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Using data from a multi-centre, randomised, double-blind, placebo-controlled trial of a neuro-repair treatment (NeuroAiD/MLC601) with a long-term follow-up, this study analysed the savings in time to functional recovery. The results showed that approximately 40% cumulative incidence of functional recovery was achieved within 6 months after stroke onset in the MLC601 group versus 24 months in the placebo group. The main findings are that MLC601 reduced the time to achieve functional recovery 18 months earlier compared to placebo.

J. Cardiovasc. Dev. Dis. 2023, 10(3), 117; https://doi.org/10.3390/jcdd10030117

The CHIMES-E study, a planned extension study of the CHIMES study, aimed to evaluate the effects of an initial 3-month treatment with NeuroAiD on long-term outcomes of up to 2 years. This study has showed that NeuroAiD increases significantly the odds of achieving functional independence at 6 months and persisted up to 18 months after a stroke, as measured by mRS dichotomy 0-1. It also provided further long-term safety data on NeuroAiD, even when combined with other stroke treatments. The authors concluded that an initial 3-month treatment with NeuroAiD increased the odds of functional independence after a stroke, “providing level 1 evidence of benefit in ischaemic stroke”*.*

Venketasubramanian N, et al. Cerebrovascular Diseases 2015.

In this study, the CHIMES investigators assess the effects of combining NeuroAiD and rehabilitation. While patients show substantial neurological improvement due to endogenous mechanisms after stroke, they are often not sufficient to achieve complete recovery in many patients. Hence neurorehabilitation remains one of the cornerstones for poststroke management. NeuroAiD has been shown to enhance the inherent neurorestorative and neurorecovery mechanisms after stroke. This paper reports a more significant effect size in the NeuroAiD and persistent rehabilitation vs placebo and persistent rehabilitation group, in comparison with the NeuroAiD vs Placebo effect size in the overall population. NeuroAiD and rehabilitation together can enable more than double the chance to reach independence at 6 months and 1 year. This study supports a probable beneficial effect of combining NeuroAiD and rehabilitation brain repair processes.

This is a sub-analysis of the CHIMES-E study. The researchers aimed to evaluate the recovery pattern and the influence of prognostic factors on treatment effect of NeuroAiD over 2 years. The sustained benefits of NeuroAiD over 2 years were due to more subjects with poorer prognosis improving to functional independence at month 6 and beyond compared to placebo. Selection of subjects with poorer prognosis, particularly those with more severe NIHSS score and longer OTT delay, as well as a long follow-up period, may improve the power of future trials investigating the treatment effect of neuroprotective or neurorestorative therapies.

This publication is a post-hoc analysis performed on data from subjects included in the CHInese Medicine Neuroaid Efficacy on Stroke recovery (CHIMES) study. The CHIMES study is an academic international double-blind placebo-controlled clinical trial which treated and monitored 1100 patients from several countries who had suffered an ischemic stroke of intermediate severity within 72 hours, for 3 months. Early vascular events were defined as a composite of recurrent stroke, acute coronary syndrome, and vascular death occurring within 3 months of stroke onset. The research concluded that the risk of early vascular events during the 3-month follow-up was significantly reduced by half in the MLC601 group as compared to the placebo group without an increase in nonvascular deaths. Kaplan–Meier survival analysis demonstrated the difference in risk as early as the first 14 days after stroke.

The CHIMES study is an academic international double-blind placebo-controlled clinical trial which treated and monitored 1100 patients from several countries who had suffered an ischemic stroke of intermediate severity within 72 hours, for 3 months. The research concluded that NeuroAiD is statistically no better than placebo in improving outcomes at 3 months when used among patients with acute ischemic stroke of intermediate severity. However the results of the study confirmed the overall benefit of NeuroAiD in stroke recovery and showed that treatment effect for achieving functional independence was greater among non-acute strokes, consistent with previous studies. In addition the study showed that NeuroAiD had an excellent safety profile.

