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levodopa + benserazide (Madopar HBS / Levopar Plus / Prolopa)

✓ Approved

Roche · DDC · 小分子

什么是 levodopa + benserazide？

levodopa + benserazide 是一种小分子，由Roche研发。该药已获批，用于治疗相关适应症，给药途径：Oral (PO)。

药物档案

商品名Madopar HBS, Levopar Plus, Prolopa
公司Roche
药物类别小分子
分子靶点DDC
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, Roche

作用机制

分子靶点

levodopa + benserazide 作用于 1 个分子靶点：

DDCdopa decarboxylase (AADC)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

levodopa + benserazide 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Nervous system disordersParkinson's disease✓ Approved

相关研究文献

PubMedArchiv der Pharmazie2026-10-26

Clarifying Problems in the Synthetic Pathway Towards Methylene-Type Levodopa Acylals as Potential Prodrugs.

Keydel Tobias T, Theele Yann Y, Link Andreas A

Here, we report a practical synthetic pathway towards levodopa (l-DOPA) acylals with a special emphasis on problems occurring during preparation, low yields or unmanageable side reactions, and how to circumvent them. The key step can be performed rapidly by microwave irradiation in a green chemistry manner. Final compounds can be achieved after deprotection approaches but exhibit inadequate properties in terms of stability, thwarting the adaptation of the double ester concept discussed here to the important active pharmaceutical ingredient levodopa. However, a future outlook is provided, discussing potential structural and chemical changes for stable levodopa acylals.

PMID 42929392
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PubMedEuropean journal of neurology2026-10-26

Continuous Subcutaneous Foslevodopa/Foscarbidopa Improves Nonmotor Symptoms and Fluctuations in Parkinson's Disease.

De Micco Rosa R, Ciaramaglia Oriana O, Siciliano Mattia M, Sant'Elia Valeria V et al.

Nonmotor fluctuations (NMFs) in Parkinson's disease (PD) represent a heterogeneous and disabling feature often linked to pulsatile dopaminergic stimulation from oral levodopa. Continuous subcutaneous foslevodopa/foscarbidopa infusion (CSFLI) provides 24-h levodopa delivery, with established motor benefits but limited real-world data on NMFs. We investigated changes in motor complications, nonmotor symptoms, and NMFs over 3 months after initiation of CSFLI. In this prospective, single-center, real-world study, 66 patients with advanced PD initiated CSFLI. Longitudinal 3-month data were available for 40 patients. Motor complications were assessed with the Unified Parkinson's Disease Rating Scale (UPDRS) Part IV, motor severity with UPDRS Part III, and nonmotor symptoms with the Nonmotor Symptom Scale (NMSS); nonmotor fluctuations were evaluated with the Nonmotor Fluctuation Assessment questionnaire (NoMoFa). Additional validated scales assessed sleep, mood, fatigue, autonomic, and behavioral symptoms. Longitudinal changes were analyzed using paired parametric or non-parametric tests, as appropriate, with FDR correction. After 3 months, motor complications significantly improved, with reductions in OFF time and ON time with dyskinesias. Nonmotor symptom burden also improved, with significant reductions in NoMoFa total and NMF-OFF scores, whereas NMF-ON remained unchanged. Improvements were also observed in sleep-related symptoms, depressive symptoms, and quality of life, whereas apathy, autonomic symptoms, and daytime sleepiness did not significantly change. CSFLI was associated with improvements in motor complications and nonmotor fluctuations, particularly OFF-related NMFs, together with benefits in specific nonmotor symptoms. These findings provide preliminary real-world evidence supporting a potential role of CSFLI in the management of NMFs in PD.

PMID 42929191
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PubMedAmerican journal of translational research2026-10-25

Effects of butylphthalide plus donepezil on symptoms, cognitive function, and oxidative stress in patients with cognitive impairment in Parkinson's disease.

