12-week course of 15 mg/d escitalopram or placebo in 84 participants with a clinical diagnosis of AD, reported no differences outcomes of depression and cognition (An et al., 2017).

Starting in July 2017, a Phase 1 study at NYU began comparing 5 mg/d of escitalopram with 37.5 mg/d of venlafaxine, a different antidepressant medication, and with placebo, in 31 people with subjective memory concerns. The study was to evaluate the drugs' ability to slow down progression to mild cognitive impairment or Alzheimer's disease, using EEG and metabolic imaging in the hippocampal formation as primary outcome measures. This trial was terminated in September 2019 due to insufficient enrollment.

In February 2022, a trial began to assess the effects of eight weeks of escitalopram on Aβ dynamics in adults with major depression. Participants must be at least 60 years old and have normal cognitive function. They will take 10 or 20 mg escitalopram daily as tolerated, or placebo. The primary endpoints are change in CSF Aβ40, Aβ42, and vascular dysfunction biomarkers, plus depressive symptoms. Other outcomes include plasma Aβ and CSF total tau and phosphorylated tau. The study, at two sites in New York, will run until early 2026.

For details on citalopram and escitalopram trials in Alzheimer's disease, see clinicaltrials.gov.

Last Updated: 15 Aug 2024

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Therapeutics

Guanfacine

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Overview

Name: Guanfacine
Synonyms: Intuniv, SPD503, Afken, Estulic, Tenex
Chemical Name: N-amidino-2-(2,6dichlorophenyl) acetamide monohydrochloride
Therapy Type: Small Molecule (timeline)
Target Type: Other Neurotransmitters (timeline)
Condition(s): Alzheimer's Disease
U.S. FDA Status: Alzheimer's Disease (Phase 3)
Approved for: Attention-deficit hyperactivity disorder, hypertension

Background

This drug is an α2A adrenergic receptor agonist. It acts in the central nervous system and is used to treat high blood pressure and attention-deficit/hyperactivity disorder (ADHD). An extended-release formulation, approved as a once-a-day medication for ADHD in children, is available as a generic. Side effects include blurred vision, confusion, faintness, sweating, fatigue, and others.

Guanfacine works in the prefrontal cortex to increase attention and cognition by activating postsynaptic norepinephrine receptors. In preclinical studies, the drug improved working memory of aged rodents and monkeys (Arnsten and Jin, 2012). People with AD show impairment in attention, which may contribute to memory problems (Malhotra, 2018). In addition, degeneration of norepinephrine-producing locus coeruleus neurons, and noradrenergic dysfunction, are recognized features of Alzheimer’s and Parkinson’s diseases (Weinshenker, 2018; Jacobs et al., 2019).

Findings

The idea that guanfacine might boost cognition in Alzheimer’s disease has been around for two decades, but not supported by trial data. The first small studies using guanfacine alone in people with AD were negative (Crook et al., 1992; Schlegel et al., 1989). Likewise, a larger trial in people with age-associated memory impairment found no benefit on learning or memory (McEntee et al., 1991). In more recent work, three months of treatment with extended-release guanfacine at one-half, and one-tenth, the dose used for ADHD did not improve attention or cognitive function in 154 healthy elderly controls (Barcelos et al., 2018).

In January 2019, a study began to evaluae guanfacine as an add-on to cholinergic treatment in people with AD. The single-center Phase 3 trial at Imperial College London is enrolling 160 participants who meet clinical criteria for probable AD and have been taking a stable dose of donepezil, galantamine, or rivastigmine for three months. They will receive 2 mg per day of extended-release guanfacine or placebo for three months. The primary outcome is performance on the ADAS-Cog; secondary outcomes include additional cognitive tests focusing on attention, plus neuropsychiatric symptoms, daily activities, and caregiver burden. Blood pressure and sleepiness will be tracked. The trial will end in early 2021. 

Guanfacine is also being studied for stress disorders, Tourette’s syndrome, and for alcohol, opioid, nicotine, or cannabis withdrawal. 

For details on guanfacine trials, see clinicaltrials.gov.

