Overview
SCIENTIFIC SCORE
Moderately Effective
Based on 7 Researches
8.7
USERS' SCORE
Good
Based on 23 Reviews
8.5
Supplement Facts
Serving Size: 1 Veg Capsule
Amount Per Serving
%DV
Potassium (from 310 mg Potassium Citrate)
99 mg
2%
Top Medical Research Studies
9
We explored the role of potassium in the inflammatory response to gout, specifically focusing on a potassium channel called TWIK2. This channel significantly contributes to the release of potassium ions, an important step in activating a particle known as the NLRP3 inflammasome, which triggers inflammation.
Our study examined the effects of a compound named ML335, known to modulate potassium channels, on inflammation caused by MSU crystals in gout. Notably, ML335 showed the best results among five tested compounds when it came to inhibiting potassium efflux through TWIK2. This means that ML335 can keep potassium levels balanced, making it a potential new treatment approach for gout.
In our investigations, we found that ML335 effectively limited the release of the inflammatory molecule IL-1β and prevented mitochondrial damage by blocking the expression of MARCH5, a protein that contributes to this injury. Through its actions, ML335 showed promise in improving mitochondrial function and reducing overall inflammation induced by MSU crystals, both in lab settings and in live animal models.
Overall, our findings suggest that targeting potassium channels, particularly using ML335, may pave the way for innovative treatments for gout, addressing both the inflammatory response and the associated cellular damage.
Our study examined the effects of a compound named ML335, known to modulate potassium channels, on inflammation caused by MSU crystals in gout. Notably, ML335 showed the best results among five tested compounds when it came to inhibiting potassium efflux through TWIK2. This means that ML335 can keep potassium levels balanced, making it a potential new treatment approach for gout.
In our investigations, we found that ML335 effectively limited the release of the inflammatory molecule IL-1β and prevented mitochondrial damage by blocking the expression of MARCH5, a protein that contributes to this injury. Through its actions, ML335 showed promise in improving mitochondrial function and reducing overall inflammation induced by MSU crystals, both in lab settings and in live animal models.
Overall, our findings suggest that targeting potassium channels, particularly using ML335, may pave the way for innovative treatments for gout, addressing both the inflammatory response and the associated cellular damage.
Read More
9
We aimed to understand the impact of potassium channel antagonists on inflammation associated with gout. Using specially designed models, we looked at how these antagonists affect levels of interleukin-1β (IL-1β), a key player in gout flare-ups.
In our experiments, we cultivated human macrophage cells to observe the effects of monosodium urate (MSU), which is known to trigger gout inflammation. We also treated these cells with potassium channel blockers like oxidized ATP (oATP) to examine their potential anti-inflammatory properties.
Our findings were promising, showing that oATP significantly reduced IL-1β production in lab tests. When we moved to in vivo models, we observed that treatment with oATP decreased inflammation and damage in the affected joints of mice. This suggests that potassium treatments could pave the way for new local therapies for gout.
Overall, this study highlights that potassium channel inhibitors, particularly oATP, could be beneficial in managing acute gout inflammation. However, it’s essential to continue exploring their direct effects and potential applications.
In our experiments, we cultivated human macrophage cells to observe the effects of monosodium urate (MSU), which is known to trigger gout inflammation. We also treated these cells with potassium channel blockers like oxidized ATP (oATP) to examine their potential anti-inflammatory properties.
Our findings were promising, showing that oATP significantly reduced IL-1β production in lab tests. When we moved to in vivo models, we observed that treatment with oATP decreased inflammation and damage in the affected joints of mice. This suggests that potassium treatments could pave the way for new local therapies for gout.
Overall, this study highlights that potassium channel inhibitors, particularly oATP, could be beneficial in managing acute gout inflammation. However, it’s essential to continue exploring their direct effects and potential applications.
Read More
9
We explored the effects of TCI227 in addressing hyperuricemia (HC), a condition closely linked to gout and other cardiovascular issues. To investigate this, we induced HC in male SD rats using potassium oxonate (PO) and then treated them with varying doses of TCI227 over four weeks.
Throughout the study, we meticulously measured organ weight and conducted biochemical analyses of blood and urine. Our findings revealed that TCI227 significantly improved body weight, reduced levels of creatinine and serum uric acid, and interestingly increased urinary uric acid compared to the HC group.
Moreover, TCI227 was found to enhance short-chain fatty acids (SCFAs), essential for gut health. When examining the fecal microbiota, TCI227 influenced the composition by increasing specific beneficial bacteria while reducing others that could be detrimental.
