NCT00951834: SUN-AK

Sunphenon EGCg (Epigallocatechin-Gallate) in the Early Stage of Alzheimer´s Disease

Completed Phase 2/Phase 3 Last updated 28 July 2021

What this trial tests

Phase 2/Phase 3 trial testing Epigallocatechin-Gallate in Alzheimer's Disease in 21 participants. Completed in 1 February 2015.

Timeline

1 October 2009

Primary endpoint
1 February 2015

1 February 2015

Quick facts

Lead sponsor	Charite University, Berlin, Germany
Phase	Phase 2/Phase 3
Status	Completed
Study type	INTERVENTIONAL
Allocation	randomized
Design	parallel
Masking	quadruple
Primary purpose	treatment
Enrollment	21
Start date	1 October 2009
Primary completion	1 February 2015
Estimated completion	1 February 2015
Sites	3 locations across Germany

Drugs / interventions tested

• Epigallocatechin-Gallate — full drug profile →
• Placebo

Conditions studied

• Alzheimer's Disease — all drugs for Alzheimer's Disease →

Sponsor

Charite University, Berlin, Germany

Who can join

60 and older, any sex, with Alzheimer's Disease. Patients with the condition only — healthy volunteers not accepted.

What's being measured

Primary outcomes are the specific endpoints the trial is designed to prove or disprove.

• ADAS-COG (Score 0-70) (Baseline to treatment)
  Time frame: 18 months

Sponsor's own description

EGCG has shown a neuroprotective effect in cell-experimental and animal studies. The neuroprotective mechanism of EGCG probably bases - besides the known antioxidant effect - amongst others on the modulation of several signal transduction pathways, the influence on the expression of genes which regulate cell survival resp. programmed cell death, as well as the modulation of the mitochondrial function. In different Alzheimer models EGCG seems to cause an induction of alpha-secretase and the endothelin-converting-enzyme, as well as to prevent the aggregation of beta-amyloid to toxic oligomers through the direct binding to the unfolded peptide.

The investigators therefore expect EGCG to have a positive influence on the course of the Alzheimer´s Disease.

Publications & conference data

8 peer-reviewed publications reference this trial (live from Europe PMC):

1. Amyloid β Protein and Alzheimer's Disease: When Computer Simulations Complement Experimental Studies.
   Nasica-Labouze J, Nguyen PH, Sterpone F, Berthoumieu O, et al · · 2015 · cited 446× · PMID 25789869 · DOI 10.1021/cr500638n
2. Mitochondrial dysfunction in Alzheimer's disease: Role in pathogenesis and novel therapeutic opportunities.
   Perez Ortiz JM, Swerdlow RH. · · 2019 · cited 341× · PMID 30675901 · DOI 10.1111/bph.14585
3. Natural products as a source of Alzheimer's drug leads.
   Williams P, Sorribas A, Howes MJ. · · 2011 · cited 232× · PMID 21072430 · DOI 10.1039/c0np00027b
4. New pharmacological strategies for treatment of Alzheimer's disease: focus on disease modifying drugs.
   Salomone S, Caraci F, Leggio GM, Fedotova J, et al · · 2012 · cited 197× · PMID 22035455 · DOI 10.1111/j.1365-2125.2011.04134.x
5. Oxidative damage in neurodegeneration: roles in the pathogenesis and progression of Alzheimer disease.
   Perluigi M, Di Domenico F, Butterfield DA. · · 2024 · cited 154× · PMID 37843394 · DOI 10.1152/physrev.00030.2022
6. Tau Protein Interaction Partners and Their Roles in Alzheimer's Disease and Other Tauopathies.
   Sinsky J, Pichlerova K, Hanes J. · · 2021 · cited 139× · PMID 34502116 · DOI 10.3390/ijms22179207
7. Preventive and Therapeutic Strategies in Alzheimer's Disease: Focus on Oxidative Stress, Redox Metals, and Ferroptosis.
   Plascencia-Villa G, Perry G. · · 2021 · cited 130× · PMID 32486897 · DOI 10.1089/ars.2020.8134
8. Mitochondrial Dysfunction in Alzheimer's Disease: Opportunities for Drug Development.
   Bhatia S, Rawal R, Sharma P, Singh T, et al · · 2022 · cited 121× · PMID 33998995 · DOI 10.2174/1570159x19666210517114016