CLINICAL TRIALS PROFILE FOR LEVODOPA

505(b)(2) Clinical Trials for levodopa

This table shows clinical trials for potential 505(b)(2) applications. See the next table for all clinical trials

Trial Type	Trial ID	Title	Status	Sponsor	Phase	Start Date	Summary
New Formulation	NCT00363727 ↗	Onset Motor Complications Using REQUIP CR (Ropinirole Controlled-release) As Add-on Therapy To L-dopa In Parkinson's	Completed	GlaxoSmithKline	Phase 3	2003-12-01	This study evaluates how effective a new formulation of a marketed drug is in increasing the time to onset of dyskinesia (abnormal twisting, writhing movements) in patients with Parkinson's Disease who have been taking levodopa for less than 2 years.
New Formulation	NCT00640159 ↗	Tolerability and Efficacy of Switch From Oral Selegiline to Orally Disintegrating Selegiline (Zelapar) in Patients With Parkinson's Disease	Completed	Baylor College of Medicine	Phase 4	2007-01-01	Parkinson's disease (PD) is a progressive neurodegenerative disease. Symptomatic therapy is primarily aimed at restoring dopamine function in the brain. Oral selegiline in conjunction with L-dopa has been a mainstay of therapy for PD patients experiencing motor fluctuations for many years. The mechanisms accounting for selegiline's beneficial adjunctive action in the treatment of PD are not fully understood. Inhibition of monoamine oxidase (MAO) type B (MAO-B) activity is generally considered to be of primary importance. Oral selegiline has low bio-availability and is typically dosed BID, for a total of 5-10 mg daily. Recently, the FDA approved a new orally disintegration tablet (ODT) formulation of selegiline, called ZelaparTM. This new formulation utilizes Zydis technology to dissolve in the mouth, with absorption through the oral mucosa, thereby largely bypassing the gut and avoiding first pass hepatic metabolism. This allows more active drug to be delivered at a lower dose. Consequently, Zelapar is dosed once-daily, up to 2.5 mg per day. There are no empirical data indicating whether the use of the new approved formulation of selegiline ODT (Zelapar) is superior or preferred by patients compared to traditional oral selegiline. It is believed that clinical efficacy will be preserved or enhanced, by delivering more active drug, with improved patient preference for the ODT formulation due to the once-daily dosing . The effectiveness of orally disintegrating selegiline as an adjunct to carbidopa/levodopa in the treatment of PD was established in a multicenter randomized placebo-controlled trial (n=140; 94 received orally disintegrating selegiline, 46 received placebo) of three months' duration. Patients randomized to orally disintegrating selegiline received a daily dose of 1.25 mg for the first 6 weeks and a daily dose of 2.5 mg for the last 6 weeks. Patients were all treated with levodopa and could additionally have been on dopamine agonists, anticholinergics, amantadine, or any combination of these during the trial. At 12 weeks, orally disintegrating selegiline-treated patients had an average of 2.2 hours per day less "OFF" time compared to baseline. Placebo treated patients had 0.6 hours per day less "OFF" time compared to baseline. These differences were significant (p < 0.001). Adverse events were very similar between drug and placebo.
New Combination	NCT01766258 ↗	Efficacy and Safety Proof of Concept Study in Patients With Parkinson's Disease and End-of-dose Motor Fluctuations	Completed	Orion Corporation, Orion Pharma	Phase 2	2011-05-01	The primary objective of the study is to assess the efficacy, carbidopa dose response and safety of ODM-101, a new combination of levodopa, carbidopa and entacapone in the treatment of Parkinson's disease (PD) patients with end-of-dose motor fluctuations.
New Formulation	NCT06817200 ↗	The Effect of Amantadine as add-on Therapy for Motor Fluctuations in Advanced Parkinson's Disease: a Randomized Double-blinded Placebo-controlled Trial	NOT_YET_RECRUITING	University Hospital, Toulouse	PHASE2	2025-05-01	Motor fluctuations are identified as the most challenging symptoms by parkinson disease patients. A recent post-hoc analysis of ADS-5012 trials (new formulation of ER Amantadine), revealed a significant improvement in OFF-time. No randomized clinical trial has ever specifically investigated to date the effect of amantadine IR on motor fluctuations. The main objective of this study is to evaluate the effect of amantadine (300 mg/day) as add-on therapy for the treatment of motor fluctuations (Off-time) in advanced Parkinson's disease patients versus placebo after 3 months of treatment.

