Bienvenido

Gracias por su interés en NeuroAiD*.

Esta sección está dedicada a los profesionales médicos. A continuación puede revisar los datos clínicos de NeuroAiD, leer acerca de su farmacología, consultar publicaciones y evaluar la relevancia de NeuroAiD en su centro y para aquellos de sus pacientes que hayan sufrido un accidente cerebrovascular o un traumatismo craneoencefálico. Para obtener más información, no dude en ponerse en contacto con nosotros por correo electrónico a través de medical@moleac.com

* Nota: NeuroAiD™ (MLC601) es la fórmula original compuesta por 14 ingredientes. NeuroAiD™ II y NurAiD™ II (MLC901) son formulas simplificadas de NeuroAiD™ (MLC601) compuestas por 9 ingredientes herbarios de la fórmula original. Se ha demostrado que MLC901 y MLC601 son farmacológicamente equivalentes. A efectos de simplificación, en la siguiente información se utilizará NeuroAiD como nombre global para designar a los productos, con la excepción de casos en los que se mencionen específicamente.

NeuroAiD es un producto natural indicado para tratamiento de recuperación después de sufrir un accidente cerebrovascular o un traumatismo craneoencefálico.

 

De acuerdo con la normativa nacional de cada país, NeuroAiD está registrado con varias denominaciones, como suplemento alimenticio, medicina tradicional y fitoterapia. Hasta la fecha, NeuroAiD está a la venta en más de 32 países y está expandiendo de forma continua su desarrollo.

Con la asistencia y participación de los principales líderes de opinión internacionales en neurología e investigadores expertos, NeuroAiD ha compilado más de 45 publicaciones, desde estudios de fase I a ensayos clínicos aleatorizados, con el objetivo de atender una necesidad médica mundial.

  1. Young S y cols. Safety profile of MLC601 (NeuroAiD) in acute ischemic stroke patients: A Singaporean substudy of the Chinese medicine NeuroAiD efficacy on stroke recovery study. Cerebrovascular Diseases 2010;30:1-6. 2. Gan R y cols. Danqi Piantan Jiaonang does not modify haemostasis, haematology, and biochemistry in normal subjects and stroke patients. Cerebrovascular Diseases 2008;25:450-456

Información de prescripción general

La dosis recomendada es de 2 cápsulas, 3 veces al día durante un mínimo de 3 meses.

 

Vía de administración

Vía oral con un vaso de agua. Para personas con dificultades de deglución, las cápsulas se pueden abrir y el contenido se puede diluir en agua. También es posible administrar el contenido diluido a través de sonda nasogástrica.

 

Interacciones

Hasta la fecha, no se han notificado interacciones farmacológicas con NeuroAiD. Si desea obtener más información sobre el perfil de seguridad de NeuroAiD, haga clic AQUÍ.

 

Efectos secundarios

Los ensayos clínicos publicados han confirmado que NeuroAiD no tiene efecto anticoagulante ni efecto sobre la función hepática ni renal. Asimismo, NeuroAiD tampoco afecta a la tensión arterial y no provoca cambios en los parámetros cardíacos, hematológicos, hemostáticos y bioquímicos1,2.

En los ensayos clínicos sobre NeuroAiD se comunicaron solo casos raros de náuseas, cefalea leve, polidipsia, xerostomía y vómitos en pacientes que tomaron NeuroAiD. En estos casos, se recomienda recudir a la mitad la dosis de NeuroAiD durante varios días y aumentarla después progresivamente.

 

Contraindicaciones

El uso de NeuroAiD en mujeres embarazadas o en estado de lactancia y niños no está documentado, por lo que no se puede recomendar. Hasta la fecha, no se conoce ninguna otra contraindicación.

 

Clinical Data

Amplification of brain self-repair processes translating into persistent functional recovery.

A 3-month course with NeuroAiD:

  • Increases by 50% the odds of achieving functional independence at 6 months.1

  • Enhances persistent functional recovery and independence on top of rehabilitation for up to 2 years.1,2,3

  • Improves motor recovery with benefits observed as early as 1 month of treatment and at each time point up to 3 months.4

The CHIMES-E Study, functional recovery over 2 years.1

  • Pre-planned study on 880 subjects* with Acute Ischaemic Stroke followed up for 2 years.