A pre-specified country analysis of subjects from the Philippines in the CHInese Medicine NeuroAiD Efficacy on Stroke recovery (CHIMES) Study, published in 2014, showed significantly improved functional and neurological outcomes on NeuroAiD at month 3. With this new analysis, the researchers showed that the beneficial effect of NeuroAiD seen at month 3 in the Filipino cohort is durable up to two years after stroke.

This study of 150 Iranian patients with a recent ischemic stroke (within 1 month) shows that MLC601 improves motor recovery as early as 4 weeks and persisted up to 12 weeks after stroke. Moreover, good tolerability to treatment was shown and adverse events were mild and transient. No severe adverse event leading to drug discontinuation was reported.

This paper reviews the important findings on NeuroAiD™, from pharmacological properties to efficacy and safety data in Stroke recovery. It reminds that NeuroAiD has demonstrated neurorestorative and neuroprotective properties and this justifies its use from the postacute to chronic phase of stroke. Clinical benefits have shown that it helps achieve functional independence with 63% increase in the odds of achieving independence in patients with established deficits and enhances recovery of motor functions. In addition, NeuroAiD offers a better protection by reducing early cardiovascular events and deaths by 50% after a stroke.

In the clinic, the natural recovery rate of homonymous hemianopsia caused by occipital lobe infarction is low. This prospective study compared the effects of NeuroAiD (MLC601) versus piracetam in improving visual field defects in 40 patients matched for age and sex within 1 week of PCA infarction with pure homonymous hemianopsia. After 3 months of treatment, the findings suggest that MLC601 is superior to piracetam for reducing quantitative visual field defects in homonymous hemianopsia patients.

The authors’ purpose was to verify if patient selection based on two prognostic actors (ie, stroke severity and time to treatment) improves detection of a treatment effect with MLC601. Analyses were performed using data from the CHIMES Study (international, randomized, placebo-controlled, double-blind trials comparing MLC601 to placebo in patients with ischemic stroke of intermediate severity in the preceding 72 hours). MLC601 treatment effects were much higher in the subgroups with prognostic factors than for the entire group and the highest treatment effect was seen among patients with both prognostic factors. It can be concluded that patient selection appears to be an important factor for consideration when designing clinical trials in stroke to better reveal the treatment effect and provides new insights for futures trials.

This publication updates the 2-study meta-analysis published in Stroke journal in 2009 with all clinical data available since on NeuroAiD and provides an overall assessment of the effects of NeuroAiD in improving functional and motor outcomes by the end of treatment. In a systematic review this paper shows that previous studies on NeuroAiD in ischemic stroke in general were of low risk of bias. The meta-analysis showed a statistically significant beneficial effect in favor of NeuroAiD on functional outcome when assessed at the end of study treatment. Although the results did not reach statistical significance, the overall effects on motor recovery were also in favor of NeuroAiD.

This publication is a pre-planned analysis performed on subjects from the Philippines included in the CHIMES Study. The authors found a statistically significant treatment effect in favour of NeuroAiD™ in the primary outcome of mRS and other secondary outcomes (NIHSS and Barthel Index). This result was likely attributable to the inclusion of patients with more severe stroke and longer delay from stroke onset to treatment initiation in the Philippines cohort. Thus the favourable treatment of NeuroAiD was best demonstrated among postacute stroke patients with moderate severity.

The National Institutes of Health Stroke Scale (NIHSS) is composed of 15 items. The purpose of this study was to compare the measurement properties of the original NIHSS with shortened versions (including only 11, 8 and 5 items). The analyses were performed using the data from the CHIMES study at Day 10 and 3 months. The original 15-item NIHSS, which can be performed easily over a few minutes, retained information that made it more discriminative and responsive to change than the shortened versions. The authors recommend to use the full version NIHSS, to evaluate patients’stroke severity in clinical trials.

