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

✓ Approved

Roche · DDC · Small Molecule

What is levodopa + benserazide?

levodopa + benserazide is a small molecule developed by Roche. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesMadopar HBS, Levopar Plus, Prolopa
CompanyRoche
Drug ClassSmall Molecule
Molecular TargetDDC
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Roche

Mechanism of Action

Molecular Targets

levodopa + benserazide acts on 1 molecular target:

DDCdopa decarboxylase (AADC)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

levodopa + benserazide is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Nervous system disordersParkinson's disease✓ Approved

Related Research Articles

PubMedNeurology2026-10-20

Child Neurology: Neonatal Management of Tyrosine Hydroxylase Deficiency: How Early Is Early Enough?

Menetrey Anika A, AlFaris Haya S HS, Aljouda Liali L, Martin Nicole N et al.

Tyrosine hydroxylase deficiency is a rare, treatable, autosomal recessive disorder of monoamine neurotransmitter biosynthesis that typically presents in infancy or early childhood. Despite potential benefits of presymptomatic treatment with levodopa/carbidopa, prenatal or neonatal diagnosis remains extremely rare. We report 2 preterm neonates from unrelated families, both with known family history of tyrosine hydroxylase deficiency. After early diagnosis, levodopa/carbidopa therapy was initiated during the neonatal period. This proactive approach proved feasible and well tolerated, leading to early normalization of subtle motor abnormalities. These cases highlight the importance of early genetic diagnosis of this rare condition and the feasibility of levodopa/carbidopa treatment in neonates.

PMID 42900876
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PubMedNeural regeneration research2026-10-20

Neurodegeneration epicenters: Distinct network mechanisms of dopaminergic treatment in Parkinson's disease.

Duanmu Xiaojie X, Zhu Zihao Z, Lu Nan N, Zhang Wenzhuo W et al.

Parkinson's disease exhibits heterogeneous spatiotemporal patterns of neurodegeneration. Dopaminergic therapy improves motor symptoms by modulating brain function in affected regions, yet whether the neural mechanisms through which dopaminergic therapy exerts its effects are linked to this heterogeneity of neurodegeneration remains unclear. A connectivity-based epicenter framework combined with spectral dynamic causal modeling was applied to resting-state functional magnetic resonance imaging data from 160 drug-naïve Parkinson's disease patients and 174 healthy controls to identify subtype-specific degenerative epicenters and characterize directional interactions among affected regions. Ninety-seven patients additionally underwent an acute levodopa challenge to evaluate how dopaminergic modulation influences these interactions and relates to symptom improvements. Two distinct Parkinson's disease subtypes were identified: subtype 1 was characterized by degenerative epicenters predominantly located in subcortical and cerebellar regions, whereas subtype 2 exhibited epicenters primarily involving cortical regions. Both subtypes exhibited widespread dysregulation of directional interactions among epicenter regions relative to healthy controls. Levodopa treatment partially reversed these network abnormalities in a manner specific to each subtype, notably within cerebellar vermis in subtype 1 and frontal cortex in subtype 2. Symptom improvements were linked to distinct network interactions: in subtype 1, tremor correlated with the thalamus, midbrain nuclei, and cerebellar vermis, whereas bradykinesia primarily involved the cerebellar vermis; in subtype 2, rigidity improvements mapped to frontal cortex and limbic regions, and bradykinesia to limbic regions. These findings suggest that Parkinson's disease involves distinct epicenter networks in each subtype, with widespread directional dysregulation contributing to symptom diversity in patients. Levodopa treatment selectively modulates these network interactions, shedding light on the mechanisms underlying treatment heterogeneity and guiding precision-targeted therapeutic strategies.

PMID 42899897
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PubMedJournal of medical case reports2026-10-20

Childhood-onset parkinsonism, dystonia and severe muscle wasting in a Sudanese girl caused by a novel homozygous DnaJ heat shock protein family (heat shock protein 40) member C6 frameshift variant, with an incidental pathogenic breast cancer 1 gene secondary finding: a case report.

