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SCIENTIFIC SCORE
Moderately Effective
Based on 5 Researches
8.6
USERS' SCORE
Good
Based on 1 Review
8.5
Supplement Facts
Serving Size: 1 Veggie Capsule
Serving Per Container: 60
Amount Per Serving
%DV
Coenzyme Q10 (Ubiquinone)
200 mg
†
Black Pepper Ext. (Piper nigrum) (fruit) (standardized to contain 95% Piperine) (BioPerine®)
5 mg
†
Top Medical Research Studies
9
CoQ10 reduces glioblastoma growth
CoQ reduces glioblastoma growth and infiltration through proteome remodeling and inhibition of angiogenesis and inflammation.
Direct impact on tumor hallmarks
The study focused on understanding how coenzyme Q10 (CoQ) could help manage glioblastoma, a particularly challenging type of brain tumor. We utilized xenograft models with U251 cells implanted in mice to observe tumor growth, inflammation, and vascular changes, alongside assessing the effects of CoQ on various related behaviors, including cell migration and invasion.
We found that CoQ treatment significantly reduced tumor volume in both xenograft and orthotopic models. Interestingly, while it did not directly hinder tumor cell proliferation, it was effective in creating a less hypoxic and vascularized environment. This indicates that CoQ can influence the tumor’s growth dynamics by targeting the underlying conditions that support tumor survival and expansion.
Additionally, CoQ treatment led to a noticeable downregulation of proteins involved in inflammation and angiogenesis, like HIF-1α and NF-kB. This change in molecular activity caused an entire reshaping of the tumor's protein landscape, ultimately impacting how the tumor interacts with its environment. Notably, we observed a restriction in tumor cell migration and invasion, attributed to changes in the cell's structural components.
Overall, our findings suggest that incorporating CoQ into current treatment protocols could provide a holistic approach to combat glioblastoma by simultaneously addressing multiple pathways that facilitate tumor growth and infiltration.
We found that CoQ treatment significantly reduced tumor volume in both xenograft and orthotopic models. Interestingly, while it did not directly hinder tumor cell proliferation, it was effective in creating a less hypoxic and vascularized environment. This indicates that CoQ can influence the tumor’s growth dynamics by targeting the underlying conditions that support tumor survival and expansion.
Additionally, CoQ treatment led to a noticeable downregulation of proteins involved in inflammation and angiogenesis, like HIF-1α and NF-kB. This change in molecular activity caused an entire reshaping of the tumor's protein landscape, ultimately impacting how the tumor interacts with its environment. Notably, we observed a restriction in tumor cell migration and invasion, attributed to changes in the cell's structural components.
Overall, our findings suggest that incorporating CoQ into current treatment protocols could provide a holistic approach to combat glioblastoma by simultaneously addressing multiple pathways that facilitate tumor growth and infiltration.
Read More
9
CoQ10 shows promise in glioblastoma
High levels of ubidecarenone (oxidized CoQ) delivered using a drug-lipid conjugate nanodispersion (BPM31510) differentially affect redox status and growth in malignant glioma versus non-tumor cells.
Study explores CoQ10 effectiveness
We investigated the effects of ubidecarenone, also known as Coenzyme Q10 (CoQ10), on brain tumors, particularly glioblastoma, which are notoriously difficult to treat. The study involved both rodent and human glioma cell lines and compared them with non-tumor cells.
Our findings revealed that the glioma cells showed a significant sensitivity to ubidecarenone compared to the non-tumor cells. This sensitivity was evident as we noted increased production of mitochondrial superoxide in tumor cells before any observable changes in their growth or cell cycle.
What's interesting is that in co-culture experiments, ubidecarenone was effective in creating a balance between tumor cells and non-tumor cells. In an aggressive in vivo glioma model, we observed more than a 25% long-term survival rate, suggesting that ubidecarenone could serve as a promising therapeutic tool.
Overall, our research highlights that delivering high levels of CoQ10 through a lipid-drug conjugate could selectively target cancer cells and exploit their unique metabolic vulnerabilities.
Our findings revealed that the glioma cells showed a significant sensitivity to ubidecarenone compared to the non-tumor cells. This sensitivity was evident as we noted increased production of mitochondrial superoxide in tumor cells before any observable changes in their growth or cell cycle.
