A Phase IIb, Randomized, Double-Blind, Placebo-Controlled, Multicenter Study to Evaluate the Efficacy and Safety of Intravenous Prasinezumab in Participants with Early Parkinson's Disease - BN42358

Start Date02 Jul 2021

Sponsor / Collaborator

F. Hoffmann-La Roche Ltd.

NCT04777331 / Active, not recruitingPhase 2

A Phase IIB, Randomized, Double-Blind, Placebo-Controlled, Multicenter Study to Evaluate the Efficacy and Safety of Intravenous Prasinezumab in Participants With Early Parkinson's Disease

This is a multicenter, randomized, double-blind, placebo-controlled study that will evaluate the efficacy and safety of intravenous (IV) prasinezumab versus placebo in participants with Early Parkinson's Disease (PD) who are on stable symptomatic PD medication.

Start Date05 May 2021

Sponsor / Collaborator

Hoffmann-La Roche, Inc.

[+1]

JPRN-jRCT2080223775 / Unknown statusPhase 1

A Phase I Single-Dose Study of RO7046015 in Healthy Japanese Men

Start Date15 Jan 2018

Sponsor / Collaborator

Chugai Pharmaceutical Co., Ltd.

100 Clinical Results associated with Prasinezumab

100 Translational Medicine associated with Prasinezumab

100 Patents (Medical) associated with Prasinezumab

Literatures (Medical) associated with Prasinezumab

07 Oct 2024·MOLECULAR PHARMACEUTICS

Investigating the Mechanisms of Antibody Binding to Alpha-Synuclein for the Treatment of Parkinson’s Disease

Article

Author: Lai, Pin-Kuang ; Harrison, Malcolm C.

Parkinson's disease (PD) is an idiopathic neurodegenerative disorder with the second-highest prevalence rate behind Alzheimer's disease. The pathophysiological hallmarks of PD are both degeneration of dopaminergic neurons in the substantia nigra pars compacta and the inclusion of misfolded α-synuclein (α-syn) aggregates known as Lewy bodies. Despite decades of research for potential PD treatments, none have been developed, and developing new therapeutic agents is a time-consuming and expensive process. Computational methods can be used to investigate the properties of drug candidates currently undergoing clinical trials to determine their theoretical efficiency at targeting α-syn. Monoclonal antibodies (mAbs) are biological drugs with high specificity, and Prasinezumab (PRX002) is an mAb currently in Phase II, which targets the C-terminus (AA 118-126) of α-syn. We utilized BioLuminate and PyMol for the structure prediction and preparation of the fragment antigen-binding (Fab) region of PRX002 and 34 different conformations of α-syn. Protein-protein docking simulations were performed using PIPER, and 3 of the docking poses were selected based on the best fit. Molecular dynamics simulations were conducted on the docked protein structures in triplicate for 1000 ns, and hydrogen bonds and electrostatic and hydrophobic interactions were analyzed using MDAnalysis to determine which residues were interacting and how often. Hydrogen bonds were shown to form frequently between the HCDR2 region of PRX002 and α-syn. Free energy was calculated to determine the binding affinity. The predicted binding affinity shows a strong antibody-antigen attraction between PRX002 and α-syn. RMSD was calculated to determine the conformational change of these regions throughout the simulation. The mAb's developability was determined using computational screening methods. Our results demonstrate the efficiency and developability of this therapeutic agent.

23 Sep 2024·Journal of Physiological Sciences

Limitations and potential strategies of immune checkpoint blockade in age-related neurodegenerative disorders.

Review

Author: Mansour, Rana ; Aswa, Darin W ; Farouk, Ziad ; Lasheen, Noha N ; Elgarawany, Abdullrahman ; Allam, Salma