  • Randomised to 3 months of either NeuroAiD or placebo.

+50% in odds of achieving functional independence at 6 months.

Persistent recovery with benefits observed over 2 years

In subjects with 2 to 4 prognostic factors of poorer outcome** and receiving NeuroAiD2 :

  • More subjects achieved functional independence over time versus placebo.

  • Significant improvements observed as early as 3 months.

  • Less subjects deteriorating over time versus placebo, illustrating the persistence of the recovery

*CHIMES-E published in Cerebrovascular Diseases journal is the pre-planned extended follow-up to 24 months of the CHIMES study5, a 3-month study conducted on 1099 subjects. The CHIMES study was published in Stroke journal in 2013. **Prognostic factors are defined as older age, female sex, baseline NIHSS score ≥ 10 and time to first dose 48h.  

Combining NeuroAiD and Rehabilitation doubles the odds of achieving functional independence versus Rehabilitation alone.3  

  • Analysis of 380 subjects having received rehabilitation during 3 months of NeuroAiD (n=200) or placebo (n=180).

+50% in odds of achieving functional independence at 6 months.

Persistent recovery with benefits observed over 2 years

  • Statistically significant odds ratio at all time points from 3 months to 2 years from stroke onset.

  • Persistent recovery with benefits sustained for up to 2 years, as supported by low Numbers Needed to Treat (NNT) range from 5 to 7 over the 24-month follow-up period.

NeuroAiD improves motor recovery.4

  • Randomised double-blind study placebo-controlled study in post-acute stroke subjects with upper and lower limbs deficits, included up to one month following an ischaemic stroke (n=150).

Significantly better motor recovery observed since month 1 and sustained up to month 3.

By stimulating brain neurorepair processes, NeuroAiD enhances recovery after a TBI

  • Improves 2 of the most commonly impacted cognitive domain post-TBI6

  • Enhances functional outcome to reach independency in moderate and severe TBI7

The BRAINS study6

  • Randomized, placebo-controlled pilot trial on 79 mild to moderate TBI subjects.

  • Recruited from 1 month to 12 months from TBI.

  • Receiving 6 months of NeuroAiD or matching placebo and followed-up until 9 months.

NeuroAiD significantly improves Executive Functioning and Complex Attention at 6 months.

  • Continuous improvement of Executive Functioning, significant at 6 months.

  • Executive Functioning deficit is directly impacting activities of daily living and affecting cognitive rehabilitation.

  • Continuous improvement of Complex Attention, significant at 6 months.

  • Complex Attention is one of the most impacted cognitive domains following a TBI.

Recovering functional outcomes post-TBI7

  • Randomised, double-blind, placebo-controlled trial in 81 subjects after a moderate to severe TBI.

  • Treatment initiated within 24 hours from TBI onset from a 6-month course.

  • Dosing schedule: NeuroAiD (MLC901) or placebo at a regimen of 2 capsules, 3 times per day for 6 months.

  • Assessment: GOS and modified Rankin Scale (mRS) at month 3 and month 6.

NeuroAiD optimises recovery of moderate and severe TBI subjects over time

  • Higher rate of subjects with favourable outcome in NeuroAiD group compared to placebo group at month 3.

  • Over 86% of the subjects reached favourable outcome in NeuroAiD group after a 6-month course (including 43.2% with GOS 5).

  • Significant differences in favour of NeuroAiD at both time points.

  • More subjects reached functional independence (mRS 0-1) in NeuroAiD group vs placebo at month 3 and month 6.

  • The proportion of subjects with no symptoms (mRS 0) is superior in NeuroAiD group compared to the placebo group at both time points.

  • Significant differences in favour of NeuroAiD at both time points.

