Benzbromarone
Uricosuric Agents
Gout Suppressants
Uric Acid
Sulfinpyrazone
Gout
Flurbiprofen
Hyperuricemia
Excessive URIC ACID or urate in blood as defined by its solubility in plasma at 37 degrees C; greater than 0.42mmol per liter (7.0mg/dL) in men or 0.36mmol per liter (6.0mg/dL) in women. This condition is caused by overproduction of uric acid or impaired renal clearance. Hyperuricemia can be acquired, drug-induced or genetically determined (LESCH-NYHAN SYNDROME). It is associated with HYPERTENSION and GOUT.
Allopurinol
Probenecid
The prototypical uricosuric agent. It inhibits the renal excretion of organic anions and reduces tubular reabsorption of urate. Probenecid has also been used to treat patients with renal impairment, and, because it reduces the renal tubular excretion of other drugs, has been used as an adjunct to antibacterial therapy.
Organic Cation Transport Proteins
Vinblastine and sulfinpyrazone export by the multidrug resistance protein MRP2 is associated with glutathione export. (1/40)
The multidrug resistance proteins MRP1 and MRP2 are members of the same subfamily of ATP-binding cassette transporters. Besides organic molecules conjugated to negatively charged ligands, these proteins also transport cytotoxic drugs for which no negatively charged conjugates are known to exist. In polarized MDCKII cells, MRP1 routes to the lateral plasma membrane, and MRP2 to the apical plasma membrane. In these cells MRP1 transports daunorubicin, and MRP2 vinblastine; both transporters export reduced glutathione (GSH) into the medium. We demonstrate that glutathione transport in MDCKII-MRP1 cells is inhibited by the inhibitors of organic anion transporters sulfinpyrazone, indomethacin, probenecid and benzbromarone. In MDCKII-MRP2 cells, GSH export is stimulated by low concentrations of sulfinpyrazone or indomethacin, whereas export is inhibited down to control levels at high concentrations. We find that unmodified sulfinpyrazone is a substrate for MRP2, also at concentrations where GSH export is inhibited. We also show that GSH export in MDCKII-MRP2 cells increases in the presence of vinblastine, and that the stoichiometry between drug and GSH exported is between two and three. Our data indicate that transport of sulfinpyrazone and vinblastine is associated with GSH export. However, at high sulfinpyrazone concentrations this compound is transported without GSH. Models of MRP action are discussed that could explain these results. (+info)Effect of urate-lowering therapy on the velocity of size reduction of tophi in chronic gout. (2/40)
OBJECTIVE: The optimal serum urate levels necessary for elimination of tissue deposits of monosodium urate in patients with chronic gout is controversial. This observational, prospective study evaluates the relationship between serum urate levels during therapy and the velocity of reduction of tophi in patients with chronic tophaceous gout. METHOD: Sixty-three patients with crystal-confirmed tophaceous gout were treated with allopurinol, benzbromarone, or combined therapy to achieve serum uric acid levels less than the threshold for saturation of urate in tissues. The tophi targeted for evaluation during followup were the largest in diameter found during physical examination. RESULTS: Patients taking benzbromarone alone or combined allopurinol and benzbromarone therapy achieved faster velocity of reduction of tophi than patients taking allopurinol alone. The velocity of tophi reduction was linearly related to the mean serum urate level during therapy. The lower the serum urate levels, the faster the velocity of tophi reduction. CONCLUSION: Serum urate levels should be lowered enough to promote dissolution of urate deposits in patients with tophaceous gout. Allopurinol and benzbromarone are equally effective when optimal serum urate levels are achieved during therapy. Combined therapy may be useful in patients who do not show enough reduction in serum urate levels with single-drug therapy. (+info)Effects of aspirin and/or salicylate on hydrolysis and glucuronidation of indomethacin in rat erythrocytes and hepatocytes. (3/40)
