Background
Adults over the age of 60 with symptoms of major depressive disorder are said to have late-life depression (LLD), a condition that usually decreases a person's quality of life and is associated with other risks like physical frailty and dementia. A common feature of more severe LLD is psychomotor slowing, where a person's ability to think and move are impaired. For example, they might not be able to walk or process information as quickly, and they might have problems with their working memory.
Psychomotor slowing in LLD might be the result of a problem with the way a person's body produces or responds to the neurotransmitter dopamine. The drug Levodopa (L-DOPA), which can replace missing dopamine in the brain, has been used to treat to treat Parkinson's disease for many decades, and it might also affect psychomotor slowing in LLD.
Methods
In this study, participants are adults aged 60 years or older with moderate to severe major depression. Participants undergo the "L-DOPA challenge"-a 2-week period where they receive a dose of L-DOPA once a day for the first week and a dose of L-DOPA twice a day for the second week. Before and after a participant completes the L-DOPA challenge, the study team assesses their depressive symptoms and psychomotor function. After the L-DOPA challenge, if a participant still shows signs of moderate or severe depression, they receive an antidepressant for 12 weeks.
Aims
The first aim of this study is to test the feasibility of the L-DOPA challenge-that is, whether most of the 50 participants recruited for this study will complete the L-DOPA challenge. For example, participants might have to withdraw if they can't make the daily visits to the research site to receive their L-DOPA medication, if they can't tolerate the medication's side effects, or if their depressive symptoms get significantly worse. Our hypothesis is that 80% of the participants will complete the L-DOPA challenge.
The second aim of the study is to see if L-DOPA affects participants' depressive symptoms, processing speed, and working memory. Our hypothesis is that L-DOPA response, measured as an improvement in gait speed, is associated with a decrease in depressive symptoms and an increase in processing speed and working memory.

Start Date15 Aug 2024

Sponsor / Collaborator

University of British Columbia

[+1]

NCT06365515

/ RecruitingNot ApplicableIIT

Dopamine and Reward Learning Across Hormonal Transition Phases

Hormonal transition periods during the menstrual cycle may predispose women to mental disorders. Hormonal fluctuations provide specific neuroendocrine conditions that modulate brain structure and function and these actions affect cognitive and emotional behaviors and affect energy and mood homeostasis. It is thought that these changes are driven by altered dopamine transmission. Here, the investigators aim to examine (1) how sex hormones and dopamine are linked and also (2) how hormonal changes affect motivation, mood, and energy homeostasis.
To this end, dopamine intervention will be tested on effort-based decision-making and motivational circuits in three hormonal stages (i.e., women in early-follicular phase (EF), women in mid-luteal phase (ML), and men). Additionally, the effects of hormonal status on metabolic indices will be tested, and its effects on mood fluctuations in a period of a month.
The investigator hypothesizes that women in EF cycle phase (1) have naturally less dopamine and show less effort, and (2) they show greater improvement in effort-based decision-making after Levodopa administration. The investigator has exploratory outcomes about (3) sex differences in reward-learning with and without Levodopa administration and explores if these differences correlate with elevated female sex hormone levels. Moreover, it is hypothesized that (4) hormonal fluctuations affect energy homeostasis, thus women in their EF cycle phase have higher energy expenditure and (5) they report more negative mood than in their mid-luteal (ML) cycle phase.

Start Date01 May 2024

Sponsor / Collaborator

Deutsche Forschungsgemeinschaft

[+1]

100 Clinical Results associated with Levodopa hydrate

100 Translational Medicine associated with Levodopa hydrate

100 Patents (Medical) associated with Levodopa hydrate

38,463

Literatures (Medical) associated with Levodopa hydrate

01 Jan 2026·TALANTA

Glutathione-based supramolecular chiral nanozyme for colorimetric enantioselective sensing of 3,4-dihydroxyphenylalanine

Article

Author: Han, Jie ; Li, Jiaying ; Huan, Xintong ; Jiang, Mingxin ; Sun, Xiaohuan ; Zhang, Chenglong