All Clinical Trials for levodopa

Trial ID	Title	Status	Sponsor	Phase	Start Date	Summary
NCT00001929 ↗	Treatment of Parkinson's Disease With Eliprodil	Completed	National Institute of Neurological Disorders and Stroke (NINDS)	Phase 2	1999-03-01	Patients with Parkinson's disease are missing the chemical neurotransmitter dopamine. This occurs as a result of destructive changes in an area of the brain responsible for making dopamine, the basal ganglia. Patients with the disease experience, rigid muscles, stooped posture, and a shuffling-type walk (gait). In this study researchers plan to evaluate the effectiveness of the drug eliprodil for the treatment of Parkinson's Disease. Eliprodil works by blocking special receptors (NMDA) that are associated with the symptoms of Parkinson's Disease.
NCT00004576 ↗	Study of LY300164 for the Treatment of Parkinson's Disease	Completed	National Institute of Neurological Disorders and Stroke (NINDS)	Phase 2	2000-02-01	This study will test the effectiveness of an experimental drug called LY300164 on improving Parkinson's disease symptoms, such as movement impairments and tremor, as well as involuntary movements produced by long-term treatment with levodopa. Patients with relatively advanced (Stage II to IV) Parkinson's disease between 30 and 75 years of age may be eligible for this 8-week study. Participants will have a complete medical history and physical examination, including blood tests and an electrocardiogram, and possibly brain magnetic resonance imaging (MRI), CT scan, and chest X-ray. Patients will stop taking all anti-parkinsonism medications except levodopa (Sinemet) and the experimental drug during the study. For the first 1 to 3 days, patients will be in the hospital for a levodopa "dose-finding" procedure. For this study, levodopa is infused through a vein for up to 8 hours, with symptoms monitored frequently to determine the doses that will produce two results: 1) the dose that is less than what is needed to relieve symptoms, and 2) the dose that relieves symptoms, but may produce dyskinesias. When these dose rates are determined, patients will begin treatment in one of two groups. One will take LY300164 3 times a day, along with levodopa, for 3 weeks. The second group will take placebo tablets (a look-alike tablet with no active ingredient) and levodopa on the same schedule as the LY300164 group. A brief medical examination and routine blood and urine tests will be done weekly. The drug dose will be increased every 3 to 4 days until significant side effects occur or the maximal dose is reached. Patients will be closely monitored for 4 hours after every increase. At the end of the 3 weeks, or when the maximal dose is reached, patients will be readmitted to the hospital for 2 to 3 days for a second levodopa dose-finding study, while continuing on LY300164 or placebo. After this test, patients will resume taking levodopa and the experimental drug or placebo as before for another 2 weeks. At the end of the 2-weeks, the entire procedure will be repeated in both groups, but the treatments will be switched-that is, the patients who were taking LY300164 will now take placebo, and the patients who took placebo will now take the drug. At the end of the second 3 weeks, the levodopa infusion procedure will be repeated once more. Throughout the study, parkinsonism symptoms and dyskinesias will be evaluated and blood samples will be drawn periodically to measure drug levels.
NCT00004731 ↗	Parkinson's Disease Treatment With Coenzyme Q10	Completed	National Institute of Neurological Disorders and Stroke (NINDS)	Phase 2	1998-09-01	The purpose of this study is to compare the effects of varying dosage of coenzyme Q10 (CoQ10) versus a placebo in the treatment of Parkinson's disease (PD) in patients with early, untreated PD.
NCT00004733 ↗	Timing of Levodopa Treatment in Parkinson's Disease	Completed	National Institute of Neurological Disorders and Stroke (NINDS)	Phase 3	1998-01-01	The ELLDOPA study is a controlled clinical trial in patients with newly diagnosed PD to determine the optimal timing and dosing with levodopa (Sinemet or its generic equivalents).
NCT00006077 ↗	Effects of Monoamine Reuptake Inhibitor NS2330 in Parkinson's Disease	Completed	National Institute of Neurological Disorders and Stroke (NINDS)	Phase 2	2000-08-01	This study will evaluate the effects of an experimental drug called NS2330 on Parkinson's disease symptoms and on dyskinesias (involuntary movements) that develop as a result of long-term treatment with levodopa. This drug prevents the neurotransmitter dopamine from entering nerve cells. Patients between 18 and 75 years old who have moderately advanced Parkinson's disease and motor problems resulting from levodopa therapy may be eligible for this 5-week study. Candidates will have a complete medical history and physical examination with a detailed neurological evaluation. If needed, some patients will undergo a magnetic resonance imaging (MRI) or computerized tomography (CT) scan of the brain and a chest X-ray. All patients will have blood and urine tests and an electrocardiogram (EKG) and will take a written test for evaluation of depression. Patients enrolled in the study will, if possible, stop taking all antiparkinson medications except levodopa (Sinemet) for one month before the study begins and through its duration. For the first 1 to 3 days, patients will undergo a levodopa "dose-finding" procedure. For this study, patients will stop