Visit the Publications tab

for more information on NeuroAiD’s clinical data

Referencias:

  1. Venketasubramanian N y cols. CHInese Medicine NeuroAiD Efficacy on Stroke recovery – Extension Study (CHIMES-E): A multicenter study of long-term efficacy. Cerebrovascular Dis. 2015; 39:309-318.
  2. Venketasubramanian N y cols. Prognostic Factors and Pattern of Long-Term Recovery with MLC601 (NeuroAiD™) in the Chinese Medicine NeuroAiD Efficacy on Stroke Recovery – Extension Study. Cerebrovascular Dis. 2017; 43:36–42.
  3. Suwanwela NC y cols. Effect of Combined Treatment with MLC601 (NeuroAiDTM) and Rehabilitation on Post-Stroke Recovery: The CHIMES and CHIMES-E Studies. Cerebrovasc Dis. 2018 doi: 10.1159/000492625.
  4. Harandi AA y cols. Safety and efficacy of MLC601 in Iranian patients after stroke: a double-blind, placebo-controlled clinical trial. Stroke Research and Treatment. 2011; doi:10.4061/2011/721613.
  5. Chen C y cols. Chinese medicine Neuroaid efficacy on stroke recovery – A double-blind, placebo-controlled, randomized study. Stroke. 2013; 44:2093-2100.
  6. Theadom A y cols. MLC901 (NeuroAid II™) for cognition after traumatic brain injury: A pilot randomised clinical trial. Eur J Neurol. 2018;25(8):1055-e82.
  7. Pakdaman H y cols. MLC901 for moderate to severe traumatic brain injury: pilot, randomised, double-masked, placebo-controlled trial. Open Acc J Comp & Alt Med. 2020; 2(5).OAJCAM.MS.ID.000148. DOI: 10.32474/OAJCAM.2020.02.000148.

NeuroAiD presenta un perfil de seguridad favorable y se tolera bien

El perfil de seguridad de NeuroAiD está bien establecido en pacientes con accidente cerebrovascular isquémico y traumatismo craneoencefálico. En la mayoría de los estudios realizados sobre NeuroAiD se realizaron comparaciones con placebo. No existe mejor comparador para evaluar el perfil de seguridad de un producto.

  • No hubo ninguna interacción con los tratamientos estándar utilizados después de sufrir un accidente cerebrovascular o un traumatismo craneoencefálico1,3.

  • Sin cambios en los parámetros cardíacos, hematológicos, hemostáticos o bioquímicos3,4.

  • Ningún efecto secundario grave estuvo asociado a NeuroAiD durante el tratamiento1. Se observaron efectos secundarios raros, transitorios y leves (p. ej., síntomas gastrointestinales)1. Normalmente se resolvieron reduciendo la dosis a la mitad durante unos días.

  • No se observó ningún aumento en los acontecimientos adversos diferidos después de la finalización del tratamiento y se realizó un seguimiento de 2 años2,5.

NeuroAiD es seguro como tratamiento complementario para recuperación neurológica.

Hasta la fecha, no se han notificado interacciones farmacológicas con NeuroAiD.

NeuroAiD se debe tomar junto con tratamientos preventivos de factores de riesgo cardiovascular prescritos después de sufrir un accidente cerebrovascular; suelen incluir antiplaquetarios, antihipertensivos y hipocolesterolemiantes, además de otros como antidiabéticos.

Los ensayos clínicos sistemáticos han demostrado que NeuroAiD no presenta ninguna interacción con el ácido acetilsalicílico. No se ha observado ningún efecto sobre el INR (cociente internacional normalizado) en los pacientes que toman NeuroAiD con anticoagulantes. No obstante, se recomienda mantener la supervisión del INR al iniciar el tratamiento con NeuroAiD, ya que este es el procedimiento habitual en pacientes que toman anticoagulantes.

 

Control de la calidad

NeuroAiD se fabrica en Singapur de acuerdo con los estándares internacionales de Buenas prácticas de fabricación (GMP). Los estándares GMP se aplican a procedimientos de fabricación de suplementos alimenticios, lo que incluye la aprobación de materias primas, procesos de producción y controles de procesamiento, pruebas de laboratorio y envasado, etiquetado y distribución de productos. Estos procesos suelen ser auditados por autoridades sanitarias independientes.