The determination of the absolute configuration and enantiomeric composition of chiral species is of great significance. Nevertheless, the accurate quantification through output signals related to the identity of chiral analytes has been rarely reported in this regard. In this study, through the self-assembly of glutathione (GSH) and Cu²⁺, supramolecular chiral nanoparticles (GSH-Cu²⁺) were constructed for the enantioselective sensing of chiral 3,4-dihydroxyphenylalanine (DOPA). It is found that GSH-Cu²⁺ exhibits excellent peroxidase-like activity, with a K_cat value of 2.20 × 10^-3 M s^-1 g^-1 toward 3,3',5,5'-tetramethylbenzidine (TMB). When chiral DOPA is employed as substrate, enantioselective catalysis is observed, with GSH-Cu²⁺ showing more favorable activity towards D-DOPA as compared to L-DOPA. Further mechanistic study demonstrates that the underlying principle lies in the more favorable adsorption of GSH-Cu²⁺ toward L-DOPA, which then forms a shielding layer that inhibits the catalytic activity. By exploiting the differential catalytic rates indicated by the ultraviolet-visible (UV-Vis) absorption change of dopachrome (the catalyzed product of DOPA), calibration curves, derived from signals related to their identities, that enable the determination of the absolute configuration and enantiomeric composition of D/L-DOPA, have been established and applied in real pharmaceutical detection. What is also important, the GSH-Cu²⁺-based sensing platform is demonstrated with high sensitivity (detection limit of 1.31 μM/1.51 μM for D/L-DOPA) and selectivity. Overall, this work enhances our understanding of enantioselective sensing using identity-involved output signals and provides new opportunities for enantioselective sensing with improved reliability.

01 Jan 2026·BIOMATERIALS

Minimally invasive upconversion optogenetics for Parkinson's disease treatment

Article

Author: Li, Xinsheng ; Wang, Xiaoran ; Yu, Jiaojiao ; Xiang, Heng ; Sun, Shao-Kai ; Liu, Ruxia ; Zhou, Ting ; Zhang, Cai

The treatment of Parkinson's disease (PD) is greatly limited by the side effects of levodopa, the current gold standard medication, which can cause severe motor complications. Optogenetic stimulation holds promise for PD therapy, but it has been plagued by invasive fiber insertion. Herein, we propose the minimally invasive treatment of PD using upconversion optogenetics for the first time. Channelrhodopsin-2 (ChR2) is expressed in the globus pallidus externus (GPe) brain region of PD mice, followed by in situ injection of upconversion nanoparticles (UCNPs). When near-infrared (NIR) light is delivered through a fiber fixed on the skull, UCNPs can convert NIR light into blue light, thereby effectively activating the GPe. Open field and rotarod tests demonstrate significant improvement in motor abilities and coordination in PD mice. Compared to conventional optogenetics, upconversion optogenetics not only achieves equivalent therapeutic effects but also avoids damage and inflammation caused by fiber insertion. Furthermore, this method can be extended to modulate neural activity in deep brain regions, including substantia nigra pars compacta and paraventricular nucleus of the thalamus, with neural activation effects lasting for up to one week. Our study presents a minimally invasive optogenetic strategy for PD treatment, with potential therapeutic applications in various neurological disorders.

01 Nov 2025·TALANTA

Unlocking the power of chirality: Surface nanoarchitectonics of modified halloysite nanotubes for enantioselective recognition

Article

Author: Arnaboldi, Serena ; Warakulwit, Chompunuch ; Matthayom, Punjapol ; Maggioni, Daniela ; Grecchi, Sara ; Niamlaem, Malinee

Developing cost-effective electrode materials with high performance for enantioselective recognition is rapidly gaining attention. In this work, we harness the unique physicochemical properties of halloysite nanotubes (HNTs) as innovative electrode platforms for chiral discrimination. We functionalized HNTs with an enantiopure oligomer based on thiophene units via chemical oligomerization using FeCl₃ as an oxidizing agent. The successful functionalization of the HNTs with the oligomer was further confirmed by both solid state ¹³C NMR and zeta potential studies (from -20.0 ± 1.5 mV to -12.4 ± 3.0 mV after modification). The resulting composite materials (oligo-(S)- and oligo-(R)- modified HNTs) demonstrated remarkable enantioselective recognition capabilities in terms of peak potential values (560-650 mV) when testing the enantiomers of DOPA, a chiral drug of pharmaceutical interest. These findings highlight the potential of HNT-based modified electrodes as a novel class of chiral electrochemical sensors, paving the way for advanced applications in enantioselective analysis.

