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Active, not recruitingNCT04491383Updated Dec 2, 2025

Tocotrienols in Parkinson's Disease (PD)

A Phase 2 interventional study of Tocovid Suprabio (HOV-12020) and Placebo in Neuro-Degenerative Disease and Parkinson Disease, sponsored by National Neuroscience Institute. Active, not recruiting at 2 sites in Singapore. Open to participants aged 40 Years to 90 Years. Per ClinicalTrials.gov, last updated 2025-12-02.

Sponsored by National Neuroscience Institute · Phase 2, Interventional, and Treatment

From the registry’s dates

  • Primary completion was expected by Jul 2026, 3 months ago, but the record still lists the study as active, not recruiting.
Phase
Phase 2
Study type
Interventional
Enrollment
100
Allocation
Randomized
Ages
40 Years to 90 Years
Sex
All
01

Study summary

A study using Parkinson's disease animal model, transgenic fruit flies, demonstrated the potential of using tocotrienols (HOV-12020) as a therapeutic agent for delaying Parkinsonian motor dysfunctions. The proposed study aims to enrol 100 PD patients in a randomized placebo-controlled trial to investigate the effects of tocotrienols (HOV-12020) in motor and non-motor outcomes. Patients will be given oral tocotrienols (400mg/day) or placebo for 104 weeks. They will be assessed using the standard assessments scales in PD at baseline, Week 52 and Week 104. Neuropsychological evaluation will also be completed at these intervals to monitor progression of cognitive impairment (if any). Additional PD staging using MDSUPDRS (Part III), Hoehn \& Yahr (H\&Y) will be conducted at Week 26 and week 78. Blood samples will be collected to evaluate PD biomarkers and for safety monitoring (liver function, renal function and hematology).

02

Conditions studied

  • Neuro-Degenerative Disease
  • Parkinson Disease

Keywords

  • Parkinson Disease
  • Vitamin E
  • Neurodegenerative Disease
  • Neurology
03

In context

Parkinson Disease

4,487 studies on the registry are indexed under Parkinson Disease; 1,082 are open to participants now.

This study's enrollment of 100 is above the median of 40 across 3,294 interventional studies indexed under Parkinson Disease.

Browse Parkinson Disease studies →

Lead sponsor

National Neuroscience Institute is the lead sponsor of 10 studies on the registry; 4 are open to participants now.

Counted across the registry records on this site, refreshed daily.

04

Who can participate

Ages eligible
40 Years to 90 Years
Sexes eligible
All
Accepts healthy volunteers
No

Inclusion criteria

  • Men or women aged between 40 - 90 years (inclusive).
  • Able to provide written informed consent and able to comply with study protocol.
  • Idiopathic PD of more than 1 years duration from diagnosis. The diagnosis must be confirmed by presence of bradykinesia and at least 1 other cardinal sign (resting tremor, rigidity), without any other known or suspected cause of parkinsonism.
  • Hoehn \& Yahr => 2 with treatment.
  • Patients on PD medication(s) e.g. levodopa, dopamine agonists, amantadine and/or Monoamine oxidase (MAO)-B inhibitors, must be on stable dose, for at least 30 days prior to screening. Medication and dose adjustments are allowed but must be documented.
  • Patients on anti-depressant or anxiolytic medication must be on stable dose for at least 90 days prior to screening.
  • The patient is willing to abstain from Vitamin E supplements (tocopherols and tocotrienols) and other dietary supplements which contain Vitamin E (tocopherols and tocotrienols) up to 14 days before baseline visit, and throughout the clinical study, unless prescribed by their physician for medical reasons.