This suggests that TCI227 not only helps in managing HC but also positively alters gut microbiota in rats experiencing induced hyperuricemia. Overall, these results present an encouraging avenue for further research on TCI227’s potential in improving conditions related to gout.
Throughout the study, we meticulously measured organ weight and conducted biochemical analyses of blood and urine. Our findings revealed that TCI227 significantly improved body weight, reduced levels of creatinine and serum uric acid, and interestingly increased urinary uric acid compared to the HC group.
Moreover, TCI227 was found to enhance short-chain fatty acids (SCFAs), essential for gut health. When examining the fecal microbiota, TCI227 influenced the composition by increasing specific beneficial bacteria while reducing others that could be detrimental.
This suggests that TCI227 not only helps in managing HC but also positively alters gut microbiota in rats experiencing induced hyperuricemia. Overall, these results present an encouraging avenue for further research on TCI227’s potential in improving conditions related to gout.
Read More
Most Useful Reviews
9
Effective gout treatment
127 people found this helpful
Potassium citrate effectively treats gout and arrhythmias. Excellent quality.
Read More
9
Quick relief
16 people found this helpful
This worked better than expected. I began taking these after a severe gout flare-up. Within days, the pain from inflammation eased. This is genuinely the first remedy that worked this quickly. I highly recommend it to anyone suffering from gout; it's at least worth a try.
Read More
10
Reduced flare-ups
8 people found this helpful
I took this for gout relief after my research. It has worked wonders; I take 3 to 5 pills 2 to 3 times daily and haven’t had a flare-up in months. It has also reduced my leg cramps and lowered my blood pressure, so I no longer need medication.
Read More
Medical Researches
SCIENTIFIC SCORE
Moderately Effective
Based on 7 Researches
8.7
- All Researches
9
We explored the role of potassium in the inflammatory response to gout, specifically focusing on a potassium channel called TWIK2. This channel significantly contributes to the release of potassium ions, an important step in activating a particle known as the NLRP3 inflammasome, which triggers inflammation.
Our study examined the effects of a compound named ML335, known to modulate potassium channels, on inflammation caused by MSU crystals in gout. Notably, ML335 showed the best results among five tested compounds when it came to inhibiting potassium efflux through TWIK2. This means that ML335 can keep potassium levels balanced, making it a potential new treatment approach for gout.
In our investigations, we found that ML335 effectively limited the release of the inflammatory molecule IL-1β and prevented mitochondrial damage by blocking the expression of MARCH5, a protein that contributes to this injury. Through its actions, ML335 showed promise in improving mitochondrial function and reducing overall inflammation induced by MSU crystals, both in lab settings and in live animal models.
Overall, our findings suggest that targeting potassium channels, particularly using ML335, may pave the way for innovative treatments for gout, addressing both the inflammatory response and the associated cellular damage.
Our study examined the effects of a compound named ML335, known to modulate potassium channels, on inflammation caused by MSU crystals in gout. Notably, ML335 showed the best results among five tested compounds when it came to inhibiting potassium efflux through TWIK2. This means that ML335 can keep potassium levels balanced, making it a potential new treatment approach for gout.
In our investigations, we found that ML335 effectively limited the release of the inflammatory molecule IL-1β and prevented mitochondrial damage by blocking the expression of MARCH5, a protein that contributes to this injury. Through its actions, ML335 showed promise in improving mitochondrial function and reducing overall inflammation induced by MSU crystals, both in lab settings and in live animal models.
Overall, our findings suggest that targeting potassium channels, particularly using ML335, may pave the way for innovative treatments for gout, addressing both the inflammatory response and the associated cellular damage.
Read More
9
We developed a chronic mouse model of gout to dive deeper into the disease's mechanisms and effects. This model focuses on using potassium oxonate with a high-fat diet and additional acetic acid injections, marking a significant step away from traditional gout treatments that rely solely on monosodium urate (MSU) crystal injections.
Throughout a four-month period, we observed that mice in our model experienced significant arthritis progression, exhibiting increased joint damage and bone erosion. Notably, nearly 38% of these mice developed MSU crystal deposits in their paws, highlighting how closely our model simulates the human experience of gout.
We also explored how the treatment of benzbromarone could influence the disease's onset and severity. Encouragingly, we found that this treatment effectively halted the advancement of gout and prevented the formation of tophi in the mice.
While potassium was a key part of our methodology, it is essential to note that our findings reflect a more complex interaction of various treatments and conditions rather than isolating the effects of potassium alone.