taking their usual oral levodopa medicine and instead will have levodopa infused through a vein for up to 12 hours. During the infusions, the drug dose will be increased slowly until either 1) parkinsonism symptoms improve, 2) dyskinesias appear, 3) unacceptable side effects occur, or 4) the maximum study dose is reached. When the patient's optimal dose is determined, treatment will begin. Patients will take three pills containing NS2330 or placebo (a look-alike pill with no active ingredient) 3 days a week for up to 5 weeks, in addition to their regular levodopa medication. All participants will receive placebo at some point in the study; some patients will receive only placebo throughout the entire 5 weeks. On treatment days, patients will have a brief medical examination before receiving the drug and will then be monitored for side effects for about 6 to 8 hours after taking the drug. At the beginning of weeks 2 and 5, the levodopa infusions will be repeated at the previously determined optimum rate. Throughout the study, parkinsonism symptoms, dyskinesias and depression will be evaluated. Blood and urine samples will be collected each week for standard safety tests, and blood will also be drawn periodically to measure NS2330 levels.
NCT00006337 ↗	KW-6002 to Treat Parkinson's Disease	Completed	National Institute of Neurological Disorders and Stroke (NINDS)	Phase 2	2000-10-01	This study will evaluate the effects of an experimental drug called KW-6002 on Parkinson's disease symptoms and on dyskinesias (involuntary movements) that develop as a result of long-term treatment with levodopa. This drug blocks the action of the neurotransmitter adenosine, thought to be involved in producing Parkinson's symptoms. Patients with relatively advanced (Stage II to IV) Parkinson's disease between 30 and 80 years of age may be eligible for this 7-week study. Participants will have a complete medical history and physical examination, including blood tests and an electrocardiogram, and possibly brain magnetic resonance imaging (MRI), CT scan, and chest X-ray. Patients enrolled in the study will, if possible, stop taking all antiparkinsonian medications except levodopa (Sinemet) for one month before the study begins and throughout its duration. For the first 1 to 3 days, patients will be admitted to the NIH Clinical center to undergo a levodopa "dose-finding" procedure. For this study, patients will stop taking Sinemet and instead will have levodopa infused through a vein for up to 8 hours/day. During the infusions, the drug dose will be increased slowly until either 1) parkinsonian symptoms improve, 2) unacceptable side effects occur, or 3) the maximum study dose is reached. Symptoms will be monitored frequently to find two infusion rates: 1) one that is less than what is needed to relieve symptoms, and 2) one that relieves symptoms but may produce dyskinesias. This procedure will be repeated at the end of weeks 2, 4 and 6 of the study. When the patient's optimal dose is determined treatment will begin. Patients will take tablets or capsules containing KW-6002 or placebo (a look-alike pill with no active ingredient) once a day for 2 weeks, in addition to their regular Sinemet. All participants will receive placebo at least 2 weeks during the study; some patients will receive only placebo throughout the entire 7 weeks. At the end of weeks 1, 3 and 5, patients will be evaluated with a brief physical examination, routine blood and urine tests, and assessment of any adverse effects. Throughout the study, parkinsonian symptoms and dyskinesias will be evaluated and blood samples will be drawn periodically to measure drug levels.
NCT00006488 ↗	Continuously Infused Intracerebral (IC) Recombinant-Methionyl Human Glial Cell Line-Derived Neurotrophic Factor (r-metHuGDNF) for the Treatment of Idiopathic Parkinson's Disease	Completed	National Center for Research Resources (NCRR)	Phase 1	1969-12-31	Parkinson's disease is characterized by loss of neurons that produce dopamine in a region of the brain called the substantia nigra. In the early stages of the disease, the disease responds to agents that replace dopamine such as levodopa. Patients with more advanced disease have wide fluctuations in their response to levodopa, exhibiting on and off periods. This is due to continued degeneration of neurons. Recombinant-methionyl human glial cell line-derived neurotrophic factor (r-metHuGDNF or GDNF) is a neurotrophic factor that promotes survival of dopaminergic neurons. This is a protein produced by recombinant technology that is almost identical to the naturally produced factor. Results of animal studies indicate that GDNF has the potential to benefit patients with advanced Parkinson's disease. The purpose of this clinical trial is to determine whether GDNF works to relieve symptoms of advanced Parkinson's disease. The study will also test the delivery of GDNF using a catheter implanted into the putamen, the area of the brain associated with Parkinson's disease, and an infusion pump that is implanted under the skin in the abdomen or chest. GDNF will be placed into the pump and delivered through the catheter to the brain. The purposes of this study are to determine the potential benefits and side effects of GDNF. The performance and safety of the catheter/infusion pump system will also be assessed. The study will last for 6 months. Subjects will undergo neurological testing, computerized gait assessment and neurological imaging.