Cada lote de NeuroAiD se analiza exhaustivamente en laboratorios independientes de terceros para confirmar la conformidad con los estándares internacionales, garantizando una seguridad casi absoluta en el uso de NeuroAiD.

  1. Chen C y cols. Chinese medicine NeuroAiD efficacy on stroke recovery: A double-blind, placebo-controlled, randomized study. Stroke 2013a;44:2093-2100 2. Venketasubramanian N y cols. CHInese medicine NeuroAiD efficacy on stroke recovery – Extension study (CHIMES-E): A multicenter study of long-term efficacy. Cerebrovascular Diseases 2015;39:309-318. 3. Young S y cols. Safety profile of MLC601 (NeuroAiD) in acute ischemic stroke patients: A Singaporean substudy of the Chinese medicine NeuroAiD efficacy on stroke recovery study. Cerebrovascular Diseases 2010;30:1-6. 4. Gan R y cols. Danqi Piantan Jiaonang does not modify haemostasis, haematology, and biochemistry in normal subjects and stroke patients. Cerebrovascular Diseases 2008;25:450-456. 5. Shahripour RB y cols. A Randomized Trial to Assess the Long-Term Safety of NeuroAiD among Caucasian Patients with Acute Ischemic Stroke. Chin J Integr Med 2014;20(11):812-817.

NeuroAiD: Datos farmacológicos

NeuroAiD incorpora un mecanismo de acción multiselectivo que impulsa los principales componentes de neurorreparación endógena y ejerce un efecto de facilitador sobre la neurorreparación, al activar simultáneamente las vías farmacológicas

PLASTICIDAD DE LA RED NEURONAL1,2

  • Aumenta la supervivencia, la plasticidad y resistencia de la red neuronal y la neurogénesis, al regular al alza el factor neurotrófico derivado del cerebro (BDNF).
  • Aumenta el crecimiento neurítico y la sinaptogénesis.
  • Favorece una mayor densidad en las redes axonal y dendrítica.

NEUROGÉNESIS1,2

  • Aumenta el número de nuevas neuronas y neurogliocitos.
  • Optimiza su migración y diferenciación en células completamente funcionales.

ANGIOGÉNESIS3

  • Reduce las fugas en la barrera hematoencefálica y optimiza su reparación. Modula la expresión y actividad de los mediadores que intervienen en la neuroinflamación.
  • Amplifica el desarrollo de microvasos en el área dañada

MODULACIÓN DE LA NEUROINFLAMACIÓN4

  • Reduce las fugas en la barrera hematoencefálica y optimiza su reparación.
  • Modula la expresión y actividad de los mediadores que intervienen en la neuroinflamación.

NeuroAiD aumenta la producción del factor neurotrófico derivado del cerebro (BDNF)1

El BDNF es un factor de crecimiento que regula la supervivencia neuronal y protege a las neuronas de daños inducidos por el glutamato. El BDNF también favorece la proliferación y diferenciación de nuevas neuronas.

Efecto in vivo del tratamiento previo de NeuroAiD sobre los niveles de proteínas de BDNF en secciones de la corteza. (A) Fotografías adquiridas mediante microscopio de epifluorescencia de la inmunoexpresión de BDNF en las neuronas corticales de las secciones cerebrales. (B) Cuantificación de la intensidad de señal de BDNF en neuronas inmunoteñidas.

NeuroAiD favorece una mayor densidad en las redes neuronales1

El microscopio de epifluorescencia ha confirmado el desarrollo de una red axonal y dendrítica significativa en cultivos celulares con NeuroAiD.

El día 14, en los cultivos celulares neuronales tratados con NeuroAiD, la epifluorescencia demostró un aumento considerable de las expresiones de DCX, GAP43 y sinaptotagmina, proporcionando datos que respaldan que NeuroAiD favorece los siguientes procesos:

  • Neurogénesis

  • Crecimiento neurítico

  • Sinaptogénesis

NeuroAiD favorece tanto el desarrollo de nuevas conexiones sinápticas como la modificación de las conexiones existentes, incluido un aumento en el número y longitud de las dendritas y sinapsis. Se demostró un aumento del 60 % en la longitud de los axones en el día 14 para el grupo de NeuroAiD.