Neurological disorders such as Alzheimer's disease (AD), and Parkinson's disease (PD) have no disease-modifying treatments, resulting in a global dementia crisis that affects more than 50 million people. Amyloid-beta (Aβ), tau, and alpha-synuclein (α-Syn) are three crucial proteins that are involved in the pathogenesis of these age-related neurodegenerative diseases. Only a few approved AD medications have been used in the clinic up to this point, and their results are only partial symptomatic alleviation for AD patients and cannot stop the progression of AD. Immunotherapies have attracted considerable interest as they target certain protein strains and conformations as well as promote clearance. Immunotherapies also have the potential to be neuroprotective: as they limit synaptic damage and spread of neuroinflammation by neutralizing extracellular protein aggregates. Lately, disease-modifying therapies (DMTs) that can alter the pathophysiology that underlies AD with anti-Aβ monoclonal antibodies (MAbs) (e.g., aducanumab, lecanemab, gantenerumab, donanemab, solanezumab, crenezumab, tilavonemab). Similarly, in Parkinson's disease (PD), DMTs utilizing anti-αSyn (MAbs) (e.g., prasinezumab, cinpanemab,) are progressively being developed and evaluated in clinical trials. These therapies are based on the hypothesis that both AD and PD may involve systemic impairments in cell-dependent clearance mechanisms of amyloid-beta (Aβ) and alpha-synuclein (αSyn), respectively, meaning the body's overall inability to effectively remove Aβ and αSyn due to malfunctioning cellular mechanisms. In this review we will provide possible evidence behind the use of immunotherapy with MAbs in AD and PD and highlight the recent clinical development landscape of anti-Aβ (MAbs) and anti-αSyn (MAbs) from these clinical trials in order to better investigate the therapeutic possibilities and adverse effects of these anti-Aβ and anti-αSyn MAbs on AD and PD.

01 Apr 2024·Nature medicine

Prasinezumab slows motor progression in rapidly progressing early-stage Parkinson’s disease

Article

Author: Brockmann, Kathrin ; Kerchner, Geoffrey A ; Svoboda, Hanno ; Postuma, Ronald B ; Bonni, Azad ; Pagano, Gennaro ; Monnet, Annabelle ; Nikolcheva, Tania ; Trundell, Dylan ; Simuni, Tanya ; Marek, Kenneth ; Anzures Cabrera, Judith ; Stocchi, Fabrizio ; Pavese, Nicola ; Fontoura, Paulo ; Brundin, Patrik ; Doody, Rachelle ; Taylor, Kirsten I

Abstract:

Prasinezumab, a monoclonal antibody that binds aggregated α-synuclein, is being investigated as a potential disease-modifying therapy in early-stage Parkinson’s disease. Although in the PASADENA phase 2 study, the primary endpoint (Movement Disorder Society Unified Parkinson’s Disease Rating Scale (MDS-UPDRS) sum of Parts I + II + III) was not met, prasinezumab-treated individuals exhibited slower progression of motor signs than placebo-treated participants (MDS-UPDRS Part III). We report here an exploratory analysis assessing whether prasinezumab showed greater benefits on motor signs progression in prespecified subgroups with faster motor progression. Prasinezumab’s potential effects on disease progression were assessed in four prespecified and six exploratory subpopulations of PASADENA: use of monoamine oxidase B inhibitors at baseline (yes versus no); Hoehn and Yahr stage (2 versus 1); rapid eye movement sleep behavior disorder (yes versus no); data-driven subphenotypes (diffuse malignant versus nondiffuse malignant); age at baseline (≥60 years versus <60 years); sex (male versus female); disease duration (>12 months versus <12 months); age at diagnosis (≥60 years versus <60 years); motor subphenotypes (akinetic–rigid versus tremor-dominant); and motor subphenotypes (postural instability gait dysfunction versus tremor-dominant). In these subpopulations, the effect of prasinezumab on slowing motor signs progression (MDS-UPDRS Part III) was greater in the rapidly progressing subpopulations (for example, participants who were diffuse malignant or taking monoamine oxidase B inhibitors at baseline). This exploratory analysis suggests that, in a trial of 1-year duration, prasinezumab might reduce motor progression to a greater extent in individuals with more rapidly progressing Parkinson’s disease. However, because this was a post hoc analysis, additional randomized clinical trials are needed to validate these findings.