This publication is a post-hoc analysis performed on CHIMES study patients. The authors have identified predictors of poorer mRS at 3 months (Age > 60; Female sex; Baseline NIHSS 10-14; Stroke onset to initiation of MLC601 > 48h) and have shown that NeuroAiD™ treatment effect is statistically significant for patients with 2 or more predictors of poorer outcome. Hence this paper illustrates NeuroAiD™ efficacy at 3 months, which is best demonstrated among patients with poorer prognosis.

This paper aimed to assess the efficacy of MLC601 on functional recovery in patients given MLC601 after an ischemic stroke. This was a retrospective cohort study comparing 30 post-stroke patients given open-label MLC601 for three months and 30 matching patients who did not receive MLC601 from the Stroke Data Bank. There were positive results from this study: NeuroAiD has been shown to improve functional recovery at 3 months post-ischemic stroke.

The National Institutes of Health Stroke Scale (NIHSS) is composed of 15 items. The purpose of this study was to compare the measurement properties of the original NIHSS with shortened versions (including only 11, 8 and 5 items). The analyses were performed using the data from the CHIMES study at Day 10 and 3 months. The original 15-item NIHSS, which can be performed easily over a few minutes, retained information that made it more discriminative and responsive to change than the shortened versions. The authors recommend to use the full version NIHSS, to evaluate patients’ stroke severity in clinical trials.

The paper reports the pooled analysis of two randomized controlled clinical trials (initial stroke trials in China) that included 605 patients recruited between 2 weeks and 6 months after their stroke. The results show that patients on NeuroAiD have 2.4 times more chances of achieving independence after 1 month of treatment, and have a 25% better recovery in motor impairments. No serious adverse event was reported.

The aim of this phase II double-blind placebo controlled study was to investigate the efficacy of NeuroAiD on motor recovery in ischemic stroke patients using rehabilitation endpoints in order to provide predictive information for further larger trials. In this clinical trial, 20 patients within 1 month post-stroke received 4 capsules of NeuroAiD 3 times a day for 4 weeks and 20 other patients received placebo. While no statistical significance was detected for all primary and secondary endpoints due to the small sample size, subgroup analysis show trends for better outcome with NeuroAiD for more severe strokes, posterior strokes, and strokes with potential for recovery at 8 weeks.

This case series report deals with 10 patients who received NeuroAiD after an ischemic stroke as confirmed on brain imaging (MRI). Conducted in an outpatient private clinic in Mount Alvernia Hospital in Singapore, the report suggests that NeuroAiD can be considered as an add-on treatment to other medications including anti-platelet, warfarin, lipid-lowering, anti-hypertensive, anti-diabetic, and antidepressant medications.

Siow C, Eur Neurol 2008.

This exploratory post-hoc analysis from the CHIMES study compared MLC601 vs. placebo in terms of serious adverse events (SAEs) and their clinical impact. Among 1087 subjects from CHIMES, there were 135 subjects with SAEs: 60 on MLC601 and 75 on placebo. Subjects on MLC601 had lower rates of harmful clinical impacts. The rate of subjects with prolonged hospitalisation was threefold lower with MLC601. These findings could translate to reduced healthcare burden and reduced medical costs from stroke.

This study on 150 patients with acute ischemic stroke within 1 week of onset demonstrates the long-term (up to 6 months) safety of NeuroAiD in a Caucasian population. While mild nausea was more commonly reported in the NeuroAiD group, none of the reported adverse events were serious or required discontinuation of treatment. There was no significant change observed in blood pressure, hematologic, hepatic, and renal functions during treatment with NeuroAid and up to 3 months after completion of a 3-month regimen. These data confirm the excellent safety profile of NeuroAiD in patients with acute ischemic stroke during treatment and long after completion of treatment.

This study on 114 patients with acute ischemic stroke randomized within 48 hours of onset shows that serious adverse events (SAEs) were similar between the group treated with placebo and the group treated with MLC601. The SAEs reported were those commonly seen in stroke patients. There were neither statistically or clinically significant differences between treatment groups in biochemical, haematological, or electrocardiogram tests at 3 months, nor any statistically or clinically significant differences in the absolute and relative changes of the various parameters between baseline and 3 months. Thus, MLC601 is safe for patients with acute stroke receiving a 3-month treatment.

