CoQ10 Supplement for Glioblastoma
Recruiting in Palo Alto (17 mi)
Overseen byLawarence Recht
Age: 18+
Sex: Any
Travel: May Be Covered
Time Reimbursement: Varies
Trial Phase: Phase 2
Recruiting
Sponsor: Stanford University
Must not be taking: Insulin
Disqualifiers: Refuse IV, Allergy MRI contrasts, others
No Placebo Group
Prior Safety Data
Trial Summary
What is the purpose of this trial?The goal of this study is to evaluate the prognostic capacity of DMI in a trial assessing the efficacy of adding BPM31510, a lipid nano dispersion of CoQ10 to standard treatment of Glioblastoma (GBM).
Will I have to stop taking my current medications?
The trial does not specify whether you need to stop taking your current medications, but if you are diabetic and taking insulin, you cannot participate.
What evidence supports the effectiveness of the CoQ10 supplement treatment for glioblastoma?
Research suggests that CoQ10 can reduce glioblastoma growth and invasion by acting as an antioxidant and improving the effectiveness of standard treatments like temozolomide. It may also help in reducing the spread of cancer cells and improving the body's response to treatment.
12345Is CoQ10 safe for use in humans, particularly in the context of glioblastoma treatment?
CoQ10, also known as BPM31510, has been studied for its safety in humans, showing potential to improve the tolerability of cancer treatments and selectively target cancer cells without harming non-cancer cells. It has been used in various studies, including those involving glioblastoma, with no major safety concerns reported.
12356How does CoQ10 differ from other treatments for glioblastoma?
CoQ10 is unique because it can cross the blood-brain barrier and acts as an antioxidant, helping to reduce tumor growth and invasion by remodeling proteins and inhibiting blood vessel formation and inflammation. Unlike standard treatments, CoQ10 also enhances the effectiveness of temozolomide, a common chemotherapy drug, by increasing the cancer cells' sensitivity to it.
12345Eligibility Criteria
This trial is for individuals with Glioblastoma who can consent to the study and are part of a Phase II trial for BPM31510. Women able to have children must test negative for pregnancy. It's not suitable for insulin-dependent diabetics, those who refuse IVs, or people allergic to MRI contrast agents.Inclusion Criteria
Ability to understand and the willingness to provide written informed consent.
Any participant that consents to entry into the Phase II BPM31510 parent study (BPM31510IV-11)
I am capable of becoming pregnant and have a negative pregnancy test.
Exclusion Criteria
I am diabetic and take insulin.
I refuse to receive treatments through an IV.
Allergy to MRI contrasts
Trial Timeline
Screening
Participants are screened for eligibility to participate in the trial
2-4 weeks
Treatment
Participants receive BPM31510, a lipid nano dispersion of CoQ10, along with standard treatment for Glioblastoma. They will also undergo metabolic imaging with deuterated glucose and MRI.
Varies
1 visit for MRI and DMI study
Follow-up
Participants are monitored for overall survival and progression-free survival.
up to 36 months
Participant Groups
The study aims to assess how well DMI (using [6,6-²H₂]-Glucose) predicts treatment success when adding BPM31510 (a CoQ10 lipid nano dispersion) to standard GBM therapy.
1Treatment groups
Experimental Treatment
Group I: Deuterated Glucose + MRIExperimental Treatment1 Intervention
Participants will receive \[6,6-²H₂\]-glucose orally at a dose of 0.75g per kg of body weight (maximum 60g), dissolved in 200-500mL of water. Approximately 45 minutes after ingestion, participants will undergo an MRI scan consisting of a 30-minute conventional MRI brain study followed by a 1-hour Deuterium Metabolic Imaging (DMI) study. A Gadolinium contrast agent may be administered if more than 4 weeks have passed since the last enhanced MRI scan.
Find a Clinic Near You
Research Locations NearbySelect from list below to view details:
Stanford UniversityPalo Alto, CA
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Who Is Running the Clinical Trial?
Stanford UniversityLead Sponsor
National Institutes of Health (NIH)Collaborator
National Cancer Institute (NCI)Collaborator
References
CoQ10 reduces glioblastoma growth and infiltration through proteome remodeling and inhibition of angiogenesis and inflammation. [2023]Label="PURPOSE" NlmCategory="OBJECTIVE">Most monotherapies available against glioblastoma multiforme (GBM) target individual hallmarks of this aggressive brain tumor with minimal success. In this article, we propose a therapeutic strategy using coenzyme Q10 (CoQ10) as a pleiotropic factor that crosses the blood-brain barrier and accumulates in cell membranes acting as an antioxidant, and in mitochondrial membranes as a regulator of cell bioenergetics and gene expression.
Efficacy of coenzyme Q10 for improved tolerability of cancer treatments: a systematic review. [2022]The aim of this systematic review was to summarize and evaluate the evidence available for oral supplementation with coenzyme Q10 (CoQ10) to improve the tolerability of cancer treatments.