Throughout a four-month period, we observed that mice in our model experienced significant arthritis progression, exhibiting increased joint damage and bone erosion. Notably, nearly 38% of these mice developed MSU crystal deposits in their paws, highlighting how closely our model simulates the human experience of gout.
We also explored how the treatment of benzbromarone could influence the disease's onset and severity. Encouragingly, we found that this treatment effectively halted the advancement of gout and prevented the formation of tophi in the mice.
While potassium was a key part of our methodology, it is essential to note that our findings reflect a more complex interaction of various treatments and conditions rather than isolating the effects of potassium alone.
Read More
9
We aimed to understand the impact of potassium channel antagonists on inflammation associated with gout. Using specially designed models, we looked at how these antagonists affect levels of interleukin-1β (IL-1β), a key player in gout flare-ups.
In our experiments, we cultivated human macrophage cells to observe the effects of monosodium urate (MSU), which is known to trigger gout inflammation. We also treated these cells with potassium channel blockers like oxidized ATP (oATP) to examine their potential anti-inflammatory properties.
Our findings were promising, showing that oATP significantly reduced IL-1β production in lab tests. When we moved to in vivo models, we observed that treatment with oATP decreased inflammation and damage in the affected joints of mice. This suggests that potassium treatments could pave the way for new local therapies for gout.
Overall, this study highlights that potassium channel inhibitors, particularly oATP, could be beneficial in managing acute gout inflammation. However, it’s essential to continue exploring their direct effects and potential applications.
In our experiments, we cultivated human macrophage cells to observe the effects of monosodium urate (MSU), which is known to trigger gout inflammation. We also treated these cells with potassium channel blockers like oxidized ATP (oATP) to examine their potential anti-inflammatory properties.
Our findings were promising, showing that oATP significantly reduced IL-1β production in lab tests. When we moved to in vivo models, we observed that treatment with oATP decreased inflammation and damage in the affected joints of mice. This suggests that potassium treatments could pave the way for new local therapies for gout.
Overall, this study highlights that potassium channel inhibitors, particularly oATP, could be beneficial in managing acute gout inflammation. However, it’s essential to continue exploring their direct effects and potential applications.
Read More
9
We set out to understand how potassium, through the use of kidney tea (KT), impacts uric acid levels in the body and consequently affects gout. In our study, we administered potassium oxonate to mice to induce hyperuricemia, a condition characterized by excess uric acid, similar to what people with gout experience.
After treatment with KT, we noticed significant reductions in uric acid levels and improvements in kidney function among the affected mice. Our analysis revealed that KT positively altered the gut microbiome by increasing beneficial bacteria while decreasing those potentially harmful to metabolic health.
Additionally, we observed a return to normal levels in various metabolites in both fecal and serum samples after KT administration. These findings indicate that potassium, via kidney tea, may aid in managing gout by regulating gut health and restoring metabolic balance. This establishes a foundation for further exploration of KT as a natural treatment for gout.
After treatment with KT, we noticed significant reductions in uric acid levels and improvements in kidney function among the affected mice. Our analysis revealed that KT positively altered the gut microbiome by increasing beneficial bacteria while decreasing those potentially harmful to metabolic health.
Additionally, we observed a return to normal levels in various metabolites in both fecal and serum samples after KT administration. These findings indicate that potassium, via kidney tea, may aid in managing gout by regulating gut health and restoring metabolic balance. This establishes a foundation for further exploration of KT as a natural treatment for gout.
Read More
9
We explored the effects of TCI227 in addressing hyperuricemia (HC), a condition closely linked to gout and other cardiovascular issues. To investigate this, we induced HC in male SD rats using potassium oxonate (PO) and then treated them with varying doses of TCI227 over four weeks.
Throughout the study, we meticulously measured organ weight and conducted biochemical analyses of blood and urine. Our findings revealed that TCI227 significantly improved body weight, reduced levels of creatinine and serum uric acid, and interestingly increased urinary uric acid compared to the HC group.
Moreover, TCI227 was found to enhance short-chain fatty acids (SCFAs), essential for gut health. When examining the fecal microbiota, TCI227 influenced the composition by increasing specific beneficial bacteria while reducing others that could be detrimental.
This suggests that TCI227 not only helps in managing HC but also positively alters gut microbiota in rats experiencing induced hyperuricemia. Overall, these results present an encouraging avenue for further research on TCI227’s potential in improving conditions related to gout.
Throughout the study, we meticulously measured organ weight and conducted biochemical analyses of blood and urine. Our findings revealed that TCI227 significantly improved body weight, reduced levels of creatinine and serum uric acid, and interestingly increased urinary uric acid compared to the HC group.