Clinical Trial Conditions for levodopa

Condition Name

Condition Name for levodopa
Intervention	Trials
Parkinson's Disease	174
Parkinson Disease	127
Idiopathic Parkinson's Disease	21
Parkinson's Disease (PD)	15

Condition MeSH

Condition MeSH for levodopa
Intervention	Trials
Parkinson Disease	374
Dyskinesias	49
Parkinsonian Disorders	7
Atrophy	7

Clinical Trial Locations for levodopa

Trials by Country

Trials by Country for levodopa
Location	Trials
Germany	109
Japan	100
Canada	95
Spain	67
Italy	62

Trials by US State

Trials by US State for levodopa
Location	Trials
California	79
Florida	77
New York	66
Michigan	63
Illinois	59

Clinical Trial Progress for levodopa

Clinical Trial Phase

Clinical Trial Phase for levodopa
Clinical Trial Phase	Trials
PHASE4	5
PHASE3	4
PHASE2	8

Clinical Trial Status

Clinical Trial Status for levodopa
Clinical Trial Phase	Trials
Completed	297
Recruiting	64
Terminated	27

Clinical Trial Sponsors for levodopa

Sponsor Name

Sponsor Name for levodopa
Sponsor	Trials
Bial - Portela C S.A.	23
National Institute of Neurological Disorders and Stroke (NINDS)	20
Oregon Health and Science University	14

Sponsor Type

Sponsor Type for levodopa
Sponsor	Trials
Industry	350
Other	329
NIH	39

Levodopa Clinical Trials Update, Market Analysis, and 2026–2035 Projections

Last updated: May 20, 2026

Levodopa remains the core symptomatic therapy for Parkinson’s disease (PD) and is widely used via multiple branded and generic formulations. Patent exclusivity is largely irrelevant for most markets because key levodopa actives are long off-patent; competitive pressure is driven by formulation differentiation (controlled release, ER/ODT, combination platforms), device-adjacent delivery concepts, and payer preference rather than new active-drug patent estates.

How are current clinical trials updating the levodopa pipeline (2024–2026)?

Featured trial activity in levodopa is concentrated in three buckets: (1) reformulations and delivery systems that aim to reduce motor fluctuations, (2) combination regimens (levodopa with COMT inhibitors, MAO-B inhibitors, or novel adjuncts), and (3) early-stage platform studies of patient-centric dosing modalities.

Where trial activity is clustering

• Motor fluctuation control: trials evaluating levodopa formulations designed to smooth plasma exposure to reduce OFF time.
• On-demand or rapid onset dosing: studies tied to breakthrough symptom patterns.
• Adherence and tolerability: trials focused on administration convenience (oral dispersion, sublingual approaches where applicable), gastrointestinal tolerability, and reduction in dyskinesia triggers.
• Combination optimization: trials comparing dosing schedules and titration strategies for established combinations.

What these updates mean for R&D

• Without new active-drug patent cliffs to manage, pipeline advantage comes from measurable clinical endpoints tied to motor outcomes (OFF time reduction, dyskinesia metrics) and safety/tolerability.
• Trial endpoints skew toward digital-motor scales, patient diaries, and investigator-rated dyskinesia because these map to payer and guideline decision-making.

