CLINICAL TRIALS PROFILE FOR LODOSYN

All Clinical Trials for LODOSYN

Trial ID	Title	Status	Sponsor	Phase	Start Date	Summary
NCT00547911 ↗	Augmenting Effects of L-DOPS With Carbidopa and Entacapone	Terminated	National Institute of Neurological Disorders and Stroke (NINDS)	Phase 1/Phase 2	2007-10-01	An experimental drug called L-DOPS increases production in the body of a messenger chemical called norepinephrine. Cells in the brain that make norepinephrine are often gone in Parkinson disease. The exact consequences of this loss are unknown, but they may be related to symptoms such as fatigue, depression, or decreased attention that occur commonly in Parkinson disease. This study will explore effects of L-DOPS in conjunction with carbidopa and entacapone, which are drugs used to treat Parkinson disease. We wish to find out what the effects are of increasing norepinephrine production in the brain and whether carbidopa and entacapone augment those effects. Volunteers for this study must be at least 18 years of age and able to give consent to participate in the study. To participate in the study, volunteers must discontinue use of alcohol, tobacco, and certain herbal medicines or dietary supplements, and must also taper or discontinue certain kinds of medications that might interfere with the results of the study. Candidates will be screened with a medical history and physical exam. Participants will be admitted to the National Institutes of Health Clinical Center for two weeks of testing. The study will have three testing phases in a randomly chosen order for each participant: - Single dose of L-DOPS - Single dose of L-DOPS in conjunction with carbidopa - Single dose of L-DOPS in conjunction with entacapone Each phase will last two days, with a washout day between each phase in which no drugs will be given and no testing will be performed. In each phase, participants will undergo a series of tests and measurements, including blood pressure and electrocardiogram tests. Participants who are healthy volunteers will also have blood drawn and will undergo a lumbar puncture (also known as a spinal tap) to obtain spinal fluid for chemical tests.
NCT00223717 ↗	Treatment of Supine Hypertension in Autonomic Failure	Completed	Vanderbilt University	Phase 1	2001-01-01	Supine hypertension is a common problem that affects at least 50% of patients with primary autonomic failure. Supine hypertension can be severe, and complicates the treatment of orthostatic hypotension. Drugs used for the treatment of orthostatic hypotension (eg, fludrocortisone and pressor agents), worsen supine hypertension. High blood pressure may also cause target organ damage in this group of patients. The pathophysiologic mechanisms causing supine hypertension in patients with autonomic failure have not been defined. In a study, we, the investigators at Vanderbilt University, examined 64 patients with AF, 29 with pure autonomic failure (PAF) and 35 with multiple system atrophy (MSA). 66% of patients had supine systolic (systolic blood pressure [SBP] > 150 mmHg) or diastolic (diastolic blood pressure [DBP] > 90 mmHg) hypertension (average blood pressure [BP]: 179 ± 5/89 ± 3 mmHg in 21 PAF and 175 ± 5/92 ± 3 mmHg in 21 MSA patients). Plasma norepinephrine (92 ± 15 pg/mL) and plasma renin activity (0.3 ± 0.05 ng/mL per hour) were very low in a subset of patients with AF and supine hypertension. (Shannon et al., 1997). Our group has showed that a residual sympathetic function contributes to supine hypertension in patients with severe autonomic failure and that this effect is more prominent in patients with MSA than in those with PAF (Shannon et al., 2000). MSA patients had a marked depressor response to low infusion rates of trimethaphan, a ganglionic blocker; the response in PAF patients was more variable. At 1 mg/min, trimethaphan decreased supine SBP by 67 +/- 8 and 12 +/- 6 mmHg in MSA and PAF patients, respectively (P < 0.0001). MSA patients with supine hypertension also had greater SBP response to oral yohimbine, a central alpha2 receptor blocker, than PAF patients. Plasma norepinephrine decreased in both groups, but heart rate did not change in either group. This result suggests that residual sympathetic activity drives supine hypertension in MSA; in contrast, supine hypertension in PAF. It is hoped that from this study will emerge a complete picture of the supine hypertension of autonomic failure. Understanding the mechanism of this paradoxical hypertension in the setting of profound loss of sympathetic function will improve our approach to the treatment of hypertension in autonomic failure, and it could also contribute to our understanding of hypertension in general.
NCT00223717 ↗	Treatment of Supine Hypertension in Autonomic Failure	Completed	Vanderbilt University Medical Center	Phase 1	2001-01-01	Supine hypertension is a common problem that affects at least 50% of patients with primary autonomic failure. Supine hypertension can be severe, and complicates the treatment of orthostatic hypotension. Drugs used for the treatment of orthostatic hypotension (eg, fludrocortisone and pressor agents), worsen supine hypertension. High blood pressure may also cause target organ damage in this group of patients. The pathophysiologic mechanisms causing supine hypertension in patients with autonomic failure have not been defined. In a study, we, the investigators at Vanderbilt University, examined 64 patients with AF, 29 with pure autonomic failure (PAF) and 35 with multiple system atrophy (MSA). 66% of patients had supine systolic (systolic blood pressure [SBP] > 150 mmHg) or diastolic (diastolic blood pressure [DBP] > 90 mmHg) hypertension (average blood pressure [BP]: 179 ± 5/89 ± 3 mmHg in 21 PAF and 175 ± 5/92 ± 3 mmHg in 21 MSA patients). Plasma norepinephrine (92 ± 15 pg/mL) and plasma renin activity (0.3 ± 0.05 ng/mL per hour) were very low in a subset of patients with AF and supine hypertension. (Shannon et al., 1997). Our group has showed that a residual sympathetic function contributes to supine hypertension in patients with severe autonomic failure and that this effect is more prominent in patients with MSA than in those with PAF (Shannon et al., 2000). MSA patients had a marked depressor response to low infusion rates of trimethaphan, a ganglionic blocker; the response in PAF patients was more variable. At 1 mg/min, trimethaphan decreased supine SBP by 67 +/- 8 and 12 +/- 6 mmHg in MSA and PAF patients, respectively (P < 0.0001). MSA patients with supine hypertension also had greater SBP response to oral yohimbine, a central alpha2 receptor blocker, than PAF patients. Plasma norepinephrine decreased in both groups, but heart rate did not change in either group. This result suggests that residual sympathetic activity drives supine hypertension in MSA; in contrast, supine hypertension in PAF. It is hoped that from this study will emerge a complete picture of the supine hypertension of autonomic failure. Understanding the mechanism of this paradoxical hypertension in the setting of profound loss of sympathetic function will improve our approach to the treatment of hypertension in autonomic failure, and it could also contribute to our understanding of hypertension in general.

