BIIB122 for Early-Stage Parkinson's Disease
(LUMA Trial)
Recruiting in Palo Alto (17 mi)
+124 other locations
Age: 18+
Sex: Any
Travel: May Be Covered
Time Reimbursement: Varies
Trial Phase: Phase 2
Recruiting
Sponsor: Biogen
Disqualifiers: Stroke, Dementia, Seizure, others
Prior Safety Data
Trial Summary
What is the purpose of this trial?
This trial is testing a new drug called BIIB122 to see if it can slow down symptoms in people with early-stage Parkinson's disease. The drug works by blocking a protein that may cause the disease to get worse. Participants will take the drug for several years to see if it helps.
Will I have to stop taking my current medications?
The trial information does not specify whether you need to stop taking your current medications. It's best to discuss this with the study team or your doctor.
How is the drug BIIB122 different from other Parkinson's disease treatments?
Eligibility Criteria
This trial is for people aged 30-80 with early-stage Parkinson's disease, diagnosed within the last two years. Participants should have mild symptoms (stages 1 to 2 on a specific scale) and score ≤40 on a PD symptom questionnaire. They can't join if they have other significant neurological issues, atypical parkinsonism, drug-induced parkinsonism, or cognitive impairment as indicated by a MoCA score <24.Inclusion Criteria
My Parkinson's is in the early to mid stages.
I was diagnosed with Parkinson's disease within the last 2 years and was over 30 at diagnosis.
MDS-UPDRS Parts II and III (in OFF state) combined score ≤40 at screening
Exclusion Criteria
I haven't had a major neurological issue like stroke or dementia in the last 5 years.
I have a rare form of Parkinson's or my Parkinson's may be caused by medication.
My memory and thinking test score was below 24.
Trial Timeline
Screening
Participants are screened for eligibility to participate in the trial
2-4 weeks
Treatment
Participants receive BIIB122 or placebo tablets by mouth once daily
48 to 144 weeks
Up to 29 visits
Follow-up
Participants are monitored for safety and effectiveness after treatment
2 weeks
Treatment Details
Interventions
- BIIB122 (Monoclonal Antibodies)
Trial OverviewThe study tests BIIB122 tablets against placebo to see if it slows down symptom worsening in early Parkinson's over a period of up to three years. Patients will take either the drug or placebo daily and attend clinic visits every three months. The effectiveness will be measured using the MDS-UPDRS questionnaire assessing PD symptoms' impact on daily life.
Participant Groups
2Treatment groups
Experimental Treatment
Placebo Group
Group I: BIIB122 225 mgExperimental Treatment1 Intervention
Participants will receive BIIB122, 225 mg tablets, by mouth, once daily (QD) for up to a minimum of 48 weeks and a maximum of 144 weeks.
Participants who received BIIB122 and completed the ET visit of study 283PD302 (NCT05418673) will continue to receive BIIB122, 225 mg tablets, by mouth, QD for up to a minimum of 48 weeks and a maximum of 144 weeks.
Group II: BIIB122 Matching PlaceboPlacebo Group1 Intervention
Participants will receive BIIB122 matching placebo tablets, by mouth, QD for up to a minimum of 48 weeks and a maximum of 144 weeks.
Participants who received placebo and completed the ET visit of study 283PD302 (NCT05418673) will continue to receive BIIB122 matching placebo tablets, by mouth, QD for up to a minimum of 48 weeks and a maximum of 144 weeks.
Find a Clinic Near You
Research Locations NearbySelect from list below to view details:
Research SiteSpokane, WA
Research SiteHonolulu, HI
CenExel Rocky Mountain Movement Disorders CenterEnglewood, CO
InvicroNew Haven, CT
More Trial Locations
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Who Is Running the Clinical Trial?
BiogenLead Sponsor
Denali Therapeutics Inc.Industry Sponsor
References
Priorities in Parkinson's disease research. [2022]The loss of dopaminergic neurons in the substantia nigra pars compacta leads to the characteristic motor symptoms of Parkinson's disease: bradykinesia, rigidity and resting tremors. Although these symptoms can be improved using currently available dopamine replacement strategies, there is still a need to improve current strategies of treating these symptoms, together with a need to alleviate non-motor symptoms of the disease. Moreover, treatments that provide neuroprotection and/or disease-modifying effects remain an urgent unmet clinical need. This Review describes the most promising biological targets and therapeutic agents that are currently being assessed to address these treatment goals. Progress will rely on understanding genetic mutations or susceptibility factors that lead to Parkinson's disease, better translation between preclinical animal models and clinical research, and improving the design of future clinical trials.