This study was conducted to explore the mechanism of the pharmacokinetic interaction between aspirin (ASP) and indomethacin (IND) using rat erythrocytes (RBCs) and hepatocytes. ASP was hydrolyzed to salicylic acid (SA) in both the RBCs and hepatocytes. Within RBCs, aspirin and/or salicylate (ASP/SA) increased the concentration of IND, accompanied by a constant hydrolysis of IND. In hepatocytes, a low dose of IND was subjected to glucuronidation rather than hydrolysis, and ASP/SA inhibited both the acylglucuronidation of IND and hydrolysis of IND glucuronide. A high dose of IND underwent hydrolysis with about double the glucuronidation, and ASP/SA decreased the ratio of hydrolysis to glucuronidation, accompanied by a loss of ASP, IND and their metabolites from the medium. Collectively, the results provide metabolic insight into the mechanism of drug-drug interaction between ASP/SA and IND in the hepatocytes and RBCs. (+info)A new class of CYP2C9 inhibitors: probing 2C9 specificity with high-affinity benzbromarone derivatives. (4/40)
Noncovalent forces, other than hydrophobic interactions, are important determinants of substrate bias exhibited by some cytochromes P450. The CYP2C9 pharmacophore is proposed to include either an anionic group or hydrogen bond donor in addition to its hydrophobic groups. By constructing analogs of benzbromarone, evidence supporting the existence of a 2C9 anion-binding site was revealed. A nonsubstituted phenol analog was determined to have a pKa of 8.4 and a Ki of 414 nM whereas those with dihalogenated benzoyl phenols had pKa values between 4.2 to 5.2 and Ki values as low as 1 nM. The nonhalogenated, nonionizable analog is the poorest binder at 796 nM. The Ki range covers around three orders of magnitude with even the weakest binder being a more potent inhibitor than 2C9 substrate phenytoin. Thus, benzbromarone derivatives represent a class of molecules with the potential to reveal more structural details of the 2C9 active site. (+info)A case of exercise-induced acute renal failure in a patient with idiopathic renal hypouricemia developed during antihypertensive therapy with losartan and trichlormethiazide. (5/40)
Exercise-induced acute renal failure (ARF) developed in a 45-year-old man during antihypertensive therapy with losartan and trichlormethiazide. The antihypertensive therapy was stopped and marked hypouricemia became apparent during improvement of his renal function. The daily urinary excretion of uric acid was normal and an increased fractional excretion of uric acid was observed. Renal biopsy revealed that the kidney was recovering from acute tubular necrosis with interstitial fibrosis. Based on the results of pyrazinamide and benzbromarone tests, we classified this case as one of presecretory reabsorption defect of uric acid. Antihypertesive therapy with benidipine and candesartan was initiated, and the patient has not had any ARF episodes since. Because idiopathic renal hypouricemia can be associated with exercise-induced ARF and chronic renal dysfunction, careful antihypertensive therapy and follow-up evaluation of renal function might be necessary for hypertensive patients with idiopathic renal hypouricemia. (+info)Circadian rhythm of plasma uric acid and handling stress-induced hyperuricemia in conscious cebus monkeys. (6/40)
An apparent circadian rhythm of plasma uric acid and the effect of handling stress on plasma uric acid level in conscious cebus monkeys were demonstrated. The lowest level of plasma uric acid in the circadian rhythm occurred early in the morning and the highest, before bedtime at night. With experimental handling stress, the plasma uric acid level rose to much more than the maximum level of the circadian rhythm. Stress-induced hyperuricemia could be inhibited without an increase of urinary uric acid excretion by the minor tranquilizer diazepam at doses of more than 1 mg/kg, p.o. On the other hand, benzbromarone at 20 mg/kg, p.o. significantly inhibited the hyperuricemia with a hyperuricosuric effect, while probenecid at 50 mg/kg, p.o. had no effect on either the increased plasma uric acid or urinary uric acid excretion. Accordingly, it is concluded that the plasma uric acid level in conscious cebus monkeys easily fluctuates with experimental conditions and that the animals can be utilized to evaluate the hypouricemic and hyperuricosuric property of benzbromarone-like agents. (+info)CYP2C9 genotype-dependent effects on in vitro drug-drug interactions: switching of benzbromarone effect from inhibition to activation in the CYP2C9.3 variant. (7/40)