What's interesting is that in co-culture experiments, ubidecarenone was effective in creating a balance between tumor cells and non-tumor cells. In an aggressive in vivo glioma model, we observed more than a 25% long-term survival rate, suggesting that ubidecarenone could serve as a promising therapeutic tool.
Overall, our research highlights that delivering high levels of CoQ10 through a lipid-drug conjugate could selectively target cancer cells and exploit their unique metabolic vulnerabilities.
Read More
9
CoQ boosts glioblastoma therapy effectiveness
Regulation of the oxidative balance with coenzyme Q10 sensitizes human glioblastoma cells to radiation and temozolomide.
Relevant research on glioblastoma treatment
We examined how coenzyme Q10 (CoQ), a natural antioxidant, affects the response of glioblastoma cells to radiation and chemotherapy, specifically temozolomide (TMZ). Using human glioblastoma cell lines, we loaded them with CoQ and assessed various parameters, including oxidative stress and cytotoxicity from treatments.
Our results showed that CoQ did not impact oxygen consumption but significantly reduced levels of harmful mitochondrial superoxides and hydrogen peroxide. This change shifted the cells into a more vulnerable state, which we linked to decreased activity of enzymes like catalase and a reduction in important metabolites crucial for antioxidant defenses.
When we treated glioblastoma cells with radiation and TMZ, those preloaded with CoQ exhibited double the sensitivity to DNA damage and apoptosis. Importantly, this sensitivity was observed without harming normal astrocytes, which suggests that CoQ could be a valuable adjunct in glioblastoma treatment, enhancing the effectiveness of existing therapies while sparing healthy cells.
Our results showed that CoQ did not impact oxygen consumption but significantly reduced levels of harmful mitochondrial superoxides and hydrogen peroxide. This change shifted the cells into a more vulnerable state, which we linked to decreased activity of enzymes like catalase and a reduction in important metabolites crucial for antioxidant defenses.
When we treated glioblastoma cells with radiation and TMZ, those preloaded with CoQ exhibited double the sensitivity to DNA damage and apoptosis. Importantly, this sensitivity was observed without harming normal astrocytes, which suggests that CoQ could be a valuable adjunct in glioblastoma treatment, enhancing the effectiveness of existing therapies while sparing healthy cells.
Read More
Most Useful Reviews
8.8
Disease delay
My father has Paskin's disease. The doctor recommends this treatment to help delay its progression, though higher doses are necessary. For ongoing maintenance, a dosage of 200 can be taken, which may protect the heart and brain.
Read More
Medical Researches
SCIENTIFIC SCORE
Moderately Effective
Based on 5 Researches
8.6
9
CoQ10 reduces glioblastoma growth
CoQ reduces glioblastoma growth and infiltration through proteome remodeling and inhibition of angiogenesis and inflammation.
Direct impact on tumor hallmarks
The study focused on understanding how coenzyme Q10 (CoQ) could help manage glioblastoma, a particularly challenging type of brain tumor. We utilized xenograft models with U251 cells implanted in mice to observe tumor growth, inflammation, and vascular changes, alongside assessing the effects of CoQ on various related behaviors, including cell migration and invasion.
We found that CoQ treatment significantly reduced tumor volume in both xenograft and orthotopic models. Interestingly, while it did not directly hinder tumor cell proliferation, it was effective in creating a less hypoxic and vascularized environment. This indicates that CoQ can influence the tumor’s growth dynamics by targeting the underlying conditions that support tumor survival and expansion.
Additionally, CoQ treatment led to a noticeable downregulation of proteins involved in inflammation and angiogenesis, like HIF-1α and NF-kB. This change in molecular activity caused an entire reshaping of the tumor's protein landscape, ultimately impacting how the tumor interacts with its environment. Notably, we observed a restriction in tumor cell migration and invasion, attributed to changes in the cell's structural components.
Overall, our findings suggest that incorporating CoQ into current treatment protocols could provide a holistic approach to combat glioblastoma by simultaneously addressing multiple pathways that facilitate tumor growth and infiltration.
We found that CoQ treatment significantly reduced tumor volume in both xenograft and orthotopic models. Interestingly, while it did not directly hinder tumor cell proliferation, it was effective in creating a less hypoxic and vascularized environment. This indicates that CoQ can influence the tumor’s growth dynamics by targeting the underlying conditions that support tumor survival and expansion.