News (Medical) associated with Prasinezumab

08 Oct 2024

·endpts.com

Exclusive: A small San Diego biotech wants to change how Parkinson’s disease is diagnosed

A protein called alpha-synuclein that accumulates and ravages the brains of some people with Parkinson’s disease is the target of several experimental drugs. Until recently, the only way to detect it was by opening someone’s brain when they died. That’s starting to change. Amprion, a 30-person biotech based in San Diego, has developed a way to detect small amounts of alpha-synuclein from spinal fluid. A study published last year in The Lancet Neurology suggests the method could help confirm suspected diagnoses and even predict Parkinson’s before common symptoms arise. And now Amprion is scaling up to commercialize the test. CEO and co-founder Russell Lebovitz told Endpoints News in an exclusive interview that Amprion has raised $6 million in the first portion of its Series B, which will help it hire 15 more employees and expand its salesforce and operations throughout the US. The round was led by Formation Venture Engineering, with participation from Eli Lilly. Lilly’s interest is notable because the pharma company helped pioneer the use of diagnostics to detect amyloid in the brains of people with Alzheimer’s disease. The drugmaker is also developing drugs for Parkinson’s, and the company’s scientific leaders have mentioned alpha-synuclein as an area of interest for future neurodegenerative research at the company. “They have recognized, as have a lot of the drug companies, that this is going to be important in the future,” Lebovitz said. The technology underlying Amprion’s test was forged in the early 2000s in the aftermath of the mad cow disease crisis. Claudio Soto, a biochemist and professor of neurology at the UT Health Houston McGovern Medical School in Houston, developed a way to detect prions, the misfolded proteins that cause bovine spongiform encephalopathy in cattle and Creutzfeldt-Jakob disease in humans. The infectious proteins cause natural versions of the proteins to misfold, leaving tainted and toxic prions in their wake as they spread through the brain. That natural amplification formed the basis of Soto’s test. He added highly purified and properly folded proteins to spinal fluid or blood from a patient suspected of having the disease. If prions were present in the sample, they would quickly convert the normal proteins into diseased ones. He compared the method to PCR, the technique used to make many copies of DNA for easier sequencing. Soto formed a startup with Lebovitz in 2007 that aimed to refine the technique, now dubbed a seed amplification assay. The mad cow crisis abated, but the duo believed the technique would be valuable to help detect other misfolded proteins, such as amyloid and tau in Alzheimer’s and alpha-synuclein in Parkinson’s. The first ten years were slow going. The test originally took nearly two weeks to run, but they got it down to 20 hours. And a fluorescent dye that only lights up in the presence of misfolded proteins made the results easy to interpret. The tests are currently run out of its CLIA-certified lab in San Diego. The company is developing a simplified kit of the test that other labs can run, and hopes to submit it to the FDA in about 18 months. By 2019, Amprion had developed an alpha-synuclein test for Parkinson’s that it believed would be scalable. The company raised a $13.7 million Series A over the next three years and began offering the test to doctors at major medical centers and research institutions in 2023, Lebovitz said. The study published last year revealed that the test had a sensitivity of about 88%, meaning that about 12 in 100 people with Parkinson’s had a false negative result. Among the 1,100 healthy volunteers, the test had a 97% specificity, meaning about 3 in 100 people without the disease had a false positive. The test performed more poorly for certain subsets of Parkinson’s disease, including those with mutations in the LRRK2 gene linked to the disease. Drugmakers and regulators alike are increasingly turning to biomarkers to decide which patients to include in a clinical trial and how to assess whether the drug is working. In August, the FDA issued a letter of support encouraging “further study and use of” seed amplification assays for alpha-synuclein. Amprion has worked on similar amplification assays for amyloid and tau, but these tests are still experimental. The company offers clinical tests for amyloid, tau and another brain biomarker called neurofilament using machines sold by Fujirebio. With the new funding, Leboviz said “we can hit every major medical center doing cognitive and motor disorders in the US.” He’s hoping to raise another $9 million in the Series B round this year to help the company open a lab in Europe. But Amprion’s efforts to scale up come at a challenging time. About two weeks ago, an investigation published in Science cast doubt on several research papers supporting the role of alpha-synuclein in Parkinson’s disease. More than 130 papers published by National Institutes of Health neuroscientist Eliezer Masliah had “suspect images,” including doctored and duplicated results, according to the report. Some of the questionable studies were cited as evidence underpinning the alpha-synuclein-targeting antibody prasinezumab, which is being developed by Prothena Biosciences and Roche. Lebovitz said that other scientists have consistently demonstrated alpha-synuclein’s role in Parkinson’s and other neurodegenerative diseases irrespective of Masliah’s studies. “None of Amprion’s data relies on any work ever performed or published by Eliezer Masliah,” Lebovitz said. “We have never met with Dr. Masliah, and he has never provided any advice or other counsel.”