Delaying the onset of parkinson's disease. [2016]A drug is showing promise in delaying the onset of disabling Parkinsonism.
New medical and surgical treatments for Parkinson's disease. [2019]This article reviews new medical and surgical treatments for Parkinson's disease (PD). Catechol-O-methyl-transferase (COMT) inhibitors supplement the variety of antiparkinsonian drugs interacting with the dopaminergic system. Clinical studies show that COMT inhibitors prolong the action of levodopa in patients with the "wearing off" phenomenon. The atypical antipsychotic drug clozapine is the treatment of choice for the alleviation of levodopa-induced psychosis. Clozapine also has beneficial effects on tremor and levodopa-induced dyskinesias. Thus, COMT inhibitors and clozapine provide new opportunities for the treatment of patients with longstanding PD and fluctuating responses to levodopa. Experimental evidence in animals suggests that glutamate antagonists have symptomatic and neuroprotective actions in PD. At present, however, only weak antiglutamatergic drugs that have low specificity, such as memantine, amantadine, and budipine are available for clinical studies. Neurotrophic factors, in particular ciliary neurotrophic factor and glial cell line-derived neurotrophic factor, are among the most promising new approaches for neuroprotection in PD. Problems of bioavailability, however, thus far preclude their use in patients. An improved understanding of the pathophysiology of parkinsonism has led to a renaissance of stereotaxic surgery. The subthalamic nucleus is a potential new target for surgical intervention. Ventroposterior pallidotomy has been shown to improve not only rigidity and tremor, but also akinesia. The techniques for thalamic interventions have been refined by introducing chronic thalamic stimulation. Future transplantation approaches to PD will focus on the use of genetically modified cells carrying genes for dopamine-synthesizing enzymes or neurotrophic factors. Animal studies show the feasibility of in vivo gene transfer for the treatment of PD.
Effect of a selective glutamate antagonist on L-dopa-induced dyskinesias in drug-naive parkinsonian monkeys. [2014]Alterations of striatal glutamate receptors are believed to be responsible, at least in part, for the pathogenesis of L-dopa-induced dyskinesias (LID). To evaluate whether co-administration of CI-1041, a novel NMDA receptor antagonist selective for the NR1A/NR2B subtype, with L-dopa might prevent the appearance of this side effect, eight de novo parkinsonian monkeys were treated chronically orally with either L-dopa alone or L-dopa plus CI-1041 (n= 4 for each group). After 4 weeks of treatment with L-dopa alone, all four animals developed moderate dyskinesias either choreic or dystonic in nature. CI-1041 co-treatment completely prevented the induction of dyskinesias in three animals and only one monkey developed mild dyskinesias at the end of the fourth week of treatment in the L-dopa + CI-1041 group. The magnitude and duration of the antiparkinsonian action of L-dopa was similar in both groups. These results suggest that selective NMDA receptor antagonism may be interesting for managing LID in Parkinson's disease patients.
Drugs in development for Parkinson's disease. [2007]Pharmacological treatment of Parkinson's disease (PD) is entering a new and exciting era. Real promise now exists for the clinical application of a large range of molecules in development that will combat different aspects and stages of the condition. These include methyl- and ethyl-esterified forms of L-dopa (etilevodopa and melevodopa), inhibitors of enzymes such as monoamine oxidase type-B (eg, rasagiline), catechol-O-methyl transferase (eg, BIA-3202) and the monoamine re-uptake mechanism (eg, brasofensine). In addition, a range of full and partial dopamine agonists (eg, sumanirole, piribedil and BP-897) and their new formulations, for example, patch delivery systems (eg, rotigotine) are being developed. We also highlight non-dopaminergic treatments that will have wide ranging applications in the treatment of PD and L-dopa-induced dyskinesia. These include alpha2 adrenergic receptor antagonists (eg, fipamezole), adenosine A2A receptor antagonists (eg, istradefylline), AMPA receptor antagonists (eg, talampanel), neuronal synchronization modulators (eg, levetiracetam) and agents that interact with serotonergic systems such as 5-hydroxytryptamine (5-HT)1A agonists (eg, sarizotan) and 5-HT2A antagonists (eg, quetiapine). Lastly, we examine a growing number of neuroprotective agents that seek to halt or even reverse disease progression. These include anti-apoptotic kinase inhibitors (eg, CEP-1347), modulators of mitochondrial function (eg, creatine), growth factors (eg, leteprinim), neuroimmunophilins (eg, V-10367), estrogens (eg, MITO-4509), c-synuclein oligomerization inhibitors (eg, PAN-408) and sonic hedgehog ligands.