Ahmed Khabab Abbasher Hussien Mohamed KAHM, Ahmed Razan Kamal Yousif RKY

DNAJC6-related juvenile parkinsonism is a rare autosomal recessive disorder of auxilin, a co-chaperone essential for clathrin-mediated synaptic vesicle recycling. Fewer than 50 kindreds have been reported worldwide, and the condition is easily missed when first-line investigations come back normal. We describe a Sudanese adolescent in whom a previously unreported homozygous DNAJC6 frameshift variant was identified only after a prolonged diagnostic journey that included a period during which her illness was mistakenly attributed to a functional neurological disorder. Clinical whole-exome sequencing additionally returned an incidental medically actionable BRCA1 secondary finding. A 13-year-old Sudanese girl, the eldest child of first-cousin parents, was born preterm and ventilated neonatally for severe respiratory distress. Her development was normal until age five, when an isolated upper-limb tremor first appeared. Over the next 8 years her condition progressed into severe juvenile parkinsonism: bilateral rest-and-action tremor, rigidity, bradykinesia, generalized dystonia with prominent oromandibular involvement, dysphagia, profound cachexia, cognitive and behavioral decline, sleep and autonomic disturbance, episodic oculogyric crises and three discrete seizures. By approximately 11 she was wheelchair-dependent. Earlier, unrevealing investigations had led to a psychiatric diagnosis of functional neurological disorder, and the dopamine antagonists prescribed on that basis worsened her condition. Whole-exome sequencing later identified a novel homozygous DNAJC6 frameshift deletion (NM_001256864.2:c.1480del; p.Glu494ArgfsTer12), absent from population databases, alongside a heterozygous pathogenic BRCA1 deletion reported as an actionable secondary finding. Levodopa produced partial motor benefit, complicated by on-state dyskinesias, visual hallucinations and excessive daytime somnolence. Subsequent up-titration of carbidopa/levodopa to approximately 5-hourly dosing produced a further, clinically evident improvement in gait and fine-motor function. This case adds a previously unreported allele to the DNAJC6 catalog and characterizes the severe end of its phenotype, where corticospinal signs and life-threatening cachexia accompany the more familiar extrapyramidal features. It illustrates the harm that follows premature labeling of a progressive organic movement disorder as functional, especially when dopamine antagonists are then prescribed. The accompanying pathogenic BRCA1 secondary finding shows the dual diagnostic yield that clinical whole-exome sequencing can deliver. Early genetic investigation in childhood-onset movement disorders, particularly with consanguinity, should be the rule, and cascade pathways for actionable secondary findings embedded in routine practice.

PMID 42897672
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PubMedWorld neurosurgery2026-10-20

Time To Stable Programming After Staged vs Simultaneous Bilateral Subthalamic Deep Brain Stimulation Electrode Placement for Parkinson's Disease.

Yekuno Kalkidan K, Marsans Maria M, Drolett Cari C, Roberts John J et al.

To compare programming visits and time to stable stimulation and medication management after staged versus simultaneous bilateral subthalamic nucleus deep brain stimulation (DBS) for Parkinson's disease. This retrospective study included the original selected cohort of 10 staged and 10 simultaneous bilateral DBS patients, matched during cohort selection by age, disease duration, and surgical year. Continuous and count variables were summarized as medians and interquartile ranges (IQRs). Groups were compared using exact permutation Mann-Whitney tests and Fisher's exact test, as appropriate. The simultaneous group required fewer programming visits than the staged group (median 3 [IQR 3-5] vs 7.5 [IQR 6-10], P < 0.001) and had a shorter interval from initial implantation to stable therapy (5.5 [IQR 3-7] vs 14.5 [IQR 12-17] months, P = 0.007). An exploratory comparison of recorded levodopa equivalent dose reduction did not detect a difference between groups (P = 0.905). In this small retrospective cohort, simultaneous implantation was associated with fewer programming visits and a shorter overall interval to stable bilateral therapy. The timing difference includes the interval between staged procedures and does not establish superior clinical efficacy or equivalent medication outcomes.

