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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

PubMedMaterials today. Bio2026-08-30

Intranasal L-DOPA/TPP-engineered extracellular vesicles deliver icariin to ameliorate mitochondrial dysfunction with associated sphingolipid remodeling in Alzheimer's disease models.

Wu Beibei B, Wu Junyong J, Zhu Lemei L, Li An A et al.

Alzheimer's disease (AD) is associated with mitochondrial dysfunction, oxidative stress, and disrupted lipid homeostasis, but the therapeutic translation of mitochondrial-protective agents remains limited by inefficient brain delivery, insufficient neuronal selectivity, and poor subcellular precision. Here, we developed an intranasal extracellular vesicle formulation (L-DOPA/TPP-EV-ICA) by loading icariin (ICA) into mesenchymal stem cell-derived extracellular vesicles and post-inserting DSPE-PEG-Levodopa and TPP-PEG-PE to enhance nasal environment, neuronal association, and mitochondria-associated intracellular enrichment. The engineered vesicles retained EV-like morphology, showed measurable ICA encapsulation, and maintained colloidal stability under the tested storage and simulated nasal conditions. In a human nasal epithelial Transwell model, L-DOPA/TPP-EV-ICA showed greater neuronal uptake than unmodified EVs without detectable disruption of epithelial barrier integrity and exhibited preferential colocalization with mitochondria-associated structures after cellular internalization. In Aβ-injured neuronal cells, L-DOPA/TPP-EV-ICA treatment reduced mitochondrial oxidative stress and mPTP opening, improved membrane potential, and enhanced ATP production and redox-related parameters. Following intranasal administration, the engineered formulation generated stronger and more persistent brain-associated fluorescence and showed preferential association with NeuN-positive cells. In APP/PS1 mice, treatment improved cognitive performance, and attenuated histopathological and mitochondrial abnormalities. Integrated proteomic, metabolomic analyses, and protein-level analyses further identified treatment-associated alterations in sphingolipid-related pathways. These findings support L-DOPA/TPP-EV-ICA as a promising preclinical intranasal EV platform for improving mitochondrial function and modulating sphingolipid-associated alterations in AD-related models.

PMID 42668476
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PubMedJournal of neurology2026-08-29

Neuropsychiatric and multisystem toxicity following recreational inhalation of tiletamine-zolazepam (Zoletil 50): a retrospective case series with two-year prospective follow-up.

Hua Ping P, Wang Xing X, Chen Jie J, Liu Weiguo W et al.

Tiletamine-zolazepam (Zoletil) is a veterinary anesthetic, which is increasingly being abused by humans. However, the chronic neurotoxicity of this compound in humans and its long-term clinical outcomes have rarely been reported. To characterize the neurological and systemic injury following recreational Zoletil 50 inhalation, including relapse behavior and persistent deficits. We performed a retrospective case series of patients presenting to our institution with Zoletil 50 toxicity. We analyzed the clinical features, laboratory results, and neuroimaging findings, and assessed long-term outcomes and relapse rates during a two-year observation period. All 36 subjects (100%) demonstrated postural tremor, with 22 (61.1%) showing sustained, high-amplitude tremor early after admission. Four patients (11%) presented with bradykinesia and rigidity. Cerebellar ataxia was present in 30 (83%), visual disturbance in 20 (56%), and concomitant hallucinations in 16 (44%). Biochemical abnormalities included elevated transaminases (53%) and hypokalemia (44%). Two patients died in hospital due to cardiorespiratory failure. Of 34 discharged patients, 20 (59%) relapsed, 17 within the first month. A third death occurred during follow-up after a fifth relapse. At two years, residual deficits persisted in 11 of 33 survivors: subjective memory decline in seven, visual impairment in six, and bradykinesia requiring levodopa in two. Zoletil 50 inhalation is associated with a broad spectrum of neurological and systemic injury, with tremor, ataxia, and visual disturbance as the most consistent features. Relapse is common and early; one-third of long-term survivors still had neurological deficits at two years. Clinicians should consider tiletamine-zolazepam exposure when evaluating young patients with unexplained tremor, ataxia, and perceptual disturbance as standard toxicology screens do not detect this compound. Prospective controlled studies are needed to confirm causation and define the full spectrum of toxicity.

PMID 42665695
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PubMedFrontiers in neurology2026-08-27

Levodopa exacerbated tremor in Parkinson's disease.

Baizabal-Carvallo José Fidel JF, Alonso-Juarez Marlene M, Fekete Robert R

Levodopa is considered the most effective pharmacological therapy for Parkinson's disease (PD). However, it can cause side effects including diverse types of dyskinesia. In rare cases, tremor worsening has been reported in patients with PD taking levodopa. The frequency of this effect in clinical practice is unclear, and the phenomenology is poorly characterized. We aimed to assess the frequency, clinical features, and factors associated with tremor exacerbated by levodopa in patients with PD. We studied a cohort of 274 consecutive patients with PD and determined the frequency of tremor exacerbated by levodopa. Tremor exacerbation with levodopa was identified in four patients (1.46%) and 1.55% of patients taking levodopa. There were two men and two women, with ages ranging from 53 to 73 years at the time of evaluation. All patients experienced a consistent worsening of rest tremor within 20 min of taking a low dose of levodopa (62.5 mg or 125 mg). No benefit from biperiden or amantadine was observed for levodopa-exacerbated tremor in any of the cases. None of the patients showed signs of atypical parkinsonism or abnormal MRI. Patients with levodopa-exacerbated tremor were very reluctant to take more than a small dose of levodopa or any dose at all, hampering potential benefits for other parkinsonian features such as rigidity, bradykinesia, and parkinsonian gait. Tremor exacerbated by levodopa is an uncommon side effect in patients with PD that limits the benefit of this therapy.