Additionally, CoQ treatment led to a noticeable downregulation of proteins involved in inflammation and angiogenesis, like HIF-1α and NF-kB. This change in molecular activity caused an entire reshaping of the tumor's protein landscape, ultimately impacting how the tumor interacts with its environment. Notably, we observed a restriction in tumor cell migration and invasion, attributed to changes in the cell's structural components.
Overall, our findings suggest that incorporating CoQ into current treatment protocols could provide a holistic approach to combat glioblastoma by simultaneously addressing multiple pathways that facilitate tumor growth and infiltration.
Read More
9
CoQ10 shows promise in glioblastoma
High levels of ubidecarenone (oxidized CoQ) delivered using a drug-lipid conjugate nanodispersion (BPM31510) differentially affect redox status and growth in malignant glioma versus non-tumor cells.
Study explores CoQ10 effectiveness
We investigated the effects of ubidecarenone, also known as Coenzyme Q10 (CoQ10), on brain tumors, particularly glioblastoma, which are notoriously difficult to treat. The study involved both rodent and human glioma cell lines and compared them with non-tumor cells.
Our findings revealed that the glioma cells showed a significant sensitivity to ubidecarenone compared to the non-tumor cells. This sensitivity was evident as we noted increased production of mitochondrial superoxide in tumor cells before any observable changes in their growth or cell cycle.
What's interesting is that in co-culture experiments, ubidecarenone was effective in creating a balance between tumor cells and non-tumor cells. In an aggressive in vivo glioma model, we observed more than a 25% long-term survival rate, suggesting that ubidecarenone could serve as a promising therapeutic tool.
Overall, our research highlights that delivering high levels of CoQ10 through a lipid-drug conjugate could selectively target cancer cells and exploit their unique metabolic vulnerabilities.
Our findings revealed that the glioma cells showed a significant sensitivity to ubidecarenone compared to the non-tumor cells. This sensitivity was evident as we noted increased production of mitochondrial superoxide in tumor cells before any observable changes in their growth or cell cycle.
What's interesting is that in co-culture experiments, ubidecarenone was effective in creating a balance between tumor cells and non-tumor cells. In an aggressive in vivo glioma model, we observed more than a 25% long-term survival rate, suggesting that ubidecarenone could serve as a promising therapeutic tool.
Overall, our research highlights that delivering high levels of CoQ10 through a lipid-drug conjugate could selectively target cancer cells and exploit their unique metabolic vulnerabilities.
Read More
9
CoQ10 improves brain tumor treatment
Modulation of Antioxidant Potential with Coenzyme Q10 Suppressed Invasion of Temozolomide-Resistant Rat Glioma and .
Combined effects of CoQ10 and TMZ
Our exploration of coenzyme Q10 (CoQ10) aimed to understand its role in improving the treatment of glioblastoma, particularly in cases resistant to standard therapies like temozolomide (TMZ). We worked with a specific rat glioma cell line known for its resistance to TMZ, heightened production of reactive oxygen species (ROS), and strong invasion capabilities.
Our findings revealed that combining CoQ10 with TMZ produced a stronger anti-cancer effect than using TMZ alone. The combination seemed to help CoQ10 act as a powerful scavenger of harmful ROS, leading to increased cell death in the glioma cells during tests, including advanced 3D models. This suggests that not only can CoQ10 help make tumors more sensitive to treatments, but it also supports the body's antioxidant defenses.
Furthermore, we observed that this combined treatment notably reduced the glioma's invasive nature. Tests showed a decrease in specific proteins linked to cancer spread and progression. These exciting results lead us to believe that CoQ10 could become an important addition to standard glioblastoma treatments, potentially contributing to better patient outcomes through its antioxidant properties.
Our findings revealed that combining CoQ10 with TMZ produced a stronger anti-cancer effect than using TMZ alone. The combination seemed to help CoQ10 act as a powerful scavenger of harmful ROS, leading to increased cell death in the glioma cells during tests, including advanced 3D models. This suggests that not only can CoQ10 help make tumors more sensitive to treatments, but it also supports the body's antioxidant defenses.
Furthermore, we observed that this combined treatment notably reduced the glioma's invasive nature. Tests showed a decrease in specific proteins linked to cancer spread and progression. These exciting results lead us to believe that CoQ10 could become an important addition to standard glioblastoma treatments, potentially contributing to better patient outcomes through its antioxidant properties.