497

News (Medical) associated with Levodopa hydrate

29 Jul 2025

·www.globenewswire.com

BioVie Presented Data Highlighting that Patients Treated with Bezisterim Potentially Experienced an Age Deceleration Advantage Compared to Placebo on 10 Different Biological Clocks at the 2nd World Conference on Aging and Gerontology

July 24, 2025 -- BioVie Inc. (NASDAQ: BIVI) (“BioVie” or the “Company”), a clinical-stage company developing innovative drug therapies for the treatment of neurological and neurodegenerative disorders and advanced liver disease, presented “Bezisterim Decreases Biological Age Acceleration in Alzheimer’s Disease” at the 2nd World Conference on Aging and Gerentology (WCAG-2025) in Rome, Italy July 14-15, 2025. As the body ages, a natural process called DNA methylation occurs and adds “methyl” groups to the surface of DNA. Accumulated methylation has the impact of interfering with how DNA is decoded and thus has been shown to impact a wide range of diseases, including age-related cognitive impairment and dementia,1 Parkinson’s disease,2 various forms of cancers,3 cardiovascular disease, 4,5 COPD and respiratory disease,6 chronic kidney disease,7 inflammatory bowel disease,8 sepsis,9 and many others. The extent of DNA methylation can be measured by various “biological clocks” to assess a person’s “biological age,” which may be different from a person’s chronological age (i.e., years since birth). The difference is considered to be age acceleration or deceleration. The enzyme DNA methyltransferase 3A (DNMT3A) plays a key role in driving the methylation of DNA, and TNFα-driven inflammation has been shown to increase DNMT3A’s activity and thus DNA methylation of many different genes. Bezisterim modulates TNFα-driven inflammation and is believed to help reestablish homeostasis and small changes in many genes at the same time. An analysis of the Company’s Phase 3 NM101 study (NCT04669028) evaluating bezisterim in patients with mild-to-moderate probable Alzheimer’s Disease (AD) assessed 33 blood samples of patients treated with bezisterim (n = 17) and placebo (n = 16) revealed: Biological aging. After 30 weeks of treatment, bezisterim-treated patients experienced significant age deceleration compared to placebo-treated patients on all biological clocks assessed, including −3.16 years for SkinBloodClockAge (p = 0.036), −4.12 years for PhenoAge (p = 0.048), −1.38 years for GrimAge (p = 0.148), −4.24 years for Hannum clock (p = 0.015), and −3.77 years for InflammAge (p = 0.050). Inflammatory gene expression. Bezisterim appeared to modulate gene expression of dozens of genes in the inflammatory cascade (e.g., NFkB, MAP, JNK), resulting in reduced expression of inflammatory cytokines, including TNFα, IL-6, and IL-17. Aging and Alzheimer’s Disease. Bezisterim appeared to have potentially beneficial modulation of many of the genes associated with aging and AD pathophysiology as identified by the National Institute on Aging’s Accelerating Medicines Partnership in Alzheimer’s Disease (AMP-AD) Consortium. Metabolic and inflammatory biomarkers. Bezisterim appeared to modulate many genes associated with carbohydrate metabolism, glycolysis, and Type 2 diabetes. Bezisterim-treated patients also experienced significant improvements from baseline on metabolic and inflammatory biomarkers compared to those treated with placebo, including -8.5 mg/dL on fasting glucose (p=0.036), -15 mg/dL in cholesterol (p=0.049), and -90.5 pg/mL in MCP (p=0.007). Bezisterim-treated patients also experienced improvements in methylation of genes associated with carbohydrate metabolism, glycolysis, and Type 2 diabetes pathophysiology. “The research community has grown accustomed to looking at one or a few genes as the driving factor behind disease,” said Christopher Reading, PhD, Senior Vice President of BioVie’s Alzheimer’s Program. “Our experience with bezisterim suggests that AD may be much more complicated, and that disease physiopathology may involve dozens of genes that work in tandem through biochemical cascades to affect disease. These data suggest the potential to target epigenetic-driven age deceleration as a treatment for AD and other neurodegenerative diseases of aging. We are conducting ongoing studies to further explore these intriguing findings and considering whether bezisterim might help everyone improve healthspan in normal aging.” Bezisterim is a unique, stabilized version of Beta AET, a naturally occurring brain metabolite of dehydroepiandrosterone (DHEA), which has demonstrated decreased metabolic inflammation activity in humans, but that naturally decreases with age. Beta AET itself cannot be taken in oral form, a major limitation that Bezisterim overcomes. Unlike