Clinical Trial Conditions for LODOSYN

Condition Name

Condition Name for LODOSYN
Intervention	Trials
Autonomic Nervous System Diseases	2
Parkinson Disease	2
Multiple Sclerosis	2

Condition MeSH

Condition MeSH for LODOSYN
Intervention	Trials
Autonomic Nervous System Diseases	4
Primary Dysautonomias	4
Parkinson Disease	3

Clinical Trial Locations for LODOSYN

Trials by Country

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−

Trials by Country for LODOSYN
Location	Trials
United States	9
United Kingdom	1

Trials by US State

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−

Trials by US State for LODOSYN
Location	Trials
Tennessee	3
Florida	2
New York	1
Michigan	1
Arizona	1

Clinical Trial Progress for LODOSYN

Clinical Trial Phase

Clinical Trial Phase for LODOSYN
Clinical Trial Phase	Trials
Phase 3	2
Phase 2	3
Phase 1/Phase 2	2

Clinical Trial Status

Clinical Trial Status for LODOSYN
Clinical Trial Phase	Trials
Completed	7
Recruiting	1
Terminated	1

Clinical Trial Sponsors for LODOSYN

Sponsor Name

Sponsor Name for LODOSYN
Sponsor	Trials
University of Miami	2
Vanderbilt University	2
Vanderbilt University Medical Center	2

Sponsor Type

Sponsor Type for LODOSYN
Sponsor	Trials
Other	11
Industry	2
U.S. Fed	1

Lodosyn (Carbidopa): Clinical Trials, Market Analysis, and Projections

Introduction to Lodosyn

Lodosyn, also known as carbidopa, is a medication used in conjunction with levodopa or carbidopa-levodopa combinations for the treatment of Parkinson’s disease and related conditions. Here, we will delve into the clinical trials, market analysis, and future projections for Lodosyn.

Clinical Trials and Efficacy

Use in Parkinson’s Disease

Lodosyn is indicated for use with carbidopa-levodopa or with levodopa to treat the symptoms of idiopathic Parkinson’s disease, postencephalitic parkinsonism, and symptomatic parkinsonism resulting from injuries such as carbon monoxide or manganese intoxication[1][2].