The CYP2C9.3 variant exhibits marked decreases in substrate turnover compared with the wild-type enzyme, but little is known regarding the effect this variant form may have on the occurrence of drug-drug interactions. To examine this possibility, the effect of the potent CYP2C9 inhibitor, benzbromarone, was studied with regard to CYP2C9.1- and CYP2C9.3-mediated flurbiprofen metabolism to evaluate whether the variant enzyme exhibits differential inhibition kinetics. Although benzbromarone inhibited CYP2C9.1 activity as expected, CYP2C9.3-mediated flurbiprofen 4'-hydroxylation was activated in the presence of benzbromarone. T1 relaxation studies revealed little change in distances of flurbiprofen protons from the heme iron of either CYP2C9.1 or CYP2C9.3 in the presence of benzbromarone compared with flurbiprofen alone. Spectral binding studies were also performed to investigate whether benzbromarone affected substrate binding, with the addition of benzbromarone having little effect on flurbiprofen-binding affinity in both CYP2C9.1 and CYP2C9.3. Docking studies with the 2C9.1 structure crystallized with a closed active site identified multiple but overlapping subsites with sufficient space for benzbromarone binding in the enzyme when flurbiprofen was positioned closest to the heme. If the closed conformation of 2C9.3 is structurally similar to 2C9.1, as expected for the conservative I359L mutation, then the dynamics of benzbromarone binding may account for the switching of drug interaction effects. In conclusion, the I359L amino acid substitution found in CYP2C9.3 not only reduces metabolism compared with CYP2C9.1 but can also dramatically alter inhibitor effects, suggesting that differential degrees of drug inhibition interactions may occur in individuals with this variant form of CYP2C9. (+info)Prediction of CYP2C9-mediated drug-drug interactions: a comparison using data from recombinant enzymes and human hepatocytes. (8/40)
The IC50 values of 14 drugs were determined in recombinantly expressed CYP2C9 (rCYP2C9) and human hepatocytes and the data used to simulate clinical area under the plasma concentration-time curve (AUC) changes upon coadministration with prototypic CYP2C9 substrates. There was an excellent correlation between IC(50, apparent) values determined using diclofenac and naproxen as CYP2C9 substrates (r2 = 0.82, p < 0.0001), with values being generally higher in the naproxen assay. After correcting for nonspecific binding, the IC(50, unbound) values were similar between the assays, for the majority of compounds. Two compounds, amiodarone and benzbromarone, demonstrated substrate-specific differences, activating naproxen O-demethylase to approximately 250% of control activity at 1 mM and 1 microM, respectively, while inhibiting diclofenac 4'-hydroxylation with IC(50, apparent) values of 3 microM and 0.04 microM, respectively. CYP2C9 IC(50, apparent) values generated in human hepatocytes were systematically higher than those determined with rCYP2C9. After correcting for nonspecific binding, there was an excellent correlation of IC(50, unbound) values generated in the different milieu (r2 = 0.88, p < 0.0001). The ratio of inhibitor concentration at the entrance to the liver to the inhibition constant ([I]in/Ki) was used to simulate clinical deltaAUC changes and compared with that observed in vivo. Where [I]in, total/Ki, apparent) was used, there were zero false negatives (observed deltaAUC >or=2, predicted deltaAUC <2), eight correct assignations, and seven false positives (observed deltaAUC
Benzbromarone | CAS#3562-84-3 | MedKoo
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Probenecid and Colchicine
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Celivarone
Amiodarone Benzbromarone Benziodarone Budiodarone Dronedarone Gautier, P; Guillemare, E; Djandjighian, L; Marion, A; ...
Uricosuric
In some persons with loss-of-function mutations of URAT1, the uricosurics benzbromarone and losartan had no effect, suggesting ... The primary uricosuric drugs include probenecid, benzbromarone and sulfinpyrazone. Drugs with other primary uses, that have ...
Gout
... benzbromarone, and colchicine. Long term medications are not recommended until a person has had two attacks of gout, unless ...
Xanthine oxidase inhibitor
... benzbromarone". Drug Metabolism and Disposition. 33 (12): 1791-5. doi:10.1124/dmd.105.006056. PMID 16135657. S2CID 16377221. ...
Benziodarone
Amiodarone Benzbromarone, the brominated analogue of benziodarone, used as an uricosuric Dronedarone Pizzichini M, Aleo MF, ...
List of MeSH codes (D03)
... benzbromarone MeSH D03.438.127.125 - cantharidin MeSH D03.438.127.187 - citalopram MeSH D03.438.127.250 - fura-2 MeSH D03.438. ...
Hyperuricemia
... benzbromarone, benziodarone, probenecid, lesinurad, sulfinpyrazone, ethebencid, zoxazolamine, and ticrynafen) increase the ...
ATC code M04
... combinations M04AB01 Probenecid M04AB02 Sulfinpyrazone M04AB03 Benzbromarone M04AB04 Isobromindione M04AB05 Lesinurad M04AC01 ...