PMID 42656305
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PubMedMedicina2026-08-27

[Pharmacologic treatment of dystonia].

Zea Vera Alonso A, Guerrero Ruiz Graciela Del Pilar GDP

Dystonia is a significant cause of morbidity and disability in children. Treatment aims to improve function, reduce pain and disability, and enhance the child's quality of life. This review describes the most used pharmacological options for treating persistent dystonia. The main medications used to treat dystonia include anticholinergics, baclofen, and benzodiazepines. Botulinum toxin is also effective, particularly in focal dystonias. Other drugs such as levodopa, gabapentin, clonidine, and vesicular monoamine transporter inhibitors are also frequently used. The most common adverse effects are discussed. Medication selection should consider etiology, subtype of dystonia, potential adverse effects, and associated comorbidities.

PMID 42659548
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PubMedFrontiers in neurology2026-08-27

Parkinson's disease in the United Arab Emirates (UAE): Emirates Neurology Society consensus guidelines.

Mittal Shivam Om SO, Iantorno Vittorio V, Hassan Ali A, Krystkowiak Pierre P et al.

Parkinson's disease (PD) incidence has risen by more than eightfold in the United Arab Emirates (UAE) between 1990 and 2019, representing one of the highest increases globally and creating substantial pressure on a fragmented, multi-payer health system. Region-specific guidance has been lacking, leading clinicians to extrapolate from international guidelines that do not fully address formulary heterogeneity, advanced therapy centralization, and cultural factors. Under the auspices of the Emirates Neurology Society, a national taskforce of 10 specialists representing major PD centers across the UAE used a three-round modified Delphi process informed by systematic literature review and key randomized controlled trials. Recommendations were graded using a GRADE-aligned system (A-C, Good Practice Points) and adapted to UAE formulary, service configuration, and cultural context. Consensus was achieved on 146 recommendations across eight domains: (1) mandatory adoption of MDS-2015 diagnostic criteria; (2) age-stratified pharmacologic algorithms with levodopa as first-line for older or cognitively vulnerable patients; (3) structured non-motor symptom management; (4) rehabilitation and UAE cultural lifestyle adaptations including Ramadan fasting management, DBS considerations in women, family-centered care, and multilingual practice; (5) advanced therapy referral using the 5-2-1 rule integrated with the Making Informed Decisions to Aid Timely Management of Parkinson's Disease (MANAGE-PD) tool, with five device-aided options (subcutaneous foslevodopa/foscarbidopa, apomorphine SC- subcutanous, LCIG- Levodopa Carbidopa Intestinal Gel, DBS- Deep Brain Stimulation, MRgFUS- MRI guided focussed ultrasound) presented through shared decision-making; (6) a three-tier service model; (7) UAE formulary mapping; and (8) center accreditation and registry metrics. Advanced therapies are centralized in accredited centers with clear minimum volume and multidisciplinary staffing criteria. These UAE consensus recommendations provide a pragmatic, context-adapted framework for PD management, emphasizing structured diagnosis, age-appropriate pharmacotherapy, systematic use of MANAGE-PD and 5-2-1 for advanced therapy referral, culturally sensitive practice adaptations, and a three-tier network model integrated through the Malaffi health information exchange and a planned national PD registry.

PMID 42656222
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PubMedNPJ Parkinson's disease2026-08-27

Oligomeric Alpha-Synuclein from neural-derived extracellular vesicles as possible biomarkers of non-motor symptoms in Parkinson's disease.

Meloni Mario M, Agliardi Cristina C, Salvatore Anna A, Saibene Francesca Lea FL et al.

Non-motor symptoms (NMS) in Parkinson's disease (PD) are clinically impactful and lack reliable blood-based biomarkers. Neural-derived extracellular vesicles (NDEVs) enriched from serum may reflect central neurodegenerative processes. In this cross-sectional study, we examined associations between NMS burden and NDEV-associated proteins in 68 patients with PD. NDEVs were immunocaptured from serum using an anti-L1CAM approach and characterized according to MISEV guidelines. NDEV-associated oligomeric α-synuclein, SNARE complex proteins (SNAP-25, VAMP2, STX-1A), and neurotrophic factors (BDNF, GDNF, CDNF) were quantified by ELISA and related to NMS burden and PCA-derived non-motor domains, adjusting for age, sex, disease duration, MDS-UPDRS III, and levodopa equivalent daily dose (LEDD). Higher NDEV-associated oligomeric α-synuclein correlated with total NMSS score (partial Spearman's ρ = 0.252, p = 0.02) and with hallucinations (domain 4) and attention/memory (domain 5). These associations were confirmed by multivariable regression analyses. In domain-specific models, oligomeric α-synuclein was independently associated with worse cognitive and behavioral-psychotic scores, whereas higher STX-1A and lower CDNF were associated with greater affective-motivational symptom severity. No significant associations were observed for autonomic or sleep domains. These findings support NDEV-associated oligomeric α-synuclein as a candidate biomarker of non-motor symptom burden in PD and warrant longitudinal validation.

PMID 42649220
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