its naturally occurring counterpart, Bezisterim is metabolically stable, orally available, and able to cross the blood-brain barrier. It has demonstrated anti-inflammatory effects through inhibition of NF-kappa B, a central mediator of inflammation, and has shown insulin-sensitizing properties. Notably, Bezisterim is not immunosuppressive, and has demonstrated favorable safety and tolerability profiles across in-vivo clinical trials in AD and Parkinson’s Disease (PD). Bezisterim (NE3107) is an orally bioavailable, blood-brain barrier (BBB)-permeable modulator of inflammation and insulin-sensitizer. In addition, it is not immunosuppressive and has a low risk of drug-drug interaction. By binding to ERK and selectively modulating NFκB activation and TNF-α production, BioVie believes that bezisterim may offer clinical improvements in several disease indications, including AD, PD and long COVID. In PD, BioVie is currently enrolling patients in the Phase 2 SUNRISE-PD clinical trial evaluating the safety and efficacy of bezisterim on motor and non-motor symptoms in patients who have not been treated with carbidopa/levodopa, with topline data expected in late 2025 or early 2026. A previous Phase 2 study of bezisterim in PD (NCT05083260) completed in 2022, and data presented at the AD/PD™ 2023 International Conference on Alzheimer’s and Parkinson’s Diseases and related neurological disorders in Gothenburg, Sweden in March 2023, showed significant improvements in “morning on” symptoms and clinically meaningful improvement in motor control in patients treated with a combination of bezisterim and levodopa versus patients treated with levodopa alone, and no drug-related adverse events. In long COVID, we believe bezisterim has the potential to reduce neurological symptoms, including fatigue and cognitive dysfunction. Persistently circulating viral spike proteins are believed to trigger TLR-4 driven activation of NFκB and the subsequent expression of inflammatory cytokines (IL-6, TNF, IFNg). BioVie’s Phase 2 ADDRESS-LC study, is a randomized (1:1), placebo-controlled, multicenter trial in approximately 200 patients to evaluate the safety, tolerability and potential efficacy of 3 months of treatment with bezisterim to reduce the neurocognitive symptoms associated with long COVID, including difficulty concentrating or remembering things (“brain fog”) and fatigue. In AD, BioVie conducted and reported efficacy data on its Phase 3 randomized, double-blind, placebo-controlled, parallel-group, multicenter study to evaluate bezisterim in patients who have mild-to-moderate Alzheimer’s disease (NCT04669028) in 2023. Results of a Phase 2 investigator-initiated trial (NCT05227820) showing bezisterim-treated patients experienced improved cognition and biomarker levels were presented at the Clinical Trials on Alzheimer’s Disease (CTAD) annual conference in December 2022. An estimated six million Americans suffer from AD. BioVie Inc. (NASDAQ: BIVI) is a clinical-stage company developing innovative drug therapies for the treatment of neurological and neurodegenerative disorders (AD, PD and long COVID) and advanced liver disease. In neurodegenerative disease, the Company’s drug candidate bezisterim inhibits inflammatory activation of extracellular signal-regulated kinase and the transcription factor nuclear factor-κB, and the associated neuroinflammation and insulin resistance but not ERK and NFκB homeostatic functions (e.g., insulin signaling and neuron growth and survival). Both neuroinflammation and insulin resistance are drivers of AD and PD. Persistent systematic inflammation and neuroinflammation are key features in patients with neurological symptoms of long COVID. In liver disease, the Company’s Orphan drug candidate BIV201 (continuous infusion terlipressin), with FDA Fast Track status, is being evaluated and discussed with guidance received from the FDA regarding the design of Phase 3 clinical testing of BIV201 for the reduction of further decompensation in participants with liver cirrhosis and ascites. The active agent is approved in the U.S. and in about 40 countries for related complications of advanced liver cirrhosis. 1 Sugden K Neurology 2022;99:e1402-e1413 2 Tang X DOI: 10.1002/mds.29157 3 Wang Z Nucleic Acids Research, 2020, Vol. 48, No. 5 4 Stenvinkel P doi: 10.1111/j.1365-2796.2007.01777.x 5 Tabaeia S Artificial Cells, Nanomedicine, and Biotechnology, 47:1, 2031-2041 6 Qiu W Am J Respir Crit Care Med Vol 185, Iss. 4, pp 373–381, Feb 15, 2012 7 Rysz C Int. J. Mol. Sci. 2022, 23(13), 7108 8 Kraiczy J Mucosal Immunology volume 9, pages 647–658 (2016) 9 Rump K Sci Rep 9, 18511 (2019) The content above comes from the network. if any infringement, please contact us to modify.