Budiodarone
Amiodarone Benzbromarone Benziodarone Celivarone Dronedarone Roy D, Talajic M, Dorian P, Connolly S, Eisenberg MJ, Green M, Kus ...
List of drugs: Be
Benzbromarone (INN) Benzedrex Benzestrol (INN) Benzethidine (INN) Benzethonium chloride (INN) Benzetimide (INN) Benzfetamine ( ...
Benzbromarone
... is highly effective and well tolerated, and clinical trials as early as 1981 and as recently as April 2008 have ... Benzbromarone is a very potent inhibitor of CYP2C9. Several analogues of the drug have been developed as CYP2C9 and CYP2C19 ... Benzbromarone was introduced in the 1970s and was viewed as having few associated serious adverse reactions. It was registered ... Benzbromarone is a uricosuric agent and non-competitive inhibitor of xanthine oxidase used in the treatment of gout, especially ...
Suramin
The most frequent adverse reactions are nausea, vomiting, diarrhea, abdominal pain, and a feeling of general discomfort. It is also common to experience various sensations in the skin, from crawling or tingling sensations, tenderness of palms and the soles, and numbness of hands, arm, legs or feet.[10] Other skin reactions include skin rash, swelling and stinging sensation.[10] Suramin can also cause loss of appetite and irritability.[10] Suramin causes non-harmful changes in urine during use, specifically making the urine cloudy.[10] It may exacerbate kidney disease.[11] Less common side effects include extreme fatigue, ulcers in the mouth, and painful tender glands in the neck, armpits and groin.[10] Suramin uncommonly affects the eyes causing watery eyes, swelling around the eyes, photophobia, and changes or loss of vision.[10] Rare side effects include hypersensitivity reactions causing difficulty breathing. Other rare systemic effects include decreased blood pressure, fever, rapid heart ...
അഡിനോസിൻ ഡൈഫോസ്ഫേറ്റ് - വിക്കിപീഡിയ
1/C10H15N5O10P2/c11-8-5-9(13-2-12-8)15(3-14-5)10-7(17)6(16)4(24-10)1-23-27(21,22)25-26(18,19)20/h2-4,6-7,10,16-17H,1H2,(H,21,22)(H2,11,12,13)(H2,18,19,20)/t4-,6-,7-,10-/m1/ ...
Benzbromarone - Wikipedia
Benzbromarone is highly effective and well tolerated, and clinical trials as early as 1981 and as recently as April 2008 have ... Benzbromarone is a very potent inhibitor of CYP2C9. Several analogues of the drug have been developed as CYP2C9 and CYP2C19 ... Benzbromarone was introduced in the 1970s and was viewed as having few associated serious adverse reactions. It was registered ... Benzbromarone is a uricosuric agent and non-competitive inhibitor of xanthine oxidase used in the treatment of gout, especially ...
Acute Intermittent Porphyria: Practice Essentials, Pathophysiology, Epidemiology
Acute intermittent porphyria (AIP) is one of the porphyrias, a group of diseases involving defects in heme metabolism and that results in excessive secretion of porphyrins and porphyrin precursors. AIP manifests itself by abdomen pain, neuropathies, and constipation, but, unlike most types of porphyria, patients with AIP do not have a rash.
Acute Intermittent Porphyria: Practice Essentials, Pathophysiology, Epidemiology
Acute intermittent porphyria (AIP) is one of the porphyrias, a group of diseases involving defects in heme metabolism and that results in excessive secretion of porphyrins and porphyrin precursors. AIP manifests itself by abdomen pain, neuropathies, and constipation, but, unlike most types of porphyria, patients with AIP do not have a rash.
Gout News - Index
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In the profiling of an in vivo single dose, benzbromarone and aspirin were located in the same cluster of the three PPARα ... The clustering of in vitro data revealed that benzbromarone, three NSAIDs (aspirin, indomethacin and diclofenac sodium) and ... benzbromarone- and aspirin-treated rat livers as well as rat hepatocytes, and for glutathione deficiency-related genes were ... valproic acid belonged to the same cluster of PPARα agonists, supporting the reports that benzbromarone,valproic acid and some ...
A Randomized Controlled Trial of Chuanhutongfeng Mixture for the Treatment of Chronic Gouty Arthritis by Regulating miRNAs
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Acute Intermittent Porphyria: Practice Essentials, Pathophysiology, Epidemiology
Acute intermittent porphyria (AIP) is one of the porphyrias, a group of diseases involving defects in heme metabolism and that results in excessive secretion of porphyrins and porphyrin precursors. AIP manifests itself by abdomen pain, neuropathies, and constipation, but, unlike most types of porphyria, patients with AIP do not have a rash.