NeuroAiD does not significantly affect hematological, hemostatic, and biochemical parameters in normal and stroke patients. Clinical parameters and expected effects of aspirin are not altered by co-administration of the drug even when started and maintained at the early stage of acute stroke.

This randomized controlled trial included 32 subjects with non-surgical moderate traumatic brain injury (TBI) allocated to receive standard TBI treatment with or without MLC601 over three months. The MLC601 group had a numerically higher Glasgow Outcome Scale (GOS) score than the control group at all observation timepoints. The Barthel Index (BI) values indicated a significant improvement for the MLC601 group at M3, with a favourable trend at M6. No adverse effects were noted. MLC601 showed potential for a positive effect on TBI outcome with no adverse effects.

This was a 9-month pilot, randomized placebo-controlled clinical trial to examine the safety and potential effects of the herbal supplement MLC901 (NeuroAiD II) on cognitive functioning following TBI. As rersistent cognitive deficits have been reported to affect 15 –40% of adults post-TBI, investigators wanted to evaluate the effects of MLC901 in these patients. This study demonstrated that MLC901 was safe and well tolerated post‐TBI. This study provided Class I/II evidence that, for patients with mild to moderate TBI, 6 months of MLC901 improved cognitive functioning.

A.

The study aims to evaluate the efficacy of MLC901 on the neurological outcome of patient after moderate (GCS 9-12) to severe (GCS 3-8) traumatic brain Injury. Patients were randomized to receive MLC901 or placebo for six months with an intention to treat analysis. Assessment was carried out using mRS and GOS at baseline, 3 months and at 6 months follow up. Result showed functional outcome of mRS and GOS at 3 and 6 months were significantly better compared to placebo. The study highlights the promising efficacy of MLC901 in patients suffering from moderate to severe TBI.

Hussein Pakdaman, et al Open access journal of Complementary and Alternative Medicine

This study is an open-label cohort study of patients with severe spinal cord injury (SCI), measured by American Spinal Injury Association (ASIA) Impairment Scale (AIS) A and B. Ten patients experienced 14 adverse events including one serious adverse event and six deaths, none were considered treatment-related. AIS grade improved in 25% of AIS A and 50% of AIS B. The study concluded that NeuroAiD is safe and may have a role in the treatment of patients with SCI.

Publication: Carolann Murphy, Florian P. Thomas. (2023) The Journal of Spinal Cord Medicine https://doi.org/10.1080/10790268.2022.2067972

This study is a long-term follow-up of an open-label cohort study of patients with severe spinal cord injury (SCI), measured by American Spinal Injury Association (ASIA) Impairment Scale (AIS) A and B. After 6 months of NeuroAiD treatment, patients showed durability of improvement in total motor, sensory and SCIM score. The improvement was maintained until 12, 18 and 24 months.

For more than eight years, we studied monotherapy with NeuroAid (MLC601, MLC901) in patients with AD. 8 patients out of 78 patients had mild and temporary adverse events. None of the patients stopped taking their medication because of adverse events related to the study treatment. At the end of the trial, the changes in the mean (±SD) Mini-Mental State Examination (MMSE) and the Alzheimer’s Disease Assessment Scale-Cognitive Subscale (ADAS-Cog) were 5.1 (3.09) and 12.5 (10.89), respectively. The study contributes further to the long-term safety and efficacy data of MLC in patients with AD.

Following Alzheimer’s disease (AD), Vascular Dementia (VaD) is the second most common cause of dementia in elderly people with lack of available effective treatment. Several studies and clinical trials have demonstrated the benefits of MLC601 (NeuroAiD) in post-stroke recovery and AD. This pilot trial was multicenter, randomized, double-blind, aiming to investigate the efficacy and safety of NeuroAiD in patients suffering from VaD. This is the first study conducted on NeuroAiD to investigate its efficacy in VaD as well as duration of treatment over 24 months. Repeated measures analyses showed that both MMSE and ADAS-cog scores were significantly better in the treatment group at 24 months. This long-term treatment with NeuroAiD was well-tolerated without reported serious adverse events.