Read More
9
CoQ boosts glioblastoma therapy effectiveness
Regulation of the oxidative balance with coenzyme Q10 sensitizes human glioblastoma cells to radiation and temozolomide.
Relevant research on glioblastoma treatment
We examined how coenzyme Q10 (CoQ), a natural antioxidant, affects the response of glioblastoma cells to radiation and chemotherapy, specifically temozolomide (TMZ). Using human glioblastoma cell lines, we loaded them with CoQ and assessed various parameters, including oxidative stress and cytotoxicity from treatments.
Our results showed that CoQ did not impact oxygen consumption but significantly reduced levels of harmful mitochondrial superoxides and hydrogen peroxide. This change shifted the cells into a more vulnerable state, which we linked to decreased activity of enzymes like catalase and a reduction in important metabolites crucial for antioxidant defenses.
When we treated glioblastoma cells with radiation and TMZ, those preloaded with CoQ exhibited double the sensitivity to DNA damage and apoptosis. Importantly, this sensitivity was observed without harming normal astrocytes, which suggests that CoQ could be a valuable adjunct in glioblastoma treatment, enhancing the effectiveness of existing therapies while sparing healthy cells.
Our results showed that CoQ did not impact oxygen consumption but significantly reduced levels of harmful mitochondrial superoxides and hydrogen peroxide. This change shifted the cells into a more vulnerable state, which we linked to decreased activity of enzymes like catalase and a reduction in important metabolites crucial for antioxidant defenses.
When we treated glioblastoma cells with radiation and TMZ, those preloaded with CoQ exhibited double the sensitivity to DNA damage and apoptosis. Importantly, this sensitivity was observed without harming normal astrocytes, which suggests that CoQ could be a valuable adjunct in glioblastoma treatment, enhancing the effectiveness of existing therapies while sparing healthy cells.
Read More
7
MitoQ inhibits glioma cell growth
Redox-crippled MitoQ potently inhibits breast cancer and glioma cell proliferation: A negative control for verifying the antioxidant mechanism of MitoQ in cancer and other oxidative pathologies.
Direct relevance to glioma research
We explored the effects of MitoQ, a mitochondria-targeted version of coenzyme Q10, on brain tumors, particularly glioma cells. The aim was to understand how this compound influences cell growth and whether its properties can help counteract the harmful effects of oxidative stress often found in cancer.
In our experiments, we compared MitoQ with a modified compound called DM-MitoQ, which lacks the ability to engage in redox cycling, a crucial mechanism that allows MitoQ to function as an antioxidant. Surprisingly, DM-MitoQ displayed slightly greater potency in inhibiting the proliferation of breast cancer and glioma cells than MitoQ itself.
Both compounds were shown to significantly reduce oxygen consumption related to mitochondrial function, suggesting that their interference with energy production might play a crucial role in restricting cancer cell growth. Thus, our study implies that targeting mitochondrial processes could be vital in developing treatments for tough-to-treat tumors like gliomas.
Ultimately, we concluded that MitoQ's inhibition of mitochondrial oxidative phosphorylation could be pivotal in limiting brain tumor growth and spread. The findings also suggest that using DM-MitoQ may help us better understand the role of free radical processes in other cancer-related conditions.
In our experiments, we compared MitoQ with a modified compound called DM-MitoQ, which lacks the ability to engage in redox cycling, a crucial mechanism that allows MitoQ to function as an antioxidant. Surprisingly, DM-MitoQ displayed slightly greater potency in inhibiting the proliferation of breast cancer and glioma cells than MitoQ itself.
Both compounds were shown to significantly reduce oxygen consumption related to mitochondrial function, suggesting that their interference with energy production might play a crucial role in restricting cancer cell growth. Thus, our study implies that targeting mitochondrial processes could be vital in developing treatments for tough-to-treat tumors like gliomas.
Ultimately, we concluded that MitoQ's inhibition of mitochondrial oxidative phosphorylation could be pivotal in limiting brain tumor growth and spread. The findings also suggest that using DM-MitoQ may help us better understand the role of free radical processes in other cancer-related conditions.
Read More
User Reviews
USERS' SCORE
Good
Based on 1 Review
8.5
8.8
Disease delay
My father has Paskin's disease. The doctor recommends this treatment to help delay its progression, though higher doses are necessary. For ongoing maintenance, a dosage of 200 can be taken, which may protect the heart and brain.