Modulation of Antioxidant Potential with Coenzyme Q10 Suppressed Invasion of Temozolomide-Resistant Rat Glioma In Vitro and In Vivo. [2020]The main reasons for the inefficiency of standard glioblastoma (GBM) therapy are the occurrence of chemoresistance and the invasion of GBM cells into surrounding brain tissues. New therapeutic approaches obstructing these processes may provide substantial survival improvements. The purpose of this study was to assess the potential of lipophilic antioxidant coenzyme Q10 (CoQ10) as a scavenger of reactive oxygen species (ROS) to increase sensitivity to temozolomide (TMZ) and suppress glioma cell invasion. To that end, we used a previously established TMZ-resistant RC6 rat glioma cell line, characterized by increased production of ROS, altered antioxidative capacity, and high invasion potential. CoQ10 in combination with TMZ exerted a synergistic antiproliferative effect. These results were confirmed in a 3D model of microfluidic devices showing that the CoQ10 and TMZ combination is more cytotoxic to RC6 cells than TMZ monotherapy. In addition, cotreatment with TMZ increased expression of mitochondrial antioxidant enzymes in RC6 cells. The anti-invasive potential of the combined treatment was shown by gelatin degradation, Matrigel invasion, and 3D spheroid invasion assays as well as in animal models. Inhibition of MMP9 gene expression as well as decreased N-cadherin and vimentin protein expression implied that CoQ10 can suppress invasiveness and the epithelial to mesenchymal transition in RC6 cells. Therefore, our data provide evidences in favor of CoQ10 supplementation to standard GBM treatment due to its potential to inhibit GBM invasion through modulation of the antioxidant capacity.
Levels of Coenzyme Q10 and Several COQ Proteins in Human Astrocytoma Tissues Are Inversely Correlated with Malignancy. [2022]In a previous study, we reported the alterations of primary antioxidant enzymes and decreased citrate synthase (CS) activities in different grades of human astrocytoma tissues. Here, we further investigated coenzyme Q10 (CoQ10) levels and protein levels of polyprenyl diphosphate synthase subunit (PDSS2) and several COQ proteins required for CoQ10 biosynthesis in these tissues. We found that the level of endogenous CoQ10, but not of exogenous α-tocopherol, was higher in nontumor controls than in all grades of astrocytoma tissues. The levels of COQ3, COQ5, COQ6, COQ7, COQ8A, and COQ9, but not of COQ4, were lower in Grade IV astrocytoma tissues than in controls or low-grade (Grades I and II) astrocytomas, but PDSS2 levels were higher in astrocytoma tissues than in controls. Correlation analysis revealed that the levels of CoQ10 and COQ proteins were negatively correlated with malignancy degree and positively correlated with CS activity, whereas PDSS2 level was positively correlated with malignancy. Moreover, lower level of mitochondrial DNA-encoded cytochrome c oxidase subunit 2 was not only associated with a higher malignancy degree but also with lower level of all COQ proteins detected. The results revealed that mitochondrial abnormalities are associated with impaired CoQ10 maintenance in human astrocytoma progression.
GLIOMA CELL PROLIFERATION MEDIATED BY COENZYME Q10 AT SERUM DEPRIVATION IN VITRO. [2018]Mechanisms of coenzyme Q10 effect on serum-deprived glioma cell proliferation have been studied. Our results have shown that the addition of coenzyme Q10 into serum-free culture medium leads to increase in cell viability, stimulation of cell growth, as well as restoration of mitochondrial potential and increase of quantity of energized mitochondria. It has been found out that coenzyme Q10-induced glioma cell proliferation under serum deficiency is a result of intracellular reduced glutathione concentration decrease with subsequent activation of proteinkinase C, ERK1/2 and phosphoinositol-3-kinase.
High levels of ubidecarenone (oxidized CoQ10) delivered using a drug-lipid conjugate nanodispersion (BPM31510) differentially affect redox status and growth in malignant glioma versus non-tumor cells. [2021]Metabolic reprogramming in cancer cells, vs. non-cancer cells, elevates levels of reactive oxygen species (ROS) leading to higher oxidative stress. The elevated ROS levels suggest a vulnerability to excess prooxidant loads leading to selective cell death, a therapeutically exploitable difference. Co-enzyme Q10 (CoQ10) an endogenous mitochondrial resident molecule, plays an important role in mitochondrial redox homeostasis, membrane integrity, and energy production. BPM31510 is a lipid-drug conjugate nanodispersion specifically formulated for delivery of supraphysiological concentrations of ubidecarenone (oxidized CoQ10) to the cell and mitochondria, in both in vitro and in vivo model systems. In this study, we sought to investigate the therapeutic potential of ubidecarenone in the highly treatment-refractory glioblastoma. Rodent (C6) and human (U251) glioma cell lines, and non-tumor human astrocytes (HA) and rodent NIH3T3 fibroblast cell lines were utilized for experiments. Tumor cell lines exhibited a marked increase in sensitivity to ubidecarenone vs. non-tumor cell lines. Further, elevated mitochondrial superoxide production was noted in tumor cells vs. non-tumor cells hours before any changes in proliferation or the cell cycle could be detected. In vitro co-culture experiments show ubidecarenone differentially affecting tumor cells vs. non-tumor cells, resulting in an equilibrated culture. In vivo activity in a highly aggressive orthotopic C6 glioma model demonstrated a greater than 25% long-term survival rate. Based on these findings we conclude that high levels of ubidecarenone delivered using BPM31510 provide an effective therapeutic modality targeting cancer-specific modulation of redox mechanisms for anti-cancer effects.