Moreover, TCI227 was found to enhance short-chain fatty acids (SCFAs), essential for gut health. When examining the fecal microbiota, TCI227 influenced the composition by increasing specific beneficial bacteria while reducing others that could be detrimental.
This suggests that TCI227 not only helps in managing HC but also positively alters gut microbiota in rats experiencing induced hyperuricemia. Overall, these results present an encouraging avenue for further research on TCI227’s potential in improving conditions related to gout.
Read More
User Reviews
USERS' SCORE
Good
Based on 23 Reviews
8.5
- All Reviews
- Positive Reviews
- Negative Reviews
9
Effective gout treatment
127 people found this helpful
Potassium citrate effectively treats gout and arrhythmias. Excellent quality.
Read More
9
Quick relief
16 people found this helpful
This worked better than expected. I began taking these after a severe gout flare-up. Within days, the pain from inflammation eased. This is genuinely the first remedy that worked this quickly. I highly recommend it to anyone suffering from gout; it's at least worth a try.
Read More
10
Reduced flare-ups
8 people found this helpful
I took this for gout relief after my research. It has worked wonders; I take 3 to 5 pills 2 to 3 times daily and haven’t had a flare-up in months. It has also reduced my leg cramps and lowered my blood pressure, so I no longer need medication.
Read More
9
Excellent supplement
6 people found this helpful
This product is excellent for gout.
Read More
9
Alkalises body
2 people found this helpful
Potassium citrate helps to alkalise the body, reduces gout, and assists the kidneys in excreting uric acid. It maintains normal fluid levels and is essential for proper muscle contraction and heart function.
Read More
Frequently Asked Questions
7.5
Lowered uric acid
32 people found this helpful
I began taking potassium citrate to prevent gout attacks and promote uric acid excretion. After six months, my uric acid levels decreased from 7.4 to 6.7! Although my doctor monitored my potassium due to high blood pressure, I felt a positive change.
10
Reduced flare-ups
8 people found this helpful
I took this for gout relief after my research. It has worked wonders; I take 3 to 5 pills 2 to 3 times daily and haven’t had a flare-up in months. It has also reduced my leg cramps and lowered my blood pressure, so I no longer need medication.
9
No flare-ups
1 people found this helpful
I bought these capsules to help my husband's gout. He hasn’t had any flare-ups since starting them, so they must be effective!
7.5
Pain reduction
4 people found this helpful
I’ve repurchased this product four times! The pills are convenient, and I’ve noticed a reduction in gout joint pain since taking it every day. I recommend it for those looking to lower uric acid levels.
9
Symptom relief
1 people found this helpful
This product has been a saviour for my gout symptoms. Using it has balanced my urine pH, and since then, I've experienced fewer gout recurrences. It is a highly effective supplement that I will repurchase.
9
Improved symptoms
5 people found this helpful
Potassium citrate is a well-absorbed form of potassium essential for various bodily functions. I noticed a difference in my gout symptoms after taking it alongside folic acid. The quality and packaging are commendable.
9
Pain reduction
These capsules help reduce gout pain. I had no pain after taking them, and I've managed to avoid gout despite consuming high-purine foods by using them alongside other supplements.
9
Effective substitute
3 people found this helpful
This is a reasonably priced product. I take 3-5 capsules daily after each meal, which has greatly relieved my gout pain and helped improve my body’s pH. I recommend consulting a doctor for severe gout cases.
6
Reduced symptoms
3 people found this helpful
I hope consuming potassium citrate will improve my health. It is affordable and suitable for gout patients, alleviating symptoms. However, the potassium per pill is low at 99 mg, requiring higher consumption, which can be inconvenient.
9
We explored the role of potassium in the inflammatory response to gout, specifically focusing on a potassium channel called TWIK2. This channel significantly contributes to the release of potassium ions, an important step in activating a particle known as the NLRP3 inflammasome, which triggers inflammation.
Our study examined the effects of a compound named ML335, known to modulate potassium channels, on inflammation caused by MSU crystals in gout. Notably, ML335 showed the best results among five tested compounds when it came to inhibiting potassium efflux through TWIK2. This means that ML335 can keep potassium levels balanced, making it a potential new treatment approach for gout.
In our investigations, we found that ML335 effectively limited the release of the inflammatory molecule IL-1β and prevented mitochondrial damage by blocking the expression of MARCH5, a protein that contributes to this injury. Through its actions, ML335 showed promise in improving mitochondrial function and reducing overall inflammation induced by MSU crystals, both in lab settings and in live animal models.