Clinical Trial Timeline

  • Phase 3
  • 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
Imperial College of London NCT03116126
N=160

Last Updated: 15 Dec 2019

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Research Models

SHRSP/FAD

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Species: Rat
Genes: APP, PSEN1
Mutations: PSEN1: deltaE9
Modification: APP: Transgenic; PSEN1: Transgenic
Disease Relevance: Alzheimer's Disease, Vascular Dementia
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

  • Synaptic Loss

No Data

  • Neuronal Loss
  • Changes in LTP/LTD

Plaques

Diffuse amyloid plaques observed at 16-18 months, the only age examined to date.

Tangles

Occasional neurons appear to contain globose neurofibrillary tangles, as revealed by immunostaining using an antibody directed against tau phosphorylated at serine 422, an epitope found in paired helical filaments.

Synaptic Loss

Levels of SNAP25, synaptophysin, and drebrin do not differ from non-hypertensive, non-transgenic rats at 16-18 months, the only age examined to date.

Neuronal Loss

A reduction in calbindin staining might reflect a loss of inhibitory neurons. Levels of caspase-cleaved actin, a marker of apoptosis, are elevated, compared with non-hypertensive, non-transgenic rats.

Gliosis

Hypertrophied microglia and elevated levels of GFAP observed at 16-18 months, the only age examined to date.

Changes in LTP/LTD

No data.

Cognitive Impairment

Working memory deficits as assessed by novel object recognition, but not as assessed by spontaneous alternation in the Y-maze, at 16-18 months, the only age examined to date.

Last Updated: 06 Dec 2019

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Therapeutics

ALZ-801

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Overview

Name: ALZ-801
Synonyms: valiltramiprosate, NRM-8499, homotaurine prodrug, 3-APS
Therapy Type: Small Molecule (timeline)
Target Type: Amyloid-Related (timeline)
Condition(s): Alzheimer's Disease
U.S. FDA Status: Alzheimer's Disease (Phase 3)
Company: Alzheon Inc.

Background

This is a prodrug of homotaurine, a modified amino acid previously developed under the names tramiprosate and Alzhemed™. ALZ-801 is converted to homotaurine in vivo, but is more easily absorbed and lasts longer in the blood than tramiprosate.

Tramiprosate was reported to inhibit Aβ42 aggregation into toxic oligomers (Gervais et al., 2007; Kocis et al., 2017). Both ALZ-801 and tramiprosate are metabolized to 3-sulfopranpanoic acid (3-SPA), which is normally found in brain and also inhibits Aβ42 aggregation (Hey et al., 2018). A more recent study found that homotaurine activates GABA receptors, and suggests an alternative mechanism of action for ALZ-801 (Meera et al., 2023).

After tramiprosate failed in Phase 3, its maker, NeuroChem, marketed it as a nutritional supplement. Years later, a subgroup analysis of the trial data indicated a potential positive effect in participants who carried two copies of ApoE4 (Abushakra et al., 2016; Abushakra et al., 2017). Alzheon licensed ALZ-801 from NeuroChem and is developing it for Alzheimer’s disease.

Findings

Alzheon published results of a Phase 1 study of safety, tolerability, and pharmacokinetics of single and multiple doses of ALZ-801 in 127 healthy, old volunteers (Hey et al., 2018). The prodrug caused mild nausea and vomiting, which were not dose-related and went away after a week on drug or when taking the drug with food. Other common side effects were headaches, dizziness, and falls, also not dose-related. The drug had a longer half-life and less variability in blood levels between people than tramiprosate, and could be taken with food without affecting plasma concentrations. A dose of 265 mg of ALZ-801 twice daily achieved the same blood exposure as the 150 mg dose twice daily used in the Phase 3 tramiprosate trials, and brain levels five to 15 times higher than required to inhibit Aβ42 aggregation in vitro. 

In October 2017, the U.S. Food and Drug Administration granted ALZ-801 Fast-Track designation for the treatment of Alzheimer’s disease. 

In December 2019, Alzheon announced that its analysis of ADNI and tramiprosate trial data showed differences in cortical thickness between ApoE3/3 and ApoE4/4 carriers with mild AD, and that cortical thickness would be a secondary outcome in a planned Phase 3 trial (company press release; also see Abushakra et al., 2020). In August 2020, Alzheon announced that the U.S. National Institute on Aging will fund this trial (press release).