Efectos del tratamiento con MLC601/MLC901 sobre la expresión de la sinaptotagmina 1 in vitro en cultivos de neuronas corticales. La expresión de la sinaptotagmina 1 se analizó después del tratamiento con MLC601/MLC901 (1 mg/ml) en los días 7 y 14 del tratamiento.

 

NeuroAiD favorece la neuroplasticidad y la neurogénesis para favorecer la recuperación tras accidentes cerebrovasculares1

 

  • NeuroAiD aumenta la proliferación de células progenitoras neuronales a través de un efecto triplicador significativo (p <0,01) en las células madre humanas.

  • En estudios realizados en animales, NeuroAiD aumenta de forma significativa (2,1 veces) el número de neuronas (p <0,01).

  • Los cultivos celulares tratados con NeuroAiD presentan redes de conexiones más densas con neuronas más fuertes.

Efectos neurogénicos de MLC901 sobre células progenitoras derivadas de células madre embrionarias humanas. (D) Formación espontánea de agregados radiantes, similares a una roseta, de células progenitoras neurales nestina positivas en cultivos de baja densidad. (E) Cuantificación del número de rosetas 2 días después de la adición de MLC901 (*p <0,05, **p < 0,01 frente al número de control).

 

Esta combinación de sus 9 ingredientes herbarios seleccionados tiene un efecto facilitador sobre la neurorreparación

que permite conseguir una recuperación funcional global.

 

  • Como estrategia facilitadora, NeuroAiD mejora los procesos de neurorreparación natural de neurogénesis1,2, plasticidad de la red neuronal1,2, angiogénesis3 y antiinflamación4.

  • Estos efectos se suman a los efectos de consolidación que proporciona la rehabilitación para reforzar las conexiones recién formadas y conseguir una recuperación funcional global.

Consulte la sección Publicaciones

para obtener más información sobre las propiedades y modo de acción de NeuroAiD

Referencias

  1. Heurteaux C y cols. Neuroprotective and neuroproliferative activities of NeuroAiD (MLC601, MLC901), a Chinese medicine, in vitro and in vivo. Neuropharmacology. 2010;58:987-1001.
  2. Quintard H y cols. MLC901, a Traditional Chinese Medicine induces neuroprotective and neuroregenerative benefits after Traumatic Brain Injury in rats. Neuroscience. 2014;277:72-86.
  3. Gandin C y cols. MLC901 Favors Angiogenesis and Associated Recovery after Ischemic Stroke in Mice. Cerebrovasc Dis. 2016;42:139–154.
  4. Widmann C y cols. The Traditional Chinese Medicine MLC901 inhibits inflammation processes after focal cerebral ischemia. Scientific Reports. 2018;8:18062.

 

I. Ischemic Stroke

Clinical data – Efficacy

Key Data

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. As presented at ESOC Glasgow and ESC Vienna 2015
Venketasubramanian N, et al. Cerebrovascular Diseases 2015. DOI: 10.1159/000382082
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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.
Suwanwela et al. Cerebrovasc Dis 2018. DOI: 10.1159/000492625
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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.
Venketasubramanian N, et al. Cerebrovascular Diseases 2016. DOI: 10.1159/000452285
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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.
Chen C, et al. Stroke 2013. DOI: 10.1161/STROKEAHA.113.003226
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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.
Chen C, et al. Stroke 2013. DOI: 10.1161/STROKEAHA.113.002055
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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.
Navarro JC, et al. International Journal of Stroke 2016. DOI: 10.1177/1747493016676615
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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.
Harandi AA, et al. Stroke Res Treat 2011. DOI: 10.4061/2011/721613
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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.
Dib M, et al. European Journal of Medicinal Plants 2014. DOI: 10.9734/EJMP/2015/13192
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Additional Data