The aim of this early stage “proof-of-concept” clinical study was to evaluate the efficacy and tolerability of MLC601 in patients with mild to moderate Alzheimer disease (AD). The results showed that NeuroAiD was well-tolerated even up to 18 months of treatment. This tolerability represents a key improvement compared to current AD treatments, i.e. ChEIs, in which a modest but significant therapeutic effect is often compromised by the occurrence of adverse events and discontinuation of treatment.

This was an open-label extension study evaluating the efficacy and safety of MLC601 in patients with mild to moderate AD. The rationale behind this study is supported by current evidence on the long-term efficacy of MLC601 in post-stroke recovery, by positive results in the treatment of dementia and minimal cognitive impairment. The efficacy of treating AD patients with MLC601 over 4 years has been demonstrated in the study. Overall, it seems that the safety and efficacy of MLC601 is promising compared to currently prescribed treatments.

The researchers decided to conduct this study knowing the promising effect of MLC601 (NeuroAiD) in Alzheimer’s disease. They designed a pilot, randomized, double-blind, placebo-controlled study aiming at evaluating the efficacy and the safety of MLC601 in patients with Mild Cognitive Impairments (MCI). MCI is characterized by a decline of the cognitive function greater than that expected for a person’s age, with a possible progress into dementia. Seventy-two patients were receiving NeuroAiD or placebo during 6 months (M) with an evaluation of global cognitive function performed with two different scales (MMSE and ADAScog) at baseline, M3, and M6 follow-up visits. A repeated-measures analysis carried out based on both scales’ score, showed a statistically significant difference between the placebo and the MLC601 group during the 6 months of follow-up. Overall, the tolerability of the product was good with only 5 patients reporting transient and tolerable gastrointestinal disorders.

The purpose of this paper was to investigate the effects of MLC601 (NeuroAiD) on regulation of APP (Amyloid Precursor Protein) processing. Human neuroblastoma cell line SH-SY5Y was used for all experiments. Cells were treated with different concentration of NeuroAiD before assessing changes in the levels of released lactate dehydrogenase (LDH), full-length APP and secreted sAPPα. In conclusion it appears that NeuroAiD is a possible modulator of APP processing and has implications as a putative therapeutic strategy for the treatment of post stroke dementia and AD.

The presence of neurofibrillary tangles (NFTs) in the brain is characteristic of neurodegenerative diseases including Alzheimer’s disease and frontotemporal dementia due to the hyperphosphorylation of the tau protein. The objective of this study was to assess the effects of MLC901 (NeuroAiDTMII) on ameliorating tau phosphorylation at epitopes associated with formation of NFTs. Results support evidence for a role of MLC901 in mediating this effect by inhibiting kinases (GSK3β and cdk5) leading to a significant decrease of tau phosphorylation. Previous studies (pre-clinical and clinical) having demonstrated the effect of MLC601 (NeuroAiD) as a promising therapeutic strategy for Alzheimer’s disease, this paper provides a new understanding of its multimodal mechanisms of action in this promising indication.

This paper reviews the pharmacological effects of NeuroAiD on the normal and ischemic brain and neurons. In vivo and in vitro experiments using mouse model of stroke (focal ischemia), rat model of cardiac arrest (global ischemia) and cortical neurons in culture were reviewed and summarized. In conclusion NeuroAID demonstrated both neuroprotective and neuroregenerative properties in rodent models of focal and global ischemia and in cortical cell cultures.

The paper describes the results of a series of in vivo and in vitro experiments demonstrating the neuroprotective and neuroproliferative effects of NeuroAiD when given prior to and/or after injury in rodent models of ischemic stroke and neuronal injuries, human embryonic stem cells, and neuronal cell cultures. It shows how NeuroAiD supports neuroplasticity by its effect on neurogenesis, neuritic outgrowth, and synaptogenesis. NeuroAiD provides a better milieu for post-stroke recovery and decreases neurological impairments.