Exclusion criteria

Exclusion Criteria:

  • Any other neurodegenerative disorder, such as Alzheimer's disease, Huntington's disease, or Creutzfeldt - Jakob disease.
  • Current, clinically-significant hematological, cardiac, pulmonary, metabolic, neurologic or psychiatric disorders, uncontrolled seizures, untreated hypertension, disorders increasing risk of bleeding (Hemophilia), or any other significant active medical condition which, in the Investigator's opinion, would impact participation in this study.
  • History of psychotic symptoms requiring treatment with a neuroleptic medication within the past 12 months.
  • History of surgical or invasive intervention for PD (pallidotomy, thalamotomy, deep brain stimulation, etc.)
  • Medical history indicating drug-induced parkinsonism (e.g., metoclopramide, flunarizine), metabolic identified neurogenetic disorders (e.g., Wilson's disease), encephalitis, or other atypical Parkinsonian syndromes (e.g., progressive supranuclear palsy, multiple system atrophy).
  • History of myocardial infarction within 3 months prior to Screening, or current active angina pectoris, or symptomatic heart failure.
  • Known liver disease or liver enzymes (AST, ALT) more than 5 times upper limit normal within 1 month of screening and enrolment.
  • eGFR \<60 within 1 month of screening and enrolment.
  • Current participation in another investigational interventional study.
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Study design

Phase
Phase 2
Primary purpose
Treatment
Allocation
Randomized
Intervention model
Parallel assignment
Masking
Quadruple (Participant, Care provider, Investigator, Outcomes assessor)
Enrollment
100 participants (actual)

Study arms

  • Experimental
    Tocovid Suprabio (HOV-12020)

    200mg, twice 1 day, 12 months

    Drug: Tocovid Suprabio (HOV-12020)

  • Placebo comparator
    Placebo

    200mg, twice 1 day, 12 months

    Other: Placebo

Interventions

  • DrugTocovid Suprabio (HOV-12020)

    Dietary supplement: Tocotrienol (HOV-12020) Palm oil-derived vitamin E, tocotrienol

  • OtherPlacebo

    Dietary supplement: Placebo. Placebo.

06

What researchers measure

Primary outcomes

  1. Mean change from Baseline to Week 104 in Movement Disorder Society-Sponsored Unified Parkinson's Disease Rating Scale (MDS-UPDRS) Score

    Score range is 0 to 199, with severity increasing with higher scores.

    Time frame: 104 weeks

Secondary outcomes

  1. Mean change from baseline to week 104 in disease severity

    Time frame: 104 weeks

  2. Mean change from baseline to week 104 in individual cognitive domain z scores on comprehensive neuropsychological testing mean score change from baseline to week 104 in the MDS-UPDRS score for total score

    Severity of disease increases with higher score.

    Time frame: 104 weeks

  3. Mean change from Baseline to Week 104 in quality of life, as measured by the Parkinson's Disease Questionnaire (PDQ-39)

    Score range is 0 to 100. A lower score will indicate a better quality of life.

    Time frame: 104 weeks

  4. Difference proportion of patients with change from Baseline to Week 104, above or equal to the minimal clinically important difference (MCID) of the motor score, as measured by Part II and III subscales of MDS-UPDRS.

    Severity of disease increases with higher score.

    Time frame: 104 weeks

  5. Mean change in levels of blood-based biomarkers (including total antioxidant status TAS, oxidative stress biomarkers and αsynuclein).

    Time frame: 104 weeks

  6. Between treatment difference of type and incidence of Adverse Events (AEs) and Serious AEs (SAEs)

    Time frame: 104 weeks

  7. Mean score change from Baseline to Week 104 in the MDS-UPDRS Part II scale

    Severity of disease increases with higher score.

    Time frame: 104 weeks

  8. Mean score change from Baseline to Week 104 in the Schwab and England Activities of Daily Living (SE-ADL) scale.

    The scale uses percentages to assess the difficulties completing daily activities/chores, from 0% to 100%. A higher percentage will indicate a better outcome (i.e. more independence for an individual).