26 Sep 2024

·www.fiercebiotech.com

AbbVie's dopamine-focused Parkinson's treatment reduces disease burden in phase 3 trial

AbbVie got its hands on tavapadon after buying Cerevel Therapeutics for a whopping $8.7 billion in 2023. On the same day that some Parkinson’s disease drugs are being called into question, AbbVie has announced that its late-stage monotherapy candidate has significantly reduced the burden of the disease in patients compared to placeboThe phase 3 TEMPO-1 trial tested two daily doses (5 mg and 15 mg) of tavapadon, an oral dopamine receptor agonist. Both arms beat placebo at improving disease burden at Week 26 as measured by a combined score using parts of an industry scale dubbed the Movement Disorder Society-Unified Parkinson's Disease Rating Scale, according to a Sept. 26 release.In addition to the primary endpoint, tavapadon also hit a secondary endpoint, improving the mobility of patients in their daily lives, AbbVie said in the release.Most side effects were mild to moderate in severity and consistent with past clinical trials, according to AbbVie. Tavapadon partially binds to the D1 and D5 dopamine receptors, which play a role in regulating motor activity. It’s being developed both as a monotherapy and in combination with levodopa, a biological precursor to dopamine that is often used as a first-line treatment for Parkinson’s.AbbVie plans to share results from another phase 3 trial of tavapadon later this year, the pharma said in the release. That trial is testing the drug as a flexible-dose monotherapy.The pharma got its hands on tavapadon last year after buying out Cerevel Therapeutics for a whopping $8.7 billion. The other shining star of that deal is emraclidine, which is currently being tested in schizophrenia and Alzheimer’s disease psychosis. The muscarinic M4 selective positive allosteric modulator is in the same class as Karuna Therapeutics’ KarXT, which awaits an FDA approval decision that's slated for today. The AbbVie data come amid claims that prasinezumab, a Parkinson’s drug being developed by Prothena Biosciences and Roche, was built on a foundation of shaky science, according to a Science investigation published today. More than 100 research papers by Eliezer Masliah, M.D., the longtime head of the National Institute on Aging's neuroscience division, were found to contain apparently manipulated images, including four papers that were foundational to the development of prasinezumab, according to Science.

Phase 3AcquisitionClinical Result

26 Sep 2024

·www.fiercebiotech.com

NIH neuroscience leader committed research misconduct, agency investigation finds