The paper describes the results of a series of in vivo experiments demonstrating neuroprotective and neurogenesis effects of MLC901 on hippocampal CA1 region against global ischemia in rodent models of global ischemia. It shows how neuronal protection by MLC901 is likely mediated by the Akt protein (a central mediator in the signal transduction pathway involved in cell survival) and reduction of oxidative stress. MLC901 prevents necrosis and apoptotic cell death induced by global ischemia, enhances neurogenesis, and enhances functional recovery. This makes MLC901 a potential novel therapeutic strategy in treating cognitive and neurological deficits caused by global ischemia from conditions that deprive the brain of oxygen and glucose, such as cardiac arrest.

This study was designed to learn more about NeuroAiD™II’s cellular and molecular mechanisms of action on human neurons and more precisely by investigating the impact of MLC901 on human neural progenitor cells undergoing neural differentiation. Genes having a role in neurogenesis and neural differentiation were found significantly regulated by MLC901 in three independent experiments. The researchers identified genes of functional pathways regulated by MLC901 that could promote neurogenesis and neuroprotection in the human brain, and offered some insights into the possible mechanism of action of MLC901. After extensive studies in cell and animal models previously published, this paper provides the first validation, in human cells of the neuroplasticity mechanism triggered by MLC901, and whose effects are observed in clinical trials on recovery.

This study investigates the potential anti-inflammatory effects of MLC901 (NeuroAiD™II) in a model of transient focal cerebral ischemia in mice (60-min middle cerebral artery occlusion), and analyzes the effect of MLC901 on the different mechanisms that trigger the inflammatory process. MLC901 increases survival after MCAO, reduces the infarct volume, and improves the neurological score. These are in line with previous preclinical results and clinical trials. The major effects of MLC901 are: 1) the reduction of neutrophil recruitment, 2) the reduction of microglia activation, and 3) the reduction of pro-inflammatory mediators (TNFα, IL6, IL1β, CCL2) production induced by stroke. The present work confirms that MLC901 significantly protects mice against brain injury after focal ischemia and represents a promising therapeutic strategy for brain injuries, and particularly stroke treatment.

This in-vivo study conducted by the CNRS (National Center for Scientific Research, France) is providing further evidence of MLC901 (NeuroAiD™II) multimodal mechanism of action and particularly interesting to better understand a possible cardioprotective effect.

Vincent a, et al. Scientific reports 2017.

NeuroAiD™II (MLC901) has already demonstrated neuroprotective and neuroreparative properties and is also proven to improve long-term post-stroke recovery in human. In humans, vascular remodeling takes place 3 or 4 days after stroke, facilitating the processes of neurorepair. Therapeutic angiogenesis is an approach of regenerative medicine that may help in improving the outcomes of patients after an ischemic stroke. Because the neural and vascular cell crosstalk is important in brain repair, Dr. Catherine Heurteaux and her team at CNRS (National Center for Scientific Research, France) decided to further investigate the effect of MLC901 on vascular remodeling in a model of focal ischemia in mice. This study has provided evidences that MLC901 enhances endothelial cell proliferation and vascular remodeling locally in the ipsilateral infarcted area, but not in the contralateral hemisphere, showing that MLC901 is stimulating only the natural local revascularization process. This key finding highlights the role of MLC901 in stimulating revascularization, neuroprotection and repair of the neurovascular niche after ischemic stroke.

This paper highlights the potency of NeuroAid in neuroprotection with the discovery of a key underlying mechanism of action. The activation by NeuroAid of the ATP-sensitive potassium channel located in the suffering neurons of the brain protects them from death. Indeed, the opening of the channel decreases the excitability of neurons (by hyperpolarization) preventing an overload of calcium and release of excitotoxic glutamate. Besides the beneficial effects in neuroplasticity already published, these results strengthen the interest of NeuroAid in stroke recovery.

