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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

PubMedNeurorehabilitation and neural repair2026-08-25

White Matter Diffusion Anisotropy and the Effects of Inpatient Multidisciplinary Rehabilitation in Parkinson's Disease: A Diffusion Tensor Imaging Analysis.

Marumoto Kohei K, Koyama Tetsuo T, Takahashi Ryuichi R, Yamamoto Shinji S et al.

In Parkinson's disease (PD), compensatory increases in corticospinal tract (CST) fractional anisotropy (FA) occur early; whether pretreatment white matter integrity predicts rehabilitation responsiveness is unknown. To determine whether pretreatment CST FA predicts inpatient rehabilitation response in PD. Ninety-four PD patients and 13 age-matched healthy controls underwent DTI before an 8-week inpatient multidisciplinary rehabilitation program. Patients were classified as responders (UPDRS Part III improvement ≥2.5 points; n = 61) or non-responders (n = 33). FA across 20 white matter ROIs was compared (Kruskal-Wallis; Mann-Whitney U post-hoc) and voxel-wise TBSS performed. Logistic regression adjusted for age, disease duration, H-Y stage, and levodopa dose. Responders had higher bilateral CST FA than non-responders (right: P < .001, d = 0.99; left: P < .001, d = 1.14; both FDR-corrected) and maintained CST FA comparable to healthy controls, whereas non-responders showed significantly lower CST FA. TBSS confirmed bilateral CST clusters of higher FA in responders (P < .05, TFCE-corrected). CST FA correlated inversely with H-Y stage (ρ = -0.307, P = .003) and motor improvement (ρ = -0.417, P < .001). Logistic regression identified CST FA as an independent predictor (OR = 5.51 per SD; 95% CI 2.50-12.06; Nagelkerke R² = 0.408; P < .001). Pretreatment CST FA independently predicts rehabilitation responsiveness in PD, with responder integrity comparable to healthy controls. With good internal discrimination (AUC 0.79), DTI-derived CST FA is a promising marker for stratifying rehabilitation potential, though external validation is required before clinical use. UMIN Clinical Trials Registry, https://www.umin.ac.jp/, UMIN000023641.

PMID 42638517
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PubMedFrontiers in aging neuroscience2026-08-25

Triglyceride-glucose index is associated with cerebral small vessel disease-related motor impairment in Parkinson's disease: a mediation analysis.

Zhang Meimei M, Li Wei W, Zhang Yumei Y, Feng Tao T

Cerebral small vessel disease (CSVD) may worsen motor and cognitive impairment in Parkinson's disease (PD), yet whether peripheral metabolic inflammation mediates this link remains unclear. The triglyceride-glucose (TyG) index, a surrogate for insulin resistance, has been associated with CSVD and neurodegeneration. This study examined whether the TyG index statistically accounts for the association between CSVD burden and motor or cognitive deficits in PD. This retrospective cross-sectional study enrolled 362 PD patients. The 4-point scale assessed CSVD burden. Movement Disorder Society Unified Parkinson's Disease Rating Scale part III (MDS-UPDRS III) and Montreal Cognitive Assessment (MoCA) evaluated motor and cognitive function, separately. Spearman correlation and mediation analyses were performed, adjusting for age, sex, education, hypertension, diabetes, and daily dose equivalent of levodopa. Sensitivity analyses were conducted to assess the robustness and specificity of the findings. CSVD burden was positively associated with MDS-UPDRS III (total effect = 2.309, 95% CI [0.463, 4.155, p = 0.014]) and negatively associated with TyG index (a = -0.067, p = 0.025). TyG index was negatively associated with MDS-UPDRS III (b = -6.561, p < 0.001). The indirect effect was 0.441 (95% CI [0.048, 0.958]), accounting for 19.1% of the total effect. This mediation was specific to TyG, as four alternative inflammatory indices showed no significant effects. Additional analyses adjusting for disease duration and Hoehn-Yahr staging confirmed robustness [indirect effect = 0.288, 95% CI (0.019, 0.687)]. Neither fasting triglycerides nor glucose alone mediated the effect. No mediation was found for cognition. The TyG index statistically accounts for part of the association between CSVD and motor function in PD via a negative-to-negative pathway, suggesting a hypothesis-generating metabolic target that warrants prospective investigation.

PMID 42639013
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PubMedExperimental brain research2026-08-24

Levodopa-induced alterations in vertical center of mass and muscle synergy structure during Parkinsonian gait.

Aydın Rukiye R, Oyama Genko G, Shimoda Shingo S, Garcia Alvaro Costa AC et al.

Parkinson's disease (PD) is a neurodegenerative disorder characterized by gait impairments that affect the regulation of whole-body movement, which can be quantified through metrics such as vertical center of mass (vCoM). In healthy gait, vCoM oscillations contribute to metabolic efficiency by facilitating the exchange between kinetic and potential energy; however, this mechanism is often disrupted in PD. Although levodopa improves motor impairments, its impact on vCoM and neuromuscular control remains poorly understood. This study investigated levodopa effects on vCoM and neuromuscular coordination in fifteen patients with PD (Hoehn & Yahr 2-3) during PD OFF (before levodopa) and PD ON (after levodopa) and compared to nine healthy older adults (HOA). Kinematic and electromyography data were collected during an overground walk to quantify vCoM and muscle synergies. Here we show that levodopa significantly increased maximum vCoM displacement (p = 0.002), with PD OFF showing significantly reduced displacement compared to HOA (p < 0.001) while PD ON did not differ significantly, indicating a shift in vCoM displacement towards healthy patterns. Temporal patterns of muscle synergies showed that PD OFF exhibited prolonged activation duration and slower slope-to-peak in Synergy 2 (push-off) compared to HOA while spatial patterns of Synergy 2 showed an increase in gastrocnemius muscle contribution in PD ON compared to PD OFF (p = 0.002). Together these findings demonstrate that levodopa might partially restore whole-body gait mechanics through a unique reorganization of muscle synergy structure, pointing to a possible functional link between neuromuscular coordination and gait dynamics in PD.