Acute Intermittent Porphyria: Practice Essentials, Pathophysiology, Epidemiology
Acute intermittent porphyria (AIP) is one of the porphyrias, a group of diseases involving defects in heme metabolism and that results in excessive secretion of porphyrins and porphyrin precursors. AIP manifests itself by abdomen pain, neuropathies, and constipation, but, unlike most types of porphyria, patients with AIP do not have a rash.
Code System Concept
Acute Intermittent Porphyria: Practice Essentials, Pathophysiology, Epidemiology
Acute intermittent porphyria (AIP) is one of the porphyrias, a group of diseases involving defects in heme metabolism and that results in excessive secretion of porphyrins and porphyrin precursors. AIP manifests itself by abdomen pain, neuropathies, and constipation, but, unlike most types of porphyria, patients with AIP do not have a rash.
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Pharos : Target Details - SLC22A12
Required for efficient urate re-absorption in the kidney. Regulates blood urate levels. Mediates saturable urate uptake by facilitating the exchange of urate against organic anions. The protein encoded by this gene is a member of the organic anion transporter (OAT) family, and it acts as a urate transporter to regulate urate levels in blood. This protein is an integral membrane protein primarily found in epithelial cells of the proximal tubule of the kidney. An elevated level of serum urate, hyperuricemia, is associated with increased incidences of gout, and mutations in this gene cause renal hypouricemia type 1. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Jan 2013]
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Suramin - Wikipedia
The most frequent adverse reactions are nausea, vomiting, diarrhea, abdominal pain, and a feeling of general discomfort. It is also common to experience various sensations in the skin, from crawling or tingling sensations, tenderness of palms and the soles, and numbness of hands, arm, legs or feet.[10] Other skin reactions include skin rash, swelling and stinging sensation.[10] Suramin can also cause loss of appetite and irritability.[10] Suramin causes non-harmful changes in urine during use, specifically making the urine cloudy.[10] It may exacerbate kidney disease.[11] Less common side effects include extreme fatigue, ulcers in the mouth, and painful tender glands in the neck, armpits and groin.[10] Suramin uncommonly affects the eyes causing watery eyes, swelling around the eyes, photophobia, and changes or loss of vision.[10] Rare side effects include hypersensitivity reactions causing difficulty breathing. Other rare systemic effects include decreased blood pressure, fever, rapid heart ...
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PROBENECID
If Serum Uric Acid Level is ≤2.0 mg/dl, Should You Proceed to Investigate Hypouricemia? - CME INDIA
Allopurinol4
- Benzbromarone is a uricosuric agent and non-competitive inhibitor of xanthine oxidase used in the treatment of gout, especially when allopurinol, a first-line treatment, fails or produces intolerable adverse effects. (wikipedia.org)
- Benzbromarone is highly effective and well tolerated, and clinical trials as early as 1981 and as recently as April 2008 have suggested it is superior to both allopurinol, a non-uricosuric xanthine oxidase inhibitor, and probenecid, another uricosuric drug. (wikipedia.org)
- Efficacy of allopurinol and benzbromarone for the control of hyperuricaemia. (wikipedia.org)
- These urate lowering therapies (ULTs) include the xanthine oxidase inhibitors (allopurinol, febuxostat), medications that increase urate excretion (probenecid, benzbromarone, and lesinurad), and recombinant uricase (pegloticase), which breaks down urate to water-soluble allantoin. (hindawi.com)
Management of gout2
- Ten years' experience with benzbromarone in the management of gout and hyperuricaemia" (PDF). (wikipedia.org)
- Frequency of CYP2C9 polymorphisms in Polynesian people and potential relevance to management of gout with benzbromarone. (cdc.gov)
Uricosuric1
- Benzbromarone, a uricosuric medicine which is currently unapprovedin New Zealand, is to become available, fully subsidised, under Special Authority criteria from 1 voltaren w kapsulkach April, 2013. (kr.ua)
Inhibitor2
- Benzbromarone is a very potent inhibitor of CYP2C9. (wikipedia.org)
- therefore, (16) is definitely a C-ring methoxy analog of benzbromarone 1.11 Compound 16 was a much weaker inhibitor, ~47-fold (1.2 M versus 26 nM). (woofahs.com)
Gout3