This randomized double-blind placebo-controlled study recruited 80 patients within 1 week of stroke, of which 40 received 4 capsules of NeuroAiD 3 times a day and 40 others received placebo for 3 months. The subjects were recruited at Ahvaz Golestan Hospital in Iran from April 2009 to March 2010. This study shows that MLC601 improves cerebral blood flow velocity in post-cerebral infarction subjects better than in the control group. This is associated with more improvement in functional outcome (Barthel Index of activities of daily living) as compared to placebo at 3 months.
Shahripour RB, et al. Eur Intern Med 2011. DOI: 10.1016/j.ejim.2011.01.002
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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.
Ghandehari K, et al. Neural Regen Res 2011. DOI: 10.3969/j.issn.1673-5374.2011.06.003
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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.
Venketasubramanian N, et al. Journal of Evidence-Based Medicine 2015. DOI: 10.1111/jebm.12170
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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.
Siddiqui FJ, et al. Cerebrovasc Dis 2013. DOI: 10.1159/000346231
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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.
Navarro J, et al. Int J Stroke 2014. DOI: 10.1111/ijs.12324
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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.
Fabiaña NL, et al. Journal of Clinical Neuroscience 2016. DOI: 10.1016/j.jocn.2016.04.013
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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.
Chankrachang S, et al. J. of Stroke and Cerebro Diseases 2015. DOI: 10.1016/j.jstrokecerebrovasdis.2014.11.017
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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.
Navarro JC, et al. Rehabil Res Pract 2012. DOI: 10.1155/2012/506387
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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.
Lee CF, et al. Stroke 2016. DOI: 10.1161/STROKEAHA.115.011657
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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.
Chen C, et al. Stroke 2009. DOI: 10.1161/STROKEAHA.108.531616
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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.
Kong KH, et al. Cerebrovasc Dis 2009. DOI: 10.1159/000247001
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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. DOI: 10.1159/000155220
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This paper is a review of the related Medline literature (presenting the neuroprotective and neurorestorative properties of the product demonstrated in several pre-clinical studies and also its benefits in post-stroke patients supported by clinical trials including CHIMES and CHIMES-E studies) and a primary stroke center experience to support the availability of NurAiD II for post-stroke patients.
De Le Cruz Cosme C. International Journal of Clinical Neurosciences and Mental Health 2017. ABSTRACT. http://moleac.com/pubs/nuraid-ii_in_stroke_recovery_scientific_reasoning_and_real-world_evidence_-__de_la_cruz_et_al_-_2017.pdf
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Clinical data – Safety

Key Data

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.
Venketasubramanian N, Moorakonda RB, Lu Q et al. Cerebrovasc Dis 2020. DOI: 10.1159/000506070
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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.
Shahripour RB, et al. Chin J Integr Med 2014. DOI: 10.1007/s11655-014-1687-8
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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.
Young SHY, et al. Cerebrovasc Dis 2010. DOI: 10.1159/000313398
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Additional Data

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.
Gan R, et al. Cerebrovasc Dis 2008. DOI: 10.1159/000126919
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II. Traumatic Brain Injury – Neurosurgical pathologies

Clinical data – Efficacy

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.
Fauzi AA, Prihastomo KT, Ranuh IGMAR et al. Brain Sci 2020;10;60:1-9. DOI: 10.3390/brainsci10020060
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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. Theadom et al. Eur J Neurol. 2018 Apr 3. DOI: 10.1111/ene.13653
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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 DOI: 10.32474/ OAJCAM.2020.02.000148
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This case series report of 20 patients treated with MLC601 in the Neurosurgery division of National University Hospital in Singapore. All patients received 4 capsules of MLC601 3 times a day for 3 months started within 3 months of onset of brain injury or stroke. All patients reported some improvements and good tolerance for the drug. Three cases (head injury, hemorrhagic stroke from AVM, and brain abscess) with remarkable outcomes were presented, illustrating how it may not be unreasonable to prescribe MLC601 to selected patients with difficult neurosurgical pathology in the hope that the neurological function outcome would improve.
Yeo TT, et al. Poster WSC Seoul 2010. http://moleac.com/pubs/case_report_on_the_use_of_mlc601_(neuroaid)_in_neurosurgical_pathologies_-_yeo_tt_-_2010.pdf
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III. Cognitive Disorders and Dementia