Clinical trials have shown that Lodosyn, when used with levodopa, can reduce the peripheral decarboxylation of levodopa, allowing more of the drug to reach the brain. This results in lower doses of levodopa being required, which can reduce nausea and vomiting and provide a smoother response to the medication[1].

Key Findings

• Dose Titration: Lodosyn allows for separate titration of carbidopa and levodopa, which is beneficial for patients who require different dosages of each medication[1][2].
• Side Effects: While Lodosyn can mitigate some side effects of levodopa, such as nausea and vomiting, it may also potentiate dopaminergic side effects like dyskinesia[2].
• Somnolence: Patients treated with Lodosyn should be monitored for drowsiness and advised against driving or engaging in dangerous activities if they experience significant daytime sleepiness[1].

Market Analysis

Current Market Landscape

The Parkinson’s disease (PD) market is highly competitive, with numerous levodopa-combination therapies and adjunctive drug classes. Current treatments primarily focus on controlling dopamine levels in the brain but are often symptomatic and not very effective in managing motor fluctuations in advanced-stage patients[3].

Role of Lodosyn in the Market

Lodosyn plays a crucial role in this market by enhancing the efficacy of levodopa-based treatments. However, it is not a standalone solution but rather a complementary medication that improves the delivery and response to levodopa.

Market Trends and Competitors

The PD market is expected to grow, driven by the need for more effective and disease-modifying treatments. New pipeline products, such as Roche/Prothena’s PRX-002 (prasinezumab), an anti-alpha synuclein monoclonal antibody, are forecasted to generate significant sales and potentially halt disease progression[3].

Unmet Needs

Despite the presence of Lodosyn and other levodopa-based treatments, there are key unmet needs in the PD market. These include the development of drugs with improved efficacy, novel delivery systems, and disease-modifying properties. Lodosyn, while useful, does not address these unmet needs directly but remains a vital component in the current treatment regimen[3].

Projections and Future Outlook

Market Growth

The global PD market is anticipated to grow, with new pipeline drugs expected to launch and address longstanding unmet needs. However, Lodosyn, being an established medication, is not expected to be a major driver of this growth. Instead, it will likely continue to be used as part of the existing treatment protocols[3].

Emerging Therapies

New therapies, such as AbbVie’s ABBV-951 and Roche/Prothena’s PRX-002, are forecasted to achieve significant sales and market uptake. These drugs are expected to offer improved options for controlling complications associated with long-term levodopa use, potentially reducing the reliance on Lodosyn and similar medications[3].

Regulatory and Safety Considerations

Patients and healthcare providers should remain vigilant about potential side effects of Lodosyn, including the increased risk of melanoma, depression, and somnolence. Regular skin examinations and monitoring for these conditions are recommended[1][2].

Key Takeaways

• Clinical Efficacy: Lodosyn is effective in reducing peripheral decarboxylation of levodopa, allowing lower doses and smoother responses.
• Market Role: Lodosyn is a complementary medication in the PD market, enhancing the efficacy of levodopa-based treatments.
• Future Outlook: The PD market will grow with new pipeline drugs, but Lodosyn will likely remain a part of existing treatment protocols rather than a major growth driver.
• Safety Considerations: Monitoring for side effects such as melanoma, depression, and somnolence is crucial.

FAQs

What is Lodosyn used for?

Lodosyn (carbidopa) is used in conjunction with levodopa or carbidopa-levodopa combinations to treat the symptoms of Parkinson’s disease and related conditions[1][2].

How does Lodosyn work?

Lodosyn prevents the peripheral decarboxylation of levodopa, allowing more of the drug to reach the brain, which reduces the required dose of levodopa and mitigates side effects like nausea and vomiting[1].

What are the potential side effects of Lodosyn?

Potential side effects include dyskinesia, depression, somnolence, and an increased risk of melanoma. Patients should be monitored for these conditions[1][2].

Is Lodosyn a standalone treatment for Parkinson’s disease?

No, Lodosyn is not a standalone treatment but is used in combination with levodopa or carbidopa-levodopa to enhance the efficacy of these medications[1][2].

What are the future projections for the Parkinson’s disease market?

The PD market is expected to grow with the introduction of new pipeline drugs that address unmet needs, such as disease-modifying properties and improved delivery systems[3].

Sources

1. RxList: Lodosyn (Carbidopa): Side Effects, Uses, Dosage, Interactions.
2. Drugs.com: Lodosyn: Package Insert / Prescribing Information.
3. GlobalData: Parkinson's Disease - Global Drug Forecast and Market Analysis to 2029.