Li Ni N, Li Yuqin Y, He Xuebing X, Huang Shungui S

To investigate the effects of butylphthalide combined with donepezil on clinical symptoms, cognitive function, and oxidative stress in patients with cognitive impairment associated with Parkinson's disease (PD). A total of 119 patients with PD-associated cognitive impairment who were admitted to Chengdu Sixth People's Hospital (Donghong Branch) were retrospectively included and divided into two groups. Both groups received levodopa and benserazide hydrochloride as basic treatment. In addition, patients in the control group (n = 55) received donepezil, and those in the research group (n = 64) received butylphthalide combined with donepezil. The two groups were compared in terms of therapeutic efficacy, clinical symptoms (assessed by the Unified Parkinson's Disease Rating Scale [UPDRS]), cognitive function (Montreal Cognitive Assessment [MoCA]), activities of daily living (ADLs; ADL scale), neurotransmitter levels (dopamine [DA], gamma-aminobutyric acid [GABA], 5-hydroxytryptamine [5-HT]), neurotrophic factors (neurotrophin-3 [NT-3], nerve growth factor [NGF]), oxidative stress (superoxide dismutase [SOD], malondialdehyde [MDA]), adverse events, and quality of life (QoL; the 36-Item Short Form Health Survey [SF-36]). Furthermore, exploratory subgroup analyses were performed according to Hoehn-Yahr staging (H-Y staging) and baseline MoCA scores. Compared to the control group, patients in the research group exhibited much higher overall response rate, lower post-treatment UPDRSII, UPDRSIII, and MDA levels, and higher MoCA scores, ADL scores, DA, GABA, 5-HT, NT-3, NGF, SOD levels, and SF-36 scores. The overall incidence of adverse events was comparable between groups. Neither H-Y staging nor baseline MoCA scores significantly affected the efficacy of the combination therapy. Butylphthalide combined with donepezil may exert beneficial effects on symptom improvement, cognitive function enhancement, and oxidative stress regulation in patients with PD-associated cognitive impairment.

PMID 42923556
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PubMedFrontiers in psychiatry2026-10-25

Psychotic symptoms in tyrosine hydroxylase deficiency-associated dopa-responsive dystonia treated with antipsychotics and rTMS: a case report.

Shen Yue Y, Chen Hai-Zhi HZ, Lv Liang L, Fang Lan-Lan LL

Tyrosine hydroxylase deficiency (THD) is a rare autosomal recessive disorder caused by mutations in the TH gene. THD encompasses a broad phenotypic spectrum that includes dopamine-responsive dystonia (DRD) as its milder presentation, alongside severe infantile parkinsonism and progressive infantile encephalopathy. Although non-motor manifestations-such as depression, anxiety, and sleep disturbances-have garnered increasing attention, psychotic symptoms including hallucinations and delusions remain rarely reported in THD. This report describes a genetically confirmed woman with THD who presented with infantile-onset dystonia. Auditory hallucinations and erotomanic delusions emerged approximately five years after levodopa initiation and persisted despite one-month levodopa withdrawal. Although levodopa markedly improved her dystonia, antipsychotic treatment posed a therapeutic dilemma: risperidone exacerbated motor symptoms, and aripiprazole was limited by poor adherence. A multimodal regimen comprising aripiprazole, quetiapine, and low-frequency repetitive transcranial magnetic stimulation (rTMS) targeting the left temporoparietal cortex was associated with progressive improvement of psychotic symptoms without clinically apparent worsening of dystonia. The independent contribution of rTMS could not be determined given the concurrent pharmacological titration. Selecting appropriate antipsychotic medication in THD patients with prominent psychotic symptoms poses a considerable challenge. The combination of aripiprazole, quetiapine, and rTMS may represent a potential therapeutic option. To our knowledge, this is the first reported case of genetically confirmed DRD due to THD presenting with prominent psychotic symptoms, and among the few documenting rTMS use in this population. These observations are based on clinical assessment without standardized quantitative measures; the independent efficacy of rTMS cannot be established from this case.

PMID 42923261
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PubMedmedRxiv : the preprint server for health sciences2026-10-25

The LRRK2 R1441G+M1646T haplotype is associated with slower motor symptom progression in Parkinson's disease.