This paper demonstrates how NeuroAiD™ can be beneficial in reducing the deleterious consequences induced by Traumatic Brain Injury (TBI) and highlights NeuroAiD™ properties in a rat model of TBI. This is the first publication on the pharmacological actions of NeuroAiD™ in TBI and in which its multimodal mechanisms as well as its time-effect have been demonstrated. Adding to NeuroAiD™ beneficial effects in ischemic stroke recovery, this work provides evidence that NeuroAiD™ has neuroprotective and neurorestorative actions which lead to an improvement in the recovery of cognitive functions in an animal model of TBI, hence providing a rationale for NeuroAiD™ to improve recovery of patients with TBI.

Many post-Traumatic Brain Injury’s (TBI) processes are mediated by the Transforming growth factor-beta 1 (TGF-β1) expressed by microglial cells. Previous studies identified the activity of NeuroAiD in reducing microglia activation in rats with TBI. This in-vivo studies, conducted on rats, aimed at investigating whether NeuroAiD or Astragaloside (also known to attenuate microglia activation) improves output of TBI by affecting microglial expression of TGF-β1. The researchers found that both NeuroAiD and Astragaloside significantly reduced TBI-induced brain contused volume, neurological severity score and the number of TGF-β1 containing microglia. This is another demonstration of NeuroAiD’s neuroprotective effect, already highlighted in several published pre-clinical studies.

This paper highlights the role of MLC601 in improving recovery as well as affecting microglial activation in a model of rats with induced TBI. Early treatment with MLC601 (1h post-TBI) has shown significantly better benefits in reducing TBI-induced cerebral contusion than a late treatment. Beneficial effects of MLC601 were correlated with reduction in neurological and motor deficits, neuronal apoptosis and microglial activation (microgliosis, morphological transformation of microglia and microglial overexpression of TNF-α). These results are consistent in part with the beneficial effects of MLC901 in a model of rats with induced TBI already published. This work provides further evidence and a rationale to use MLC601 or MLC901 therapy in improving functional recovery in patients with TBI.

NeuroAiD™II (MLC901) has already demonstrated neuroprotective and neuroreparative properties and is also proven to improve long-term post-stroke recovery in human. In humans, vascular remodeling takes place 3 or 4 days after stroke, facilitating the processes of neurorepair. Therapeutic angiogenesis is an approach of regenerative medicine that may help in improving the outcomes of patients after an ischemic stroke. Because the neural and vascular cell crosstalk is important in brain repair, Dr. Catherine Heurteaux and her team at CNRS (National Center for Scientific Research, France) decided to further investigate the effect of MLC901 on vascular remodeling in a model of focal ischemia in mice. This study has provided evidences that MLC901 enhances endothelial cell proliferation and vascular remodeling locally in the ipsilateral infarcted area, but not in the contralateral hemisphere, showing that MLC901 is stimulating only the natural local revascularization process. This key finding highlights the role of MLC901 in stimulating revascularization, neuroprotection and repair of the neurovascular niche after ischemic stroke.

This paper highlights the potency of NeuroAid in neuroprotection with the discovery of a key underlying mechanism of action. The activation by NeuroAid of the ATP-sensitive potassium channel located in the suffering neurons of the brain protects them from death. Indeed, the opening of the channel decreases the excitability of neurons (by hyperpolarization) preventing an overload of calcium and release of excitotoxic glutamate. Besides the beneficial effects in neuroplasticity already published, these results strengthen the interest of NeuroAid in stroke recovery.

The NeuroAiD Safe Treatment (NeST) Registry works as a product registry to provide information on the use of NeuroAiD and monitor its safety in a real world setting. The NeST Registry is a proactive industry-academic effort designed to be as unobtrusive as possible during its assessment hence an online framework was introduced for easier data entry and retrieval of clinical information. The registry also acts as a complement for more accurate pharmacovigilance, essential for patient care and surveillance. Participation is voluntary and patients' data is anonymous.