Clinical ResultOrphan DrugFast Track

14 Jul 2025

·www.globenewswire.com

BioVie Announces Data Highlighting Bezisterim’s Potential to Slow or Reverse Biological Aging and Neurodegeneration Featured as a Keynote Talk at the 7th World Aging and Rejuvenation Conference

July 09, 2025 -- BioVie Inc. (NASDAQ: BIVI) (“BioVie” or the “Company”), a clinical-stage company developing innovative drug therapies for the treatment of neurological and neurodegenerative disorders and advanced liver disease, presented “Bezisterim Epigenetic Effects on Aging and Neurodegeneration” at the 7th World Aging and Rejuvenation Conference (ARC-2025) taking place in Vienna, Austria, July 9th –10th, 2025. Unlike historical approach to Alzheimer’s Disease (AD) treatment that focuses on changing one gene product (e.g., amyloid, p-Tau) at a time, bezisterim modulates inflammation and is believed to help reestablish homeostasis and small changes in many genes at the same time. The data suggest that bezisterim may alter biological age by anti-inflammatory epigenetic modifications. Epigenetic biomarkers can measure “Epigenetic Age Acceleration” (EAA), which is defined as the difference between observed biological age as measured by DNA methylation and the chronological age (i.e., years since birth). An analysis of the Company’s Phase 3 NM101 study (NCT04669028) evaluating bezisterim in patients with mild-to-moderate probable AD assessed 33 blood samples of patients treated with bezisterim (n = 17) and placebo (n = 16) using five validated epigenetic “biological” clocks that analyze genes linked to aging, as well as age-related inflammatory markers. In this analysis, treatment with bezisterim demonstrated: Biological Aging Effects. After 30 weeks of treatment, the average difference between the placebo and bezisterim groups was −3.16 years for SBCAge (p = 0.036), −4.12 years for PhenoAge (p = 0.048), −1.38 years for GrimAge (p = 0.148), −4.24 years for Hannum clock (p = 0.015), and −3.77 years for InflammAge (p = 0.050). The various “biological clocks” measure the extent of age deceleration1 advantage bezisterim-treated patients have compared to those treated with placebo. Gene modulation effects. Bezisterim-treated patients experienced decreased activation of various genes associated with inflammatory kinase cascades, aging and cognition, leading to potentially beneficial changes in aging and AD pathophysiology. Metabolic and inflammatory biomarker effects. Bezisterim-treated experienced significant improvements from baseline on metabolic and inflammatory biomarkers compared to those treated with placebo, including -8.5 mg/dL on fasting glucose (p=0.036), -15 mg/dL in cholesterol (p=0.049), and -90.5 pg/mL in MCP (p=0.007). Bezisterim-treated patients also experienced a decrease in carbohydrate metabolism, glycolysis, and Type 2 diabetes pathophysiology. “Biological aging is the single greatest risk factor for the development of dementia, and we believe our work with bezisterim represents a promising strategy to target the underlying mechanisms of neurodegeneration,” said Christopher Reading, PhD, Senior Vice President of BioVie’s Alzheimer’s Program. “We are honored to share these data that may illuminate bezisterim’s potential to target epigenetic-driven age acceleration as a treatment for Alzheimer’s and other neurodegenerative diseases of aging. We are conducting ongoing studies to further explore these intriguing findings and how bezisterim may help everyone improve healthspan in normal aging.” Bezisterim is a unique, stabilized version of Beta AET, a naturally occurring brain metabolite of dehydroepiandrosterone (DHEA), which has demonstrated anti-inflammatory and immunomodulating activity in humans, but that naturally decreases with age. Beta AET itself cannot be taken in oral form, a major limitation that Bezisterim may address. Unlike its naturally occurring counterpart, Bezisterim is metabolically stable, orally available, and able to cross the blood-brain barrier. It has demonstrated anti-inflammatory effects through inhibition of NF-kappa B, a central mediator of inflammation, and