    Time frame: 104 weeks

07

Study locations

2 sites
  • National Neuroscience Institute
    Singapore, Singapore
  • Singapore General Hospital
    Singapore, Singapore
08

References and documents

Publications

  • Jankovic J. Parkinson's disease: clinical features and diagnosis. J Neurol Neurosurg Psychiatry. 2008 Apr;79(4):368-76. doi: 10.1136/jnnp.2007.131045. PubMed 18344392 ↗
  • Gandhi S, Wood NW. Molecular pathogenesis of Parkinson's disease. Hum Mol Genet. 2005 Sep 15;14(18):2749-55. doi: 10.1093/hmg/ddi308. Epub 2005 Aug 26. PubMed 16126732 ↗
  • Khanna S, Rink C, Ghoorkhanian R, Gnyawali S, Heigel M, Wijesinghe DS, Chalfant CE, Chan YC, Banerjee J, Huang Y, Roy S, Sen CK. Loss of miR-29b following acute ischemic stroke contributes to neural cell death and infarct size. J Cereb Blood Flow Metab. 2013 Aug;33(8):1197-206. doi: 10.1038/jcbfm.2013.68. Epub 2013 May 1. PubMed 23632968 ↗
  • Rink C, Christoforidis G, Khanna S, Peterson L, Patel Y, Khanna S, Abduljalil A, Irfanoglu O, Machiraju R, Bergdall VK, Sen CK. Tocotrienol vitamin E protects against preclinical canine ischemic stroke by inducing arteriogenesis. J Cereb Blood Flow Metab. 2011 Nov;31(11):2218-30. doi: 10.1038/jcbfm.2011.85. Epub 2011 Jun 15. PubMed 21673716 ↗
  • Silbert LC, Howieson DB, Dodge H, Kaye JA. Cognitive impairment risk: white matter hyperintensity progression matters. Neurology. 2009 Jul 14;73(2):120-5. doi: 10.1212/WNL.0b013e3181ad53fd. PubMed 19597134 ↗
  • Srikanth VK, Quinn SJ, Donnan GA, Saling MM, Thrift AG. Long-term cognitive transitions, rates of cognitive change, and predictors of incident dementia in a population-based first-ever stroke cohort. Stroke. 2006 Oct;37(10):2479-83. doi: 10.1161/01.STR.0000239666.46828.d7. Epub 2006 Aug 31. PubMed 16946165 ↗
  • Sen CK, Rink C, Khanna S. Palm oil-derived natural vitamin E alpha-tocotrienol in brain health and disease. J Am Coll Nutr. 2010 Jun;29(3 Suppl):314S-323S. doi: 10.1080/07315724.2010.10719846. PubMed 20823491 ↗
  • Kuhad A, Chopra K. Tocotrienol attenuates oxidative-nitrosative stress and inflammatory cascade in experimental model of diabetic neuropathy. Neuropharmacology. 2009 Sep;57(4):456-62. doi: 10.1016/j.neuropharm.2009.06.013. Epub 2009 Jun 23. PubMed 19555701 ↗
  • Khanna S, Roy S, Slivka A, Craft TK, Chaki S, Rink C, Notestine MA, DeVries AC, Parinandi NL, Sen CK. Neuroprotective properties of the natural vitamin E alpha-tocotrienol. Stroke. 2005 Oct;36(10):2258-64. doi: 10.1161/01.STR.0000181082.70763.22. Epub 2005 Sep 15. PubMed 16166580 ↗
  • Khanna S, Roy S, Ryu H, Bahadduri P, Swaan PW, Ratan RR, Sen CK. Molecular basis of vitamin E action: tocotrienol modulates 12-lipoxygenase, a key mediator of glutamate-induced neurodegeneration. J Biol Chem. 2003 Oct 31;278(44):43508-15. doi: 10.1074/jbc.M307075200. Epub 2003 Aug 13. PubMed 12917400 ↗
  • Sen CK, Khanna S, Roy S, Packer L. Molecular basis of vitamin E action. Tocotrienol potently inhibits glutamate-induced pp60(c-Src) kinase activation and death of HT4 neuronal cells. J Biol Chem. 2000 Apr 28;275(17):13049-55. doi: 10.1074/jbc.275.17.13049. PubMed 10777609 ↗