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.
Pakdaman H, et al. Neuropsychiatric Disease and Treatment 2017. DOI: 10.2147/NDT.S145047
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This publication is a multicenter, nonblinded, randomized controlled trial, which included 264 volunteers with AD to evaluate the effectiveness and safety of MLC601 in the treatment of mild to moderate AD as compared to 3 approved cholinesterase inhibitors (ChEIs) including donepezil, rivastigmine and galantamine. This is the second clinical study of NeuroAiD™ effectiveness and safety in Alzheimer disease. In a previous clinical trial study, NeuroAiD™ has demonstrated a favorable tolerability and encouraging effectiveness on cognitive function in Alzheimer disease patients during 18 months of treatment when compared to rivastigmine. In this study, the authors have shown that NeuroAiD™ has favorable effects on cognitive functions during 16 months of follow-up, with improvements on cognitive function specifically observed in the first 8 months of treatment. NeuroAiD™ is as effective as other commonly used Cholinesterase inhibitors (Donepazil, Rivastigmine, Galantamine) in treating cognitive deficits. Finally, NeuroAiD™ has shown a better tolerability profile compared to the 3 ChEIs, which implies a better compliance for patients.
Pakdaman, H et al. Dementia and Geriatric Cognitive Disorders 2015. DOI: 10.1159/000375295
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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.
Harandi AA, et al. Brit Med Med Res 2013. http://moleac.com/pubs/efficacy_and_tolerability_of_mlc601_in_patients_with_mild_to_moderate_alzheimer_disease_-_pakdaman_et_al_-_2013.pdf
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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.
Pakdaman et al. Dement Geriatr Cogn Disord Extra 2018. DOI: 10.1159/000488482
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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.
Pakdaman H, et al. Dementia and Geriatric Cognitive Disorders 2017. DOI: 10.1159/000458521
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IV. Preclinical Data – Pharmacology

Cognitive Disorders and Dementia

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.
Lim YA, et al. Cerebrovasc Dis 2013. DOI: 10.1159/000346236
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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.
Lee WT, et al. NeuroReport 2017. DOI: 10.1097/WNR.0000000000000884
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Stroke

Key Data

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.
Heurteaux C, et al. Cerebrovasc Dis 2013. DOI: 10.1159/000346228
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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.
Heurteaux C, et al. Neuropharmacology 2010. DOI: 10.1016/j.neuropharm.2010.01.001
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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.
Quintard H, et al. Neuropharmacology 2011. DOI: 10.1016/j.neuropharm.2011.05.003
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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.
HYA Chan, et al. The Pharmacogenomics Journal 2016. DOI: 10.1038/tpj.2016.21
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This in-vivo study conducted by the CNRS (National Center for Scientific Research, France) is providing further evidence of MLC901 (NeuroAiDTMII) multimodal mechanism of action and particularly interesting to better understand a possible cardioprotective effect. A previous study, published in Stroke in 2013, demonstrated the benefits of NeuroAiD in reducing the risk of early vascular events in post-stroke victims, up to 3 months following stroke onset (Chen C, et al. Stroke 2013.). The researchers aimed at evaluating the acute and long-term benefits of MLC901 (NeuroAiDTMII) in ischemic and reperfused mouse heart models. This paper demonstrates that MLC901 treatment was able to provide acute and long-term cardioprotective effects in a murine model of myocardial ischemia-reperfusion injury in vivo.
Vincent a, et al. Scientific reports 2017. DOI: 10.1038/s41598-017-14822-x
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Additional Data