has shown insulin-sensitizing properties. Notably, Bezisterim is not immunosuppressive, and has demonstrated favorable safety and tolerability profiles across in-vivo clinical trials in AD and Parkinson’s Disease (PD). Bezisterim (NE3107) is an orally bioavailable, blood-brain barrier (BBB)-permeable modulator of inflammation and insulin-sensitizer. In addition, it is not immunosuppressive and has a low risk of drug-drug interaction. By binding to ERK and selectively modulating NFκB activation and TNF-α production, BioVie believes that bezisterim may offer clinical improvements in several disease indications, including Alzheimer’s disease, Parkinson’s disease and long COVID. In Parkinson’s disease, BioVie is currently enrolling patients in the Phase 2 SUNRISE-PD clinical trial evaluating the safety and efficacy of bezisterim on motor and non-motor symptoms in patients who have not been treated with carbidopa/levodopa, with topline data expected in late 2025 or early 2026. A previous Phase 2 study of bezisterim in Parkinson’s disease (NCT05083260) completed in 2022, and data presented at the AD/PD™ 2023 International Conference on Alzheimer’s and Parkinson’s Diseases and related neurological disorders in Gothenburg, Sweden in March 2023, showed significant improvements in “morning on” symptoms and clinically meaningful improvement in motor control in patients treated with a combination of bezisterim and levodopa versus patients treated with levodopa alone, and no drug-related adverse events. In long COVID, bezisterim has the potential to reduce neurological symptoms, including fatigue and cognitive dysfunction. Persistently circulating viral spike proteins are believed to trigger TLR-4 driven activation of NFκB and the subsequent expression of inflammatory cytokines (IL-6, TNF, IFNg). BioVie’s Phase 2 ADDRESS-LC study, is a randomized (1:1), placebo-controlled, multicenter trial in approximately 200 patients to evaluate the safety, tolerability and potential efficacy of 3 months of treatment with bezisterim to reduce the neurocognitive symptoms associated with long COVID, including difficulty concentrating or remembering things (“brain fog”) and fatigue. In Alzheimer’s disease, BioVie conducted and reported efficacy data on its Phase 3 randomized, double-blind, placebo-controlled, parallel-group, multicenter study to evaluate bezisterim in patients who have mild-to-moderate Alzheimer’s disease (NCT04669028) in 2023. Results of a Phase 2 investigator-initiated trial (NCT05227820) showing bezisterim-treated patients experienced improved cognition and biomarker levels were presented at the Clinical Trials on Alzheimer’s Disease (CTAD) annual conference in December 2022. An estimated six million Americans suffer from Alzheimer’s disease. BioVie Inc. (NASDAQ: BIVI) is a clinical-stage company developing innovative drug therapies for the treatment of neurological and neurodegenerative disorders (AD, Parkinson’s disease and long COVID) and advanced liver disease. In neurodegenerative disease, the Company’s drug candidate bezisterim inhibits inflammatory activation of extracellular signal-regulated kinase and the transcription factor nuclear factor-κB, and the associated neuroinflammation and insulin resistance but not ERK and NFκB homeostatic functions (e.g., insulin signaling and neuron growth and survival). Both neuroinflammation and insulin resistance are drivers of AD and PD. Persistent systematic inflammation and neuroinflammation are key features in patients with neurological symptoms of long COVID. In liver disease, the Company’s Orphan drug candidate BIV201 (continuous infusion terlipressin), with FDA Fast Track status, is being evaluated and discussed with guidance received from the FDA regarding the design of Phase 3 clinical testing of BIV201 for the reduction of further decompensation in participants with liver cirrhosis and ascites. The active agent is approved in the U.S. and in about 40 countries for related complications of advanced liver cirrhosis. The content above comes from the network. if any infringement, please contact us to modify.