PMID 42901320
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PubMedMayo Clinic proceedings. Innovations, quality & outcomes2026-10-18

Chorea-Acanthocytosis Without Chorea: VPS13A Disease Manifesting as Parkinsonism.

Pecha Thomas A TA, Dewey Campbell D CD, Eidelman Benjamin H BH, Pena Ashley B AB et al.

Pathogenic variants in VPS13A cause chorea-acanthocytosis, classically presenting as chorea, dystonia, and orolingual dyskinesias. Parkinsonism is an underreported presenting symptom, particularly in the absence of these classical features, and may lead to misdiagnosis. We report the case of a 52-year-old man evaluated for heart transplantation, during which the neurology service was consulted for recently diagnosed Parkinson's disease to inform transplant candidacy. His history revealed progressive gait difficulty, falls, slurred speech, nonresponse to levodopa, and absence of resting tremor or other involuntary movements. Initial examination revealed moderate hypophonic dysarthria, reduction in facial expression, asymmetric rigidity and bradykinesia, and severe postural instability. Magnetic resonance imaging of the brain revealed basal ganglia atrophy, especially in the bilateral caudate nuclei. Bloodwork revealed a normal creatine kinase level, elevated ferritin, copper, and ceruloplasmin levels, and acanthocytosis. Genetic testing revealed heterozygous pathogenic variants in VPS13A, c.7420-2A>C, and c3961-2A>G, consistent with autosomal recessive chorea-acanthocytosis. Chorea-acanthocytosis, as discovered in this patient via genetic testing, may present without typical symptoms and lead to misdiagnosis as idiopathic Parkinson's disease. Presence of atypical parkinsonian features, acanthocytes on peripheral blood smear, and basal ganglia abnormalities on structural imaging should raise the index of suspicion for this rare disorder.

PMID 42892981
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PubMedPlant physiology and biochemistry : PPB2026-10-18

Immunolocalization of L-DOPA and differential MpPPO1-3 expression in the embryonic axis and cotyledons of germinating Mucuna pruriens var. utilis seeds.

López-Sánchez Lorena L, Camas-Reyes Alberto A, Hernández-Orihuela Ana Lilia AL, Martínez-Antonio Agustino A

The cell-specific localization of L-DOPA (levodopa) in plant tissues has not been reported previously. Here, we describe the first immunolocalization of L-DOPA in mature seeds of Mucuna pruriens var. utilis at 2-6 days after imbibition (DAI), using silver-enhanced light microscopy immunocytochemistry with a specific polyclonal anti-L-DOPA antibody. Histological sections from the embryonic axis and embryo cotyledons revealed that L-DOPA accumulates predominantly in the cytoplasm of parenchymatous and starch-containing cotyledon cells, as well as in the cells of the fundamental SAM and RAM meristems of the embryonic axis. A strong immunoreactive signal at the plasma membrane and intercellular spaces of root apical meristem cells is consistent with apoplastic L-DOPA accumulation and suggests potential export to extracellular compartments. Complementarily, we analyzed the expression of the three polyphenol oxidase genes (MpPPO1, MpPPO2, and MpPPO3) by semi-quantitative RT-PCR in germinating tissues (shoot apex, primary root, and radicle) grown under light (LG) and dark (DG) conditions, alongside L-DOPA quantification by TLC. MpPPO1 was the only isoform expressed in aerial tissues (shoot apex), whereas all three isoforms were detected in radicle and root tissues, with MpPPO3 showing the highest transcript levels in roots. L-DOPA content, as estimated by TLC densitometry, showed a positive, though not statistically significant, association with MpPPO1 expression across tissues (Spearman ρ = 0.77, p = 0.10, n = 6 tissue-condition pairs). Taken together, these results may support a model in which L-DOPA stored in embryonic tissues serves as a pre-formed deterrent. At the same time, active biosynthesis via MpPPO genes in germinating roots may contribute to allelopathic exudation during early seedling establishment.

PMID 42892094
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