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.
Widmann C, et al. Scientific reports 2018. DOI: 10.1038/s41598-018-36138-0
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This in-vivo study conducted by the CNRS (National Center for Scientific Research, France) is providing further evidence of MLC901 (NeuroAiDTMII) multimodal mechanism of action and particularly interesting to better understand a possible cardioprotective effect. A previous study, published in Stroke in 2013, demonstrated the benefits of NeuroAiD in reducing the risk of early vascular events in post-stroke victims, up to 3 months following stroke onset (Chen C, et al. Stroke 2013.). The researchers aimed at evaluating the acute and long-term benefits of MLC901 (NeuroAiDTMII) in ischemic and reperfused mouse heart models. This paper demonstrates that MLC901 treatment was able to provide acute and long-term cardioprotective effects in a murine model of myocardial ischemia-reperfusion injury in vivo.
Vincent a, et al. Scientific reports 2017. DOI: 10.1038/s41598-017-14822-x
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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.
Gandin C, et al. Cerebrovasc Diseases 2016. DOI: 10.1159/000444810
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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.
Moha Ou Maati H, et al. Neuropharmacology 2012. DOI: 10.1016/j.neuropharm.2012.05.035
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Traumatic Brain Injury

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.
Quintard H, et al. Neuroscience 2014. DOI: 10.1016/j.neuroscience.2014.06.047
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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.
Chio CC, et al. 2016. DOI: 10.1111/eci.12693
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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.
Tsai MC, et al. J Neuroimmune Pharmacol 2014. DOI: 10.1007/s11481-014-9570-0
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V. Ongoing clinical Trials

With limited therapeutic options in the current treatment of spinal cord injury (SCI), many patients with SCI remain disabled. Spinal Cord Injury—Assessing Tolerability and Use of Combined Rehabilitation and NeuroAiD (SATURN) investigates the promising role of NeuroAiD in SCI especially given its excellent safety profile. SATURN is a prospective cohort study of patients with moderately severe to severe SCI, defined as American Spinal Injury Association (ASIA) Impairment Scale (AIS) A and B. The results will provide important information on the feasibility of conducting larger controlled trials to improve long-term outcome of patients with SCI.
Kumar JC et al. JMIR Res Protoc 2016. DOI: 10.2196/resprot.6275
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This imaging substudy aims to assess the efficacy of NeuroAiD in subgroups of patients randomized in the main CHIMES Study when categorized according to baseline imaging characteristics. Acute stroke lesions on baseline CT or MRI are reviewed in terms of size, location, and extent of involvement by two readers who remain blinded to treatment allocation and outcomes of the subjects. The outcomes, namely modified Rankin Scale, National Institute of Health Stroke Scale, Barthel Index, and Mini-Mental Status Examination, will be analyzed by the sub-groups nonlacunar and lacunar, cortical and sub-cortical, hemispheric vs. brainstem, Alberta Stroke Program Early CT score.
Navarro JC et al. Int J Stroke 2013. DOI: 10.1111/ijs.12044
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VI. NeST Registry

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.
Venketasubramanian N, et al. BJM Open 2015. DOI: 10.1136/bmjopen-2015-009866
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NeuroAiD está disponible en más de 32 países.

 

Moleac ha desarrollado múltiples asociaciones con empresas que comparten los mismos valores y visión para ofrecer soluciones innovadoras en cada mercado y atender necesidades médicas no satisfechas, especialmente en el tratamiento de recuperación después de un accidente cerebrovascular y traumatismo craneoencefálico.

Nuestra cada vez mayor red de socios garantiza la disponibilidad de NeuroAiD no solo en un número incluso mayor de víctimas de accidente cerebrovascular y traumatismo craneoencefálico de todo el mundo, sino también en pacientes que experimentan deterioro cognitivo.

Desde 2006, NeuroAiD ha ampliado su presencia a más de 32 países, y mantenemos nuestro objetivo de conseguir que NeuroAiD esté disponible para más pacientes que lo necesiten de todo el mundo.

Oficinas de Moleac

Nuestros socios

Exención de responsabilidad:  En esta página web se proporcionan datos científicos e información dirigida exclusivamente a profesionales sanitarios. NeuroAiD™ II es una marca comercial de Moleac. MLC601 y MLC901 son 2 formulaciones patentadas diferentes cuya equivalencia farmacológica se ha demostrado y que se denominan NeuroAiD en esta página web.

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