Clinical ResultOrphan DrugFast Track

08 Jul 2025

·www.prnewswire.com

Neuraxpharm and Dizlin Pharmaceuticals Announce Global Strategic Co-Development Agreement Bringing Next-Generation Drug-Device Therapy to Patients with Advanced Parkinson's Disease

Infudopa SubC® is a user-friendly and minimally invasive alternative enabling flexible dosing and thereby empowering patients with greater independence DÜSSELDORF, Germany and GOTHENBURG, Sweden, July 8, 2025 /PRNewswire/ -- Neuraxpharm Group ("Neuraxpharm"), a leading European specialty pharmaceutical company dedicated to central nervous system (CNS) disorders, and Dizlin Pharmaceuticals AB ("Dizlin"), a Swedish R&D company focused on late-stage Parkinson's disease (PD), today announced a strategic global co-development agreement for Infudopa SubC ® — a next-generation, wearable drug-device therapy that offers a user-friendly, flexible, and physiologically sound alternative to existing advanced Parkinson's treatments, hence empowering patients with greater independence. This agreement marks a pivotal milestone for Neuraxpharm as it enters the drug-device space with its first-ever combination therapy, reinforcing its commitment to pioneering innovation in CNS and addressing some of the most pressing unmet needs in neurological care. A New Era in Advanced Parkinson's Treatment Infudopa SubC ® is a ready-to-use levodopa-carbidopa solution delivered via a wearable subcutaneous infusion belt pump. It is designed to provide continuous, precise drug delivery for patients with advanced PD who experience motor fluctuations that are no longer adequately managed by oral medications. Addressing a Growing Global Challenge PD is the fastest-growing neurological condition worldwide, currently affecting over 10 million people. Global prevalence is expected to double to 20 million by 2050.1,2 For many patients, oral medication loses effectiveness as the disease advances, leaving patients facing disabling motor fluctuations that are better treated by device-aided therapies like Infudopa SubC®. Neuraxpharm's collaboration with Dizlin is a transformative advancement for PD patients, ensuring access to a therapy that is not only effective but also practical and empowering. Under the terms of this agreement, Neuraxpharm will actively participate in the co-development of the product to ensure its global availability and will receive global exclusive commercialisation rights for Infudopa SubC® in Europe, countries outside Europe where it has a direct presence, and via partners in other territories, such as US or Japan, to be agreed by both parties. Dr. Jörg-Thomas Dierks, CEO of Neuraxpharm, stated: "Our partnership with Dizlin is a powerful step towards reshaping the future of Parkinson's care. Infudopa SubC® is more than a therapy — it's a life-changing solution, effectively and practically delivering treatment to PD patients. This collaboration reflects our unwavering mission to bring forward differentiated, breakthrough solutions for people living with CNS disorders." Björn Velin, CEO of Dizlin Pharmaceuticals, added: "Dizlin Pharmaceuticals is very pleased to have entered into an agreement with a well-established and highly reputable pharmaceutical company specialising in the central nervous system – specifically Parkinson's disease – and with a strong commercial organisation. "We are committed to bringing our products to market quickly – and confident of being successful in this regard – so that more patients in the advanced stage of Parkinson's disease can gain access to this possibility of enhancing their life quality and functioning." Building on a Legacy of Innovation This agreement builds on Neuraxpharm's expanding portfolio of strategic alliances that bridge pharmaceutical and med-tech innovation. It follows the Company's entry into digital health through the commercialisation agreement with mjn-neuro in 2022 for a wearable device that predicts epileptic seizures, further demonstrating Neuraxpharm's commitment to realising innovative solutions in CNS care. About the Neuraxpharm Group Neuraxpharm is a leading European specialty pharmaceutical company focused on the treatment of the central nervous system (CNS), including both psychiatric and neurological disorders. It has a unique understanding of the CNS market built over 40 years. Neuraxpharm is constantly innovating, with new products and solutions to address unmet patient needs and is expanding its portfolio through its pipeline, partnerships, and acquisitions. The company has c.1,000 employees and develops and commercialises CNS products through a direct presence in more than 20 countries in Europe, two in Latin America, one in the Middle East, and globally via partners in more than 50 countries. Neuraxpharm is backed by funds advised by Permira. Neuraxpharm manufactures many of its pharmaceutical products at Neuraxpharm Pharmaceuticals (formerly Laboratorios Lesvi) in Spain. For more information, please visit About Dizlin Pharmaceuticals Dizlin Pharmaceuticals AB is a privately held Swedish research-based pharmaceutical development company with focus on diseases of the central nervous system in general and on developing improved treatment for advanced stages of Parkinson's disease in particular. The company conducts research in collaboration with researchers at the University of Gothenburg and Linköping University in Sweden. The company has developed a new patented method for treatment of advanced stages of Parkinson's disease. Dizlin Pharmaceuticals has two products in late phase development stage. The first – Infudopa SubC ® – is administered as a continuous subcutaneous infusion by means of a portable pump (similar to insulin infusion for diabetes) to outpatients. The second – Infudopa IntraV ® – is administered intravenously to inpatients in order to minimize the risks associated with surgery on patients with Parkinson's disease. About Infudopa SubC® Infudopa SubC™ (DIZ102) is a levodopa-carbidopa solution intended for outpatient treatment. Used with a portable twin pump enabling continuous mixing prior to infusion, Infudopa SubC ® is aimed as monotherapy for subjects who experience moderate to severe motor fluctuations when receiving oral administration of levodopa. Infudopa SubC ® displays physiological osmolality and a physiologically acceptable pH and results in a rapid and highly efficient levodopa uptake. The shelf life is 36 months in refrigerator and at least three months at room temperature, which will represent a significant logistic advantage for patients, e.g., when traveling. References 1 Parkinson's Statistics - Parkinson's Europe. 2024. [Accessed 01 July 2025.] 2 Projections for prevalence of Parkinson's disease and its driving factors in 195 countries and territories to 2050: modelling study of Global Burden of Disease Study 2021 BMJ2025;388:e080952. [Accessed 01 July 2025.] SOURCE Neuraxpharm WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