Schumacher Jackson G JG, Zhang Xinyuan X, Wang Jian J, Chen Xiqun X

Mutations in leucine-rich repeat kinase 2 ( LRRK2 ) are the most common genetic risk factor for Parkinson's disease (PD). G2019S, the most common pathogenic variant, has been linked to milder motor symptoms, but the effects of other LRRK2 variants on disease trajectory remain incompletely characterized. R1441G, the second most common pathogenic variant, co-occurs with the PD risk variant M1646T on a shared haplotype. Whether this haplotype confers a distinct rate of motor progression has not been established. We analyzed up to 12 years of longitudinal data from 603 participants in the Parkinson's Progression Markers Initiative (PPMI) with PD and available whole-genome sequencing data: 394 sporadic PD, 169 G2019S carriers, 20 R1441G+M1646T carriers, and 20 M1646T carriers. Motor symptom progression (MDS-UPDRS III) was assessed using linear mixed-effects models with genotype-by-time interactions, adjusted for age at onset, disease duration at baseline, sex, race, baseline score, and levodopa equivalent daily dose. R1441G+M1646T carriers exhibited 76% slower progression in OFF-state MDS-UPDRS III than sporadic PD (0.50 vs. 2.04 points/year; β=-1.54 [95% CI: -2.48, -0.60]; p=0.001). G2019S carriers exhibited 26% slower progression (1.52 points/year; β=-0.52 [-0.99, -0.06]; p=0.03). M1646T carriers did not differ from sporadic PD (p=0.60). Slower progression in R1441G+M1646T carriers was characterized by attenuated bradykinesia (64% slower; p=0.008), axial decline (76% slower; p=0.002), and a lack of orofacial symptom progression (p<0.001). R1441G+M1646T carriers also exhibited 55% slower self-reported motor decline (MDS-UPDRS II; p=0.04). R1441G+M1646T carriers exhibit substantially slower motor progression than sporadic PD while M1646T carriers do not.

PMID 42922836
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PubMedParkinson's disease2026-10-25

Odor-Specific Symptoms in Parkinson's Disease-UPSIT-TC Odor Identification Status Versus Clinical Severity.

Lin Ting-Chun TC, Yang Lan-Yan LY, Lin Yu-Hsuan YH, Lei Hsin-Bei HB et al.

Olfactory dysfunction is a well-recognized prodromal sign of Parkinson's disease (PD). This study aimed to explore the potential of short-form olfactory tests as a more convenient method for assessing PD symptoms in clinical practice. This retrospective cross-sectional study included 176 patients with PD. For each clinical measure, 40 separate logistic regression models evaluated its association with correct identification of each UPSIT-TC odor. Odors showing nominal associations at unrounded p < 0.05 were designated candidate symptom-associated odors. A symptom-specific odor score was constructed when at least two odors (≥ 2) met this criterion. Associations of each clinical measure with the UPSIT-TC total score and its corresponding symptom-specific odor score were subsequently evaluated using correlation analyses and covariate-adjusted regression models. Across all clinical measures, 101 nominal odor-clinical associations involving 31 unique odors were identified, with 17 clinical measures meeting the ≥ 2-odor criterion. Symptom-specific odor scores generally showed stronger unadjusted correlations with their corresponding clinical measures than did the UPSIT-TC total score. After adjustment for age, sex, disease duration, and levodopa equivalent daily dose (LEDD), with false discovery rate correction across 32 models, symptom-specific odor scores remained significantly associated with MDS-UPDRS total and Parts I-III scores, bradykinesia, rigidity, axial symptoms, NMSS total and gastrointestinal and urinary domain scores, MoCA scores, and NPI total scores. In contrast, the UPSIT-TC total score remained significantly associated only with rigidity. Symptom-specific odor scores have the potential to serve as a more clinically practical tool for assessing PD symptom burden than the UPSIT-TC total score. Further large-scale, multicenter studies are needed to explore odors with higher specificity for PD clinical symptoms.

PMID 42923752
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