A team of neuroscientists and research integrity experts assembled a 300-page dossier supporting their claims of misconduct in 132 papers published by Eliezer Masliah, M.D. Separately, the NIH flagged concerns with two papers. The NIH has found evidence of research misconduct against Eliezer Masliah, M.D., the longtime head of the National Institute on Aging's (NIA) neuroscience division, the NIH said in a Sept. 26 statement. The misconduct findings—made after a 9-month investigation by the agency—involve figures being reused and relabeled between two papers despite them representing different experimental conditions, according to the NIH.“NIH will notify the two journals of its findings so that appropriate action can be taken,” the agency said in the statement. Masliah is not currently serving as the NIA’s neuroscience director, the agency added. Deputy director Amy Kelley, M.D., is serving as the acting director of the NIA’s neuroscience division. Masliah took up the NIA neuroscience division post in the summer of 2016, according to his biography on the NIH website.NIH didn't return Fierce Biotech's request for comment, but said in the release that beyond the information already provided, they don't comment on personnel matters. It's unclear whether Masliah is still employed by the agency. NIH first began reviewing misconduct allegations against Masliah in May 2023, the agency said, beginning an investigation phase in Dec. 2023 that just concluded on Sept. 15. The NIH announcement coincides with the Sept. 26 publication of an investigation by Science finding that 132 papers published by Masliah contain apparently manipulated images. Some of the challenged research includes work on drug candidates that are currently in clinical trials or are already in use, including treatments for Parkinson’s and Alzheimer’s disease, according to Science's publication.For the Science investigation, a team of neuroscientists and research integrity experts assembled a 300-page dossier supporting their claims of misconduct in papers published by Masliah. Eleven other neuroscientists then reviewed the dossier, Science says, and all agreed that the findings warranted investigations by the NIH, academic journals, funders and the University of California, San Diego, where Masliah previously ran a research lab.“These fields, both Alzheimer's and Parkinson's, need a reset,” Matthew Schrag, M.D., Ph.D., a neuroscientist at Vanderbilt University Medical Center who contributed to the dossier, told Fierce Biotech in an interview. “We need to look at this with an understanding that research integrity is a significant problem, and we need to come in and make sure that we are chasing the right targets and that we are universally committed to the well-being of our patients.” Schrag’s investigative work is independent of his job at Vanderbilt University Medical Center.One of the drugs implicated in the Science investigation is prasinezumab, an antibody treatment for Parkinson’s disease. Prasinezumab targets alpha-synuclein, a protein that aggregates pathologically in Parkinson’s. The drug is under development by Prothena Biosciences in collaboration with Roche; Prothena was co-founded by the late Dale Schenk, Ph.D., a neuroscientist who co-authored four foundational papers on alpha-synuclein with Masliah that are implicated in the dossier, according to Science.In phase 2 trial data reported in Aug. 2022, prasinezumab showed no difference to placebo on measures of Parkinson’s disease progression. Another phase 2 trial is ongoing.“Let me not put too fine a point on this: the ongoing phase 2 trial should be shut down,” Schrag said.Another implicated med is dementia treatment cerebrolysin from Austria-based Ever Pharma, which is not approved in the United States but is available in dozens of other countries, according to Science. In addition, another alpha-synuclein drug for Parkinson’s called minzasolmin, from a company Masliah co-founded named Neuropore Therapies, is also held up by suspect research, according to Science’s findings.Prothena, Ever Pharma and Neuropore all told Science that the allegations are not related to the current clinical programs of the respective drugs. Antibodies that target alpha-synuclein are based on basic science by Masliah that's now being called into question, Schrag said. “I think we're seeing a number of attempts on this particular target through this mechanism that appear to be not performing as well as we'd like,” he said. Evidence that the antibodies can reach alpha-synuclein clumped inside of neurons “came from these animal studies that appear to have been heavily manipulated," the neuroscientist said.Numerous biotechs have been rocked recently by misconduct claims. Flagship Pioneering’s Laronde had its research on a new class of genetic medicine scrutinized in a Stat and Boston Globe investigation, revealing a “bad assay” and poor note-taking. Flagship then merged Laronde with another of its companies, Senda Biosciences, to form Sail Biomedicines.Lykos Therapeutics, a company researching MDMA-assisted therapies, has also been besieged by controversy lately. After facing a rejection by the FDA, the psychedelic firm had three papers retracted from scientific journals due to misconduct. The tumult continued from there, with Lykos laying off 75% of its staff and eventually saying goodbye to CEO Amy Emerson.And in the Alzheimer’s space, Cassava Biosciences has long been dogged by accusations of faking data. Schrag played a pivotal role in investigating publications underlying Cassava’s science, identifying dozens with problematic images. The company’s CEO and senior vice president of neuroscience both departed in July.On Sept. 12, the United States Department of Health and Human Services finalized new guidelines for research misconduct investigations conducted by recipients of Public Health Services funding. The new rules clarify the requirements of misconduct investigations, give institutions 90 days to investigate claims instead of 60 and outline an appeals process and potential administrative remedies to misconduct, according to a release.“We have to acknowledge the seriousness of the problem, and we need to get serious about addressing known, obvious cases of research misconduct in a way where there's meaningful consequences,” Schrag said. “We need to focus on the next generation of scientists and ingraining the importance of doing this right.”Editor's note: This article was updated to provide further context on Masliah's current position at NIH.