In September 2020, the company began a Phase 2, open-label biomarker study enrolling 84 people with early stage AD dementia and one or two copies of ApoE4. Participants receive 265 mg of drug twice daily for two years, with primary outcomes being change from baseline in CSF p-tau181 and adverse events. Secondary measures include CSF and plasma biomarkers of neurodegeneration, amyloid load, and microglial activation, plus hippocampal volume and cortical thickness MRI. The study also assesses cognition and activities of daily living. Taking place in Czechia and the Netherlands, it was expected to finish in August 2023. In February 2022, Alzheon announced interim results on 80 patients treated for six months, reporting a 29 percent reduction in plasma p-tau181 from baseline, a comparable drop in the p-tau181/Aβ42 ratio, and claiming improvement on the Rey Auditory Verbal Learning Test (press release). There was no placebo control group. The most common adverse event was mild nausea; no serious drug-related side effects were reported. In September 2022, Alzheon released 12-month data on 75 patients, announcing a 41 percent reduction in p-tau181 from baseline, and a 37 percent reduction in the p-tau181/Aβ42 ratio (press release).

The company showed more one-year data on the same trial at the December 2022 CTAD conference, including reductions in hippocampal atrophy and decline on the RAVLT compared to historical controls. Plasma Aβ40 and Aβ42, which had increased over baseline at weeks 13 and 26, dropped to below baseline. Scores on a cognition composite that had been significantly improved at week 26 were still higher than baseline but no longer significantly so. The drug continued to be safe, with no evidence of brain edema (ARIA-E). Many participants continued into a one-year open label extension. In September 2023, the company issued a press release on final study results, reporting that, at two years, plasma p-tau181 had declined by 31 percent compared to baseline, and Aβ42 had decreased by 4 percent. Hippocampal atrophy, and decline on the RAVLT and Digital Symbol Substitution Test reportedly slowed, compared to historical (ADNI) controls (press release). This study had no placebo control. The company presented trial data at the March 2024 AD/PD conference in Lisbon. After two years, the participants appeared to have benefited on most outcomes when compared to historical controls. Plasma p-tau181 was reduced at all timepoints starting at 13 weeks. While plasma Aβ42 decreased, the Aβ42/40 ratio increased slightly, by 2.4 percent. Hippocampal atrophy was 21 percent less than in matched ADNI participants. RAVLT Total and DSST scores remained above baseline at two years, and cognitive stabilization correlated significantly with lower rates of hippocampal atrophy, cortical thinning, and ventricular volume. The most common side effects were transient, including mild nausea and loss of appetite. Trial data was published after peer review (Hey et al., 2024Hey et al., 2024). According to a presentation at the 2024 AAIC, 64 participants completed a third year of extended treatment. At 2.5 years, participants continued to show a reduction in cortical thinning and stabilization on the RAVLT. The fourth and final year started in April 2024.

The Phase 3 trial, dubbed APOLLOE4, began in May 2021 (press release). It has enrolled 325 ApoE4 homozygotes with clinically diagnosed early to mild AD. Participants will receive 265 mg of ALZ-801 or placebo twice daily for 18 months. The primary efficacy endpoint is change in ADAS-COG13; secondary endpoints include disability assessment for dementia (DAD), CDR-SB, and the Amsterdam-iADL. The trial includes as primary endpoints biomarkers of hippocampal volume MRI, and CSF and plasma measures of p-tau181. Alzheon will monitor the concentration in the CSF of Aβ oligomers, which it argues are a target of ALZ-801 (Tolar et al., 2020Tolar et al., 2021). Baseline characteristics of the participants have been published (Abushakra et al., 2024). Average age of 69 and MMSE of 25.6 were similar to the Phase 2 open-label study. Confirmation of brain amyloid by PET, CSF, or plasma tests was not required, as the prior trial had indicated that more than 95 percent of symptomatic, APOE4 homozygotes are amyloid positive. APOLLOE4 does enroll patients with evidence of moderate to severe cerebral amyloid angiopathy, which is disqualifying for amyloid antibody trials due to the risk of ARIA. Thirty percent of enrollees had one or more microhemorrhages, and 10 percent had siderosis. No symptomatic ARIA has been reported so far in the trial. Funded by the National Institutes on Aging and running at 78 sites in the U.S., Canada, and Europe, this trial is slated to be complete by June 2024. It offers a long term open-label extension.

For all ALZ-801 trials, see clinicaltrials.gov.

Last Updated: 23 Sep 2024

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