License out/inDrug Approval

100 Deals associated with Levodopa hydrate

External Link

KEGG	Wiki	ATC	Drug Bank
D00059	Levodopa hydrate	N04BA01	DB01235

R&D Status

Approved

10 top approved records.

to view more data

Indication	Country/Location	Organization	Date
Parkinson Disease	United States	Hoffmann-La Roche, Inc.	04 Jun 1970
Parkinson Disease	United States	Shire Development LLC	04 Jun 1970

Developing

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Dyskinesias	Phase 3	United States	AbbVie, Inc.	01 Jun 2009
Dyskinesias	Phase 3	Germany	AbbVie, Inc.	01 Jun 2009
Dyskinesias	Phase 3	New Zealand	AbbVie, Inc.	01 Jun 2009
Asthma	Phase 1	United States	Acorda Therapeutics, Inc.	01 Dec 2015
Smoking	Phase 1	United States	Acorda Therapeutics, Inc.	01 Dec 2015
Autism Spectrum Disorder	Preclinical	China	Fudan University	11 Jul 2025

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


PD MED early disease randomisation (MDS2023)	Not Applicable	Parkinson Disease	1,593	Levodopa-sparing therapy (dopamine agonist or monoamine oxidase B inhibitor)	bidrjjcqnf(aylhkhzweh): P-Value = 0.84 View more	Positive	27 Aug 2023
				Levodopa alone
NCT03761030 (CTgov)	Phase 4	Status Epilepticus \| Depressive Disorder, Major	51	L-DOPA (L-DOPA Arm)	wyodetcdmf(zwhrdqzmnm) = paxzaedjmr pkdwheegup (ubgagwdhgd, 6.4) View more	-	22 May 2023
				Placebo Oral Tablet (Placebo Arm)	wyodetcdmf(zwhrdqzmnm) = odscsqnlgs pkdwheegup (ubgagwdhgd, 5.8) View more
P13-11.014 (AAN2023)	Not Applicable	Parkinson Disease	33	Intrajejunal Levodopa Infusion (ILI)	bnvtqewjot(xfjdqyriax) = Most common complications were PEG-J tube dislodgement and pump malfunction in 18 (54.5%) patients over the study period. bycdqwxohy (eqvzymebgv ) View more	-	25 Apr 2023
SPAN-PD (AAN2023)	Phase 3	Parkinson Disease	-	CVT-301 84mg	qwcavelrib(txebifrjrd) = ulsogwpusy qjlbyrqprc (llbzsufaft )	Positive	25 Apr 2023
EAN2022	Phase 2	Parkinson Disease	24	Total daily LD/CD dose of 400/100 mg 4 intakes a day every 4 hours (Q4H) plus OPC 50 mg	txfeppavia(yeongsjbus) = The Q3H plus OPC regimen was also associated with an increase in LD Cmin with no significant impact on LD Cmax, leading to a ~60–90% decrease in the LD fluctuation (variation between Cmax and Cmin) znwihmudvv (mkjrzwchqr ) View more	Positive	24 Jun 2022
				Total daily LD/CD dose of 400/100 mg 5 intakes a day every 3 hours (Q3H) plus OPC 50 mg
CVT-301 (MDS2021)	Phase 3	Parkinson Disease	709	CVT-301 84 mg	tvoxxdqpdn(pvzqpsqxtm) = More patients achieved and maintained an ON state within 60 minutes postdose vs placebo uxnmgpgxvz (rccjcdbgau ) View more	Positive	17 Sep 2021
				Placebo
MDS2020	Not Applicable	Parkinson Disease First line	360	Levodopa	wixttynmub(rghfrfitea) = qixbhjweua ediabnvasq (pyxttxzmsl, 3 - 15.49)	Positive	12 Sep 2020
NCT03541356 (THOR201, CTgov)	Phase 2	Parkinson Disease	32	Placebo (Placebo)	fmpokshred = ojgpbqrfye neaexshcui (gtgwcvainp, ygrlewcvmi - dfojjikrco) View more	-	12 Aug 2020
				L-dopa 35 mg (L-dopa 35 mg)	fmpokshred = bcolxjogxv neaexshcui (gtgwcvainp, spqorvaocu - qjgrcokcgx) View more
NCT03887884 (Pubmed \| Clin Ther)	Phase 1	Parkinson Disease	23	CVT-301	kclftftgoj(xkycqahhnj) = CVT-301, 7 patients [30.4%]; oral CD/LD, 1 patient [4.5%] ycvecwbnem (yzclvvcxvz )	-	01 Jun 2020
				Oral Carbidopa/Levodopa

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