Which clinical endpoints are most used to judge levodopa efficacy and safety?

Most levodopa-centered studies use a consistent endpoint set to support claims around motor symptom control.

Common efficacy endpoints

• Mean change in daily OFF time (hours/day) from baseline.
• Responder analyses for OFF time reduction and improvement in UPDRS Part III motor scores.
• Dyskinesia assessment (change in dyskinesia duration and severity scales).
• Time to ON and ON quality metrics, including AON/OFF transitions.

Safety endpoints

• GI adverse events (nausea, vomiting, dyspepsia).
• Neuropsychiatric events (hallucinations, confusion) in sensitive subpopulations.
• Dyskinesia and orthostatic symptoms, tracked longitudinally.
• Vital sign and ECG monitoring where formulations add excipients or altered release profiles.

How large is the levodopa market today, and what products dominate?

Levodopa market value is driven by PD prevalence, long duration of therapy, and formulary coverage. The market is structurally fragmented across multiple branded products historically, but competitively anchored by generic availability for the active component.

Dominant commercial pattern

• Long-run demand is sustained because levodopa is foundational for advancing PD.
• Product competition is primarily between:
  • Immediate-release levodopa/carbidopa generics and legacy brands.
  • Controlled-release and extended-release versions aiming to improve motor fluctuations.
  • Combination therapy products (levodopa plus adjunct inhibitors).
  • Any premium brand that can demonstrate clinically meaningful reductions in OFF time or dyskinesia burden.

What market growth drivers and headwinds shape levodopa projections?

Growth drivers

• Continued diagnosis growth and aging demographics expanding the treated population.
• Medical need for motor fluctuation management as patients progress through mid-to-late PD.
• Payer willingness to cover premium formulations when they reduce healthcare utilization tied to falls, hospitalizations, and caregiver burden.

Headwinds

• Active ingredient commoditization lowers average selling prices (ASPs) unless formulation differentiation sustains premium pricing.
• Patent and exclusivity constraints are minimal for the core active, pushing differentiation to manufacturing, release tech, and combination dosing schedules.
• Treatment substitution within PD may shift modest share to dopamine agonists early on, but levodopa remains the anchor in later stages.

What is the revenue and volume outlook for levodopa through 2035?

Base-case outlook (directional)

• Volume: stable-to-growing, aligned with PD population growth and treatment penetration.
• Value: more constrained, because generics compress pricing; growth depends on premium controlled-release and combination share gains.

Projection logic used for levodopa

1. PD prevalence growth increases treated populations.
2. Portfolios tilt toward ER/controlled-release where they outperform on motor outcomes.
3. Market value grows slower than volume due to price erosion in immediate-release segments.
4. Any incremental value comes from premium share capture and bundling within combination regimens.

When does levodopa lose exclusivity in key markets (US/EU/UK)?

For most levodopa indications and generic equivalents, active-ingredient exclusivity ended years ago. Remaining exclusivity typically attaches to:

• specific formulation compositions,
• specific release technologies,
• and method-of-use or manufacturing process claims.

Practically, “exclusivity loss” for levodopa is less about an active ingredient cliff and more about whether a premium formulation has enforceable secondary IP.

What formulations of levodopa are most important for differentiation (IR vs CR vs ER)?

Immediate-release (IR)

• Lowest barrier to generic entry.
• Competitive by price and dosing convenience.

Controlled-release / extended-release (CR/ER)

• Higher differentiation potential.
• Central to claims around OFF-time reduction and smoother levodopa exposure.

Combination platforms

• Carbidopa-based combinations dominate the standard of care landscape historically.
• Value hinges on clinical convenience and motor fluctuation endpoint performance.

How strong is the patent estate for levodopa formulations (not the API)?

Patent strength for levodopa is generally concentrated in secondary IP:

• formulation composition claims,
• release profile claims,
• manufacturing process claims,
• and method-of-use claims.

Because core levodopa is long off-patent, litigation and exclusivity risk are more often tied to:

• an individual product’s specific controlled-release design, and
• any remaining blocking patents listed in regulatory databases.

What generic entry risks exist for levodopa products in 2026–2030?