- A benefit-risk assessment of benzbromarone in the treatment of gout. (wikipedia.org)
- Benzbromarone Tops Febuxostat for Gout? (medscape.com)
- In countries where available, low-dose benzbromarone may warrant stronger consideration in gout with renal uric acid underexcretion, researchers say. (medscape.com)
Probenecid2
- Further antihyperuricemic-guided purification of the fraction afforded three lignans, phyllanthin (1), hypophyllanthin (2) and phyltetralin (3), of which 1 significantly reversed the plasma uric acid level of hyperuricemic animals to its normal level in a dose-dependent manner, comparable to that of allopurinol, benzbromarone and probenecid which are used clinically for the treatment of hyperuricemia and gout. (nih.gov)
- Benzbromarone, probenecid, pravastatin, and diclofenac were able to inhibit both apical and basolateral calcein efflux. (ncl.ac.uk)
Patients3
- Here, we performed a cross-sectional survey of the implementation status of liver function tests in patients who were newly prescribed benzbromarone, using the Japanese large claims database. (elsevier.com)
- Male patients who were newly prescribed benzbromarone from January 2010 to December 2016 were included. (elsevier.com)
- We targeted patients who continued benzbromarone during the observation period (up to 180d from the start of administration). (elsevier.com)
Major2
- This graph shows the total number of publications written about "Benzbromarone" by people in Harvard Catalyst Profiles by year, and whether "Benzbromarone" was a major or minor topic of these publication. (harvard.edu)
- A major adverse effect of benzbromarone is hepatotoxicity. (elsevier.com)
Uric acid7
- Results from a randomized controlled trial conducted in China found low-dose benzbromarone to be more effective in lowering serum urate levels than low-dose febuxostat (Uloric), with a similar safety profile, in gout with renal uric acid underexcretion. (medscape.com)
- A total of 196 relatively young healthy men with gout and uric acid underexcretion were randomly assigned to receive low-dose benzbromarone (25 mg/d) or low-dose febuxostat (20 mg/d) for 12 weeks. (medscape.com)
- For most patients, benzbromarone is effective for those who have failed to achieve serum uric acid goals with allopurinol treatment. (medscape.com)
- There are many studies on the effect of uric acid lowering therapy on CV risk in gout patients, but few studies have compared allopurinol and benzbromarone. (acrabstracts.org)
- During the study period, patients who used uric acid lowering agents other than allopurinol and benzbromarone or who used both drugs in combination were also excluded from the study. (acrabstracts.org)
- Inhibitor of the renal urate transporter URAT1 with high selectivity to URAT1 over OAT1 and OAT3 in vitro (Ki values 0.057 µM, 7.2 µM, and 2.4 µM, respectively), capable of increasing the fractional excretion of urinary uric acid, and reducing plasma uric acid more effectively than Benzbromarone. (axonmedchem.com)
- The drug for excreting uric acid is benzbromarone. (zgxkx.org)
Hepatotoxicity1
- We did not find severe hepatotoxicity with low-dose benzbromarone, but ethnic background may affect drug responses, and severe hepatotoxicity of benzbromarone has rarely been reported in Asia," the authors write. (medscape.com)
Hepatotoxic2
- Benzbromarone is severely hepatotoxic in some individuals and unlikely to ever gain approval in the United States," one of the study's investigators, Robert Terkeltaub, MD, professor of medicine, University of California San Diego, told Medscape Medical News . (medscape.com)
- Using known hepatotoxic compounds (usnic acid, benzbromarone, tamoxifen, and acetaminophen) and compounds that have no reported human cases of liver toxicity (dimethyl sulfoxide, theophylline, and aminohippurate) the platform's performance was evaluated. (pubfacts.com)
Hyperuricemia1
- If there is only hyperuricemia, benzbromarone and febuxostat can be used. (zgxkx.org)
Verinurad1
- Therefore, this phenylalanine may be important in the high potency and specificity of benzbromarone and verinurad for hURAT1 (Tan et al . (iecnc.org)
Treatment1
- However, if there are urinary stones, benzbromarone can not be used for treatment, so we should also communicate with your doctor to fully improve the examination. (zgxkx.org)
Zealand1
- Benzbromarone is not approved in the United States because of concerns of acute liver injury but is approved in several other countries, including China, Brazil, and New Zealand. (medscape.com)