PMID 42635765
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PubMedParkinsonism & related disorders2026-08-24

Comparative outcomes and healthcare costs of three device-aided pharmacotherapies for patients with advanced Parkinson's disease in Sweden: A nationwide registry-based cohort study.

Nyholm Dag D, Paonessa Davide D, Bergquist Filip F, Timmermann Jan Erik JE et al.

Patients with advanced Parkinson's disease often require treatment beyond conventional oral or transdermal therapy. However, real-world evidence across emerging advanced treatment strategies remains limited. To compare patient characteristics, treatment patterns, clinical outcomes, healthcare resource utilization (HCRU), and costs among Parkinson's disease patients treated with levodopa/carbidopa dispersible microtablets (LC-5), levodopa-carbidopa intestinal gel (LCIG)/levodopa-entacapone-carbidopa intestinal gel (LECIG), or continuous subcutaneous apomorphine infusion (CSAI). Patients initiating LC-5, LCIG/LECIG, or CSAI between 2014 and 2024 were identified in Swedish national register data. Treatment groups were balanced using inverse probability weighting. Descriptive analyses, cumulative incidence estimates, and Cox proportional hazards models were used to assess outcomes. 426 LC-5, 1112 LCIG/LECIG, and 490 CSAI users were included. 63.6% of LC-5 users were women, whereas men constituted the majority in the other treatment groups. 3.5% of LCIG/LECIG and 6.1% of CSAI users discontinued treatment, compared with 28.6% of LC-5 users. Compared with LCIG/LECIG users, the mortality hazard ratio estimates were lower for LC-5 (HR 0.71, 95% CI 0.45-1.11) and CSAI users (HR 0.80, 95% CI 0.63-1.02), but neither difference was statistically significant. In the 12 months following treatment initiation, weighted estimates of healthcare costs were higher among LCIG/LECIG (€37,613) and CSAI users (€29,214) than among LC-5 users (€17,290). In this nationwide Swedish cohort, no statistically significant mortality difference was detected. Weighted one-year HCRU and cost estimates were lower among LC-5 users than among infusion-therapy users; however, residual confounding by disease severity, treatment selection, and other unmeasured clinical factors limits causal interpretation.

PMID 42636761
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PubMedNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2026-08-24

Serum pentraxin-3 and systemic inflammatory biomarkers in Parkinson's disease with and without freezing of gait.

Çelik Fatih F, Gemici Yağmur İnalkac Yİ, Aktaş Fethi F, Ulman Cevval C et al.

Freezing of gait (FOG) is one of the most disabling axial symptoms in Parkinson's disease (PD). Neuroinflammatory mechanisms have been implicated in PD progression, yet the role of systemic inflammatory biomarkers in FOG remains unclear. We investigated the association between serum inflammatory biomarkers and FOG and explored their relationships with clinical measures of motor and freezing severity. Thirty PD patients with FOG (FOG +), 31 without FOG (FOG -), and 31 age- and sex-matched healthy controls were enrolled. Serum levels of macrophage inflammatory protein-1 alpha (MIP-1α), MIP-1β, interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and pentraxin-3 (PTX-3) were measured by ELISA. Motor severity was assessed using the Unified Parkinson's Disease Rating Scale, Hoehn-Yahr stage, and the Freezing of Gait Questionnaire. Multivariable logistic regression was performed to evaluate the independent association between PTX-3 and FOG. In unadjusted analyses, serum MIP-1α levels were significantly higher in PD patients than in controls, whereas PTX-3 levels were significantly higher in FOG + than FOG - patients. In the overall PD cohort, PTX-3 correlated positively with UPDRS-II scores (r = 0.364, p = 0.004). Exploratory analyses in the FOG + subgroup showed correlations of MIP-1β and IL-6 with UPDRS-III scores and IL-1β with FOG-Q scores (all p < 0.05). However, PTX-3 was not independently associated with FOG after adjustment for age, sex, disease duration, and levodopa equivalent daily dose. Serum PTX-3 showed a preliminary association with FOG in unadjusted analyses, whereas other inflammatory biomarkers demonstrated exploratory associations with motor and freezing-related clinical measures.

PMID 42634024
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PubMedCase reports in endocrinology2026-08-21

Improvement of Multifactorial Tremor in Klinefelter Syndrome With Testosterone Replacement Therapy.

Houssarini Jared J, Hsieh Albert A, Hocking Samantha S

A man in his 50s with long-standing learning difficulties and schizophrenia currently treated with clozapine presented with gynaecomastia and a new right testicular mass. He was noted to have a severe tremor interfering with activities of daily living treated with combination levodopa + benserazide, primidone and topiramate. Investigations revealed elevated prolactin, gonadotropins, sex hormone binding globulin, total testosterone and oestradiol. Right orchidectomy revealed Leydig cell hyperplasia. Karyotyping diagnosed Klinefelter syndrome. Testosterone replacement therapy (TRT) was commenced, with subsequent marked improvement in his debilitating tremor. Tremor is a potentially disabling complication of Klinefelter syndrome with fewer than 50 cases reported in the literature. The pathophysiology of tremor in Klinefelter syndrome is unclear. Tremor in Klinefelter syndrome is often refractory to anti-tremor medical therapy; however, as reported in this case, testosterone therapy may improve tremor in Klinefelter syndrome. It is rare for TRT to significantly improve tremor as reported in this case.

PMID 42626466
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