Phase 2

100 Deals associated with Prasinezumab

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KEGG	Wiki	ATC	Drug Bank
D11420	-	-	DB14788

R&D Status

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Indication	Highest Phase	Country/Location	Organization	Date
Parkinson Disease	Phase 2	US	Prothena Biosciences Ltd.	27 Jun 2017
Parkinson Disease	Phase 2	US	Hoffmann-La Roche, Inc.	27 Jun 2017
Parkinson Disease	Phase 2	AT	Prothena Biosciences Ltd.	27 Jun 2017
Parkinson Disease	Phase 2	AT	Hoffmann-La Roche, Inc.	27 Jun 2017
Parkinson Disease	Phase 2	FR	Prothena Biosciences Ltd.	27 Jun 2017
Parkinson Disease	Phase 2	FR	Hoffmann-La Roche, Inc.	27 Jun 2017
Parkinson Disease	Phase 2	DE	Hoffmann-La Roche, Inc.	27 Jun 2017
Parkinson Disease	Phase 2	DE	Prothena Biosciences Ltd.	27 Jun 2017
Parkinson Disease	Phase 2	ES	Prothena Biosciences Ltd.	27 Jun 2017
Parkinson Disease	Phase 2	ES	Hoffmann-La Roche, Inc.	27 Jun 2017

Clinical Result

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT03100149 (PASADENA, AAN2023)	Phase 2	Parkinson Disease alpha-synuclein	316	Prasinezumab 1500 mg	djwdvzbkhl(mddkmrbate) = jmjbfpuceg hqoivrtprb (budtywvpyv ) View more	-	25 Apr 2023
				Placebo+Prasinezumab 1500 mg	djwdvzbkhl(mddkmrbate) = yplafvsusp hqoivrtprb (budtywvpyv ) View more
PASADENA (MDS2022)	Not Applicable	Parkinson Disease α-synuclein	-	Prasinezumab 1500 mg	xbgmpnoggm(nczcmzezfp) = loselviskz ujaqzugkxo (ffqotclsdq ) View more	-	15 Sep 2022
				Prasinezumab 4500 mg	xbgmpnoggm(nczcmzezfp) = vehfdztwft ujaqzugkxo (ffqotclsdq ) View more
NCT03100149 (PASADENA, Pubmed \| Br Dent J)	Phase 2	Young onset Parkinson disease	316	Prasinezumab 1500 mg	tsgzkbcvqi(otraxppqca) = infusion reactions occurred in 19.0% and 34.0%, respectively nvrkxkdaqa (eqorkvuogg ) View more	Negative	04 Aug 2022
				Prasinezumab 4500 mg
NCT03100149 (PASADENA, CTgov)	Phase 2	Parkinson Disease	316	Placebo (Part 1: Placebo)	ndcemyvhtk(slcstkdjds) = meaggtcysh pkfypejlgc (lrismfejng, wbsaesfwky - xeorzxtatw) View more	-	08 Feb 2021
				RO7046015 (Part 1: RO7046015 Low Dose)	ndcemyvhtk(slcstkdjds) = vlvgtifhih pkfypejlgc (lrismfejng, mmvvfdjygf - asgcjwnaxu) View more
NCT03100149 (PASADENA, Pubmed \| Front Neurol)	Phase 2	Young onset Parkinson disease	316	Prasinezumab 1,500 mg	gbikcdoiiv(wlrvnviier) = rmaaihamua fmvbyvgzti (kwszxxynml )	-	01 Jan 2021
				Prasinezumab 4,500 mg	gbikcdoiiv(wlrvnviier) = pqseogfnnp fmvbyvgzti (kwszxxynml )
NCT02157714 (Pubmed \| JAMA Neurol) Manual	Phase 1	Parkinson Disease	80	PRX002	zcvggnhzrc(txxzbcwten) = smijhiwvnz rashnxjrfi (aykahwdyyj ) View more	Positive	01 Oct 2018
				Placebo	zcvggnhzrc(txxzbcwten) = kvhjwockzn rashnxjrfi (aykahwdyyj )
phase 1b multiple ascending-dose study of PRX002 (EAN)	Phase 1	Parkinson Disease alpha-synuclein	80	PRX002 0.3 mg/kg	qswirfiurp(bevhpdrcmk) = TEAEs experienced by â¥5% of patients and >placebo were constipation bqmctnzwkh (trxfnwytem ) View more	Positive	13 Jul 2017
				PRX002 1 mg/kg

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