Generic entry risk is structurally high for IR levodopa due to commodity economics. For premium CR/ER and any product with remaining patents:

• the risk is tied to patent status and whether ANDA litigation or settlement exists for that exact formulation.
• bioequivalence requirements reduce but do not eliminate clinical differentiation risk because premium claims may rely on release kinetics.

How does levodopa compare with device-aided and advanced PD therapies?

Levodopa competes less with device-aided therapies on core efficacy and more on:

• access and cost,
• patient suitability,
• and ease of administration.

Advanced therapies (pump-based or device-associated approaches) typically serve subsets of mid-to-late PD patients with disabling motor fluctuations. That limits share gains but does not displace levodopa as the baseline cornerstone.

What is the Orange Book status of levodopa (active ingredient and key formulations)?

Orange Book listing status varies by specific formulation. The active ingredient levodopa is generally represented by older or long-expired exclusivity. Any actionable listings tend to be:

• formulation-specific patents,
• manufacturing process patents,
• or method-of-use patents.

As a practical market matter, the competitive landscape is usually dominated by generics for IR and by formulation-specific differentiation for CR/ER.

Which companies hold meaningful levodopa branded exposure today?

Market leadership is typically spread across:

• legacy branded product holders with historical market share,
• generics manufacturers with strong cost advantages,
• and formulation-focused brand owners with controlled-release/combination portfolios.

The commercial outcome depends more on formulary inclusion and pricing strategy than on active-drug exclusivity.

What patent litigation or Paragraph IV challenges have mattered for levodopa?

Because levodopa is long off-patent at the active ingredient level, litigation that matters is usually tied to:

• specific formulation patents,
• remaining secondary IP for ER/CR products,
• or process patents protecting manufacturing controls.

Litigation affects timing of generic launches only when a target product has enforceable patents still listed and not yet expired.

How do biosimilar dynamics apply to levodopa?

Levodopa is a small-molecule drug, so biosimilar frameworks do not apply. Competition is via generic and formulation-based innovation rather than biologic follow-ons.

What manufacturing and IP barriers protect premium levodopa products?

For differentiated levodopa formulations, barriers typically include:

• proprietary release-control methods (tablet matrices, coatings, microstructures),
• validated manufacturing process controls to preserve release kinetics,
• and any remaining composition or method patents.

These can raise time-to-market even when ANDA-type routes are available, but they do not prevent generic entry if patents expire and bioequivalence is met.

Clinical trial update summary for decision-makers

• Trial activity is concentrated on improving motor control using formulation and combination optimization.
• Endpoint discipline is consistent: OFF time, ON quality, dyskinesia burden, and tolerability.
• Market outlook depends on premium formulation share and pricing resilience rather than new active-drug exclusivity.

Key Takeaways

• Levodopa demand is durable due to PD prevalence growth and long-term use patterns.
• Market value is capped by active-ingredient commoditization; growth depends on controlled-release/combination premium share.
• Clinical trial updates focus on smoothing levodopa exposure, reducing OFF time, and managing dyskinesia and GI tolerability.
• Patent and litigation risk is formulation-specific and process- or method-driven, not active-drug exclusivity.

FAQs

1. What trial endpoints best predict payer coverage for levodopa controlled-release products?
   OFF time reduction, dyskinesia burden metrics, and safety/tolerability signals tied to discontinuation rates.

2. Which levodopa formulation types have the highest generic substitution risk?
   Immediate-release formats typically face the fastest substitution due to lower technical differentiation barriers.

3. How do combination levodopa regimens influence clinical trial design?
   Trials often compare dosing schedules and titration strategies to isolate additive benefit on OFF time and motor scores.

4. Do levodopa patents cover the API or only formulation/manufacturing methods?
   For actionable, current protection, it is typically formulation, release mechanics, manufacturing process, or method-of-use related.

5. What are the most important real-world outcomes for levodopa market access?
   Reduction in caregiver burden, falls/hospitalization proxies, adherence outcomes, and discontinuation due to adverse events.

References

1. FDA. Orange Book: Approved Drug Products with Therapeutic Equivalence Evaluations. U.S. Food and Drug Administration.
2. ClinicalTrials.gov. Levodopa-related Interventional Studies. U.S. National Library of Medicine.
3. EMA. European Public Assessment Reports (EPARs) for levodopa-containing products. European Medicines Agency.