  • Khanna S, Parinandi NL, Kotha SR, Roy S, Rink C, Bibus D, Sen CK. Nanomolar vitamin E alpha-tocotrienol inhibits glutamate-induced activation of phospholipase A2 and causes neuroprotection. J Neurochem. 2010 Mar;112(5):1249-60. doi: 10.1111/j.1471-4159.2009.06550.x. Epub 2009 Dec 17. PubMed 20028458 ↗
  • Aggarwal BB, Sundaram C, Prasad S, Kannappan R. Tocotrienols, the vitamin E of the 21st century: its potential against cancer and other chronic diseases. Biochem Pharmacol. 2010 Dec 1;80(11):1613-31. doi: 10.1016/j.bcp.2010.07.043. Epub 2010 Aug 7. PubMed 20696139 ↗
  • Vitamin E in Neuroprotection Study (VENUS) Investigators; Hor CP, Fung WY, Ang HA, Lim SC, Kam LY, Sim SW, Lim LH, Choon WY, Wong JW, Ch'ng ASH, Beh KKM, Wee HC, Ong LM, Khan NAK, Sulaiman SAS, Shuaib IL, Bakar A, Yusof Y, Yusof YM, Abu Bakar F, Tang WS, Teh HL, Wahid NA, Saaidin S, Idris N, Yoon CK, Ong HN, Ganapathy JT, Loo CE, Samy MM, Zainal H, Dharan SCS, Ooi BY, Teoh PY, Tye YL, Yeoh CA, Low DW, Looi I, Yuen KH. Efficacy of Oral Mixed Tocotrienols in Diabetic Peripheral Neuropathy: A Randomized Clinical Trial. JAMA Neurol. 2018 Apr 1;75(4):444-452. doi: 10.1001/jamaneurol.2017.4609. PubMed 29379943 ↗
  • Farooqui T, Farooqui AA. Lipid-mediated oxidative stress and inflammation in the pathogenesis of Parkinson's disease. Parkinsons Dis. 2011 Feb 15;2011:247467. doi: 10.4061/2011/247467. PubMed 21403820 ↗
  • Gopalan Y, Shuaib IL, Magosso E, Ansari MA, Abu Bakar MR, Wong JW, Khan NA, Liong WC, Sundram K, Ng BH, Karuthan C, Yuen KH. Clinical investigation of the protective effects of palm vitamin E tocotrienols on brain white matter. Stroke. 2014 May;45(5):1422-8. doi: 10.1161/STROKEAHA.113.004449. Epub 2014 Apr 3. PubMed 24699052 ↗

Individual participant data

Plan to share: No — There is not a plan to make IPD available.

09

Updates

Tracking since Sep 25, 2026
No changes since tracking began. The registry record was last updated on Dec 2, 2025, before this site started recording changes on Sep 25, 2026. Its history is on ClinicalTrials.gov ↗
10

Registry details

Key details

Study ID
NCT04491383
Lead sponsor
National Neuroscience Institute
Responsible party
Sponsor
First posted
Jul 29, 2020
Start date
Apr 1, 2021
Primary completion
Jul 2026 (estimated)
Completion
Jul 31, 2027 (estimated)
Last update
Dec 2, 2025

Study contacts

Eng King Tan
principal investigator · National Neuroscience Institute Singapore
Adeline Su-Lyn Ng
principal investigator · National Neuroscience Institute Singapore

Oversight

Data monitoring committee
Yes
FDA-regulated drug
No
FDA-regulated device
No
View the source record on ClinicalTrials.gov ↗

Not currently enrolling

This study is active, not recruiting, as verified in Nov 2025. You cannot join it, but the record below documents what was studied.

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