Overall, our findings suggest that targeting potassium channels, particularly using ML335, may pave the way for innovative treatments for gout, addressing both the inflammatory response and the associated cellular damage.
Our study examined the effects of a compound named ML335, known to modulate potassium channels, on inflammation caused by MSU crystals in gout. Notably, ML335 showed the best results among five tested compounds when it came to inhibiting potassium efflux through TWIK2. This means that ML335 can keep potassium levels balanced, making it a potential new treatment approach for gout.
In our investigations, we found that ML335 effectively limited the release of the inflammatory molecule IL-1β and prevented mitochondrial damage by blocking the expression of MARCH5, a protein that contributes to this injury. Through its actions, ML335 showed promise in improving mitochondrial function and reducing overall inflammation induced by MSU crystals, both in lab settings and in live animal models.
Overall, our findings suggest that targeting potassium channels, particularly using ML335, may pave the way for innovative treatments for gout, addressing both the inflammatory response and the associated cellular damage.
9
We aimed to understand the impact of potassium channel antagonists on inflammation associated with gout. Using specially designed models, we looked at how these antagonists affect levels of interleukin-1β (IL-1β), a key player in gout flare-ups.
In our experiments, we cultivated human macrophage cells to observe the effects of monosodium urate (MSU), which is known to trigger gout inflammation. We also treated these cells with potassium channel blockers like oxidized ATP (oATP) to examine their potential anti-inflammatory properties.
Our findings were promising, showing that oATP significantly reduced IL-1β production in lab tests. When we moved to in vivo models, we observed that treatment with oATP decreased inflammation and damage in the affected joints of mice. This suggests that potassium treatments could pave the way for new local therapies for gout.
Overall, this study highlights that potassium channel inhibitors, particularly oATP, could be beneficial in managing acute gout inflammation. However, it’s essential to continue exploring their direct effects and potential applications.
In our experiments, we cultivated human macrophage cells to observe the effects of monosodium urate (MSU), which is known to trigger gout inflammation. We also treated these cells with potassium channel blockers like oxidized ATP (oATP) to examine their potential anti-inflammatory properties.
Our findings were promising, showing that oATP significantly reduced IL-1β production in lab tests. When we moved to in vivo models, we observed that treatment with oATP decreased inflammation and damage in the affected joints of mice. This suggests that potassium treatments could pave the way for new local therapies for gout.
Overall, this study highlights that potassium channel inhibitors, particularly oATP, could be beneficial in managing acute gout inflammation. However, it’s essential to continue exploring their direct effects and potential applications.
References
- Song D, Zhou X, Yu Q, Li R, Dai Q, et al. ML335 inhibits TWIK2 channel-mediated potassium efflux and attenuates mitochondrial damage in MSU crystal-induced inflammation. J Transl Med. 2024;22:785. doi:10.1186/s12967-024-05303-7
- Wang J, Hao P, Sun X, Ward R, Tang T, et al. New animal model of chronic gout reproduces pathological features of the disease in humans. RMD Open. 2023;9. doi:10.1136/rmdopen-2023-003499
- Zhao Y, Li Z, Chen Y, Li Y, Lu J. Suppression of P2X7R by Local Treatment Alleviates Acute Gouty Inflammation. J Inflamm Res. 2023;16:3581. doi:10.2147/JIR.S421548
- Chen Y, Pei C, Chen Y, Xiao X, Zhang X, et al. Kidney tea ameliorates hyperuricemia in mice via altering gut microbiota and restoring metabolic profile. Chem Biol Interact. 2023;376:110449. doi:10.1016/j.cbi.2023.110449
- Huang KC, Chang YT, Pranata R, Cheng YH, Chen YC, et al. Alleviation of Hyperuricemia by Strictinin in AML12 Mouse Hepatocytes Treated with Xanthine and in Mice Treated with Potassium Oxonate. Biology (Basel). 2023;12. doi:10.3390/biology12020329
- Chien CY, Chien YJ, Lin YH, Lin YH, Chan ST, et al. Supplementation of (TCI227) Prevented Potassium-Oxonate-Induced Hyperuricemia in Rats. Nutrients. 2022;14. doi:10.3390/nu14224832
- Hao Q, Jiang L, Ma J, Wang H, Liu Y, et al. C. Z. Tang and S. J. Cheng can be prepared as a food with the ability to prevent and treat hyperuricaemia. Front Nutr. 2025;12:1518014. doi:10.3389/fnut.2025.1518014
