Uricosuric that acts by increasing uric acid clearance. It is used in the treatment of gout.
Gout suppressants that act directly on the renal tubule to increase the excretion of uric acid, thus reducing its concentrations in plasma.
A xanthine oxidase inhibitor.
Agents that increase uric acid excretion by the kidney (URICOSURIC AGENTS), decrease uric acid production (antihyperuricemics), or alleviate the pain and inflammation of acute attacks of gout.
An oxidation product, via XANTHINE OXIDASE, of oxypurines such as XANTHINE and HYPOXANTHINE. It is the final oxidation product of purine catabolism in humans and primates, whereas in most other mammals URATE OXIDASE further oxidizes it to ALLANTOIN.
A uricosuric drug that is used to reduce the serum urate levels in gout therapy. It lacks anti-inflammatory, analgesic, and diuretic properties.
Hereditary metabolic disorder characterized by recurrent acute arthritis, hyperuricemia and deposition of sodium urate in and around the joints, sometimes with formation of uric acid calculi.
An anti-inflammatory analgesic and antipyretic of the phenylalkynoic acid series. It has been shown to reduce bone resorption in periodontal disease by inhibiting CARBONIC ANHYDRASE.
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.
A XANTHINE OXIDASE inhibitor that decreases URIC ACID production. It also acts as an antimetabolite on some simpler organisms.
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.
A pyrazine that is used therapeutically as an antitubercular agent.
A family of proteins involved in the transport of organic cations. They play an important role in the elimination of a variety of endogenous substances, xenobiotics, and their metabolites from the body.
Proteins involved in the transport of organic anions. They play an important role in the elimination of a variety of endogenous substances, xenobiotics and their metabolites from the body.

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 2. Where [I]in, unbound/Ki, unbound was used, there was one false negative, 14 correct assignations, and zero false positives. In summary, the data presented here suggest that for CYP2C9 interactions, the use of total liver inhibitor concentrations may indeed avoid false negatives, but more realistic predictions may be achieved using unbound liver inhibitor concentrations and unbound in vitro inhibition parameters.  (+info)

Benzbromarone is a medication that was previously used to treat gout and hyperuricemia (elevated levels of uric acid in the blood). It works by increasing the excretion of uric acid through the kidneys. However, due to concerns about its potential hepatotoxicity (liver toxicity), it is no longer widely used and has been discontinued or restricted in many countries.

The chemical structure of benzbromarone is characterized by a benzene ring substituted with bromine and a propylamino group, which is further substituted with a carbamoyl group. This gives the compound its unique properties as a uricosuric agent.

It's important to note that benzbromarone should only be used under the supervision of a healthcare professional, and patients should be closely monitored for signs of liver toxicity. Additionally, there are many alternative medications available to treat gout and hyperuricemia, so benzbromarone is typically reserved for use in specific cases where other treatments have failed or are contraindicated.

Uricosuric agents are a class of medications that work by increasing the excretion of uric acid through the kidneys, thereby reducing the levels of uric acid in the blood. This helps to prevent the formation of uric acid crystals, which can cause joint inflammation and damage leading to conditions such as gout.

Uricosuric agents achieve this effect by inhibiting the reabsorption of uric acid in the kidney tubules or by increasing its secretion into the urine. Examples of uricosuric agents include probenecid, sulfinpyrazone, and benzbromarone. These medications are typically used to manage chronic gout and hyperuricemia (elevated levels of uric acid in the blood). It is important to note that uricosuric agents may increase the risk of kidney stones due to increased excretion of uric acid in the urine, so it is essential to maintain adequate hydration while taking these medications.

Oxypurinol is not exactly a medical term itself, but it's the main metabolite (a substance that your body makes when it breaks down another substance) of allopurinol, which is a medication commonly used to treat gout and kidney stones. Allopurinol works by reducing the production of uric acid in your body, and oxypurinol helps to continue this effect even after the allopurinol has been metabolized.

So, in a broader medical context, you could define Oxypurinol as:

The primary active metabolite of allopurinol, a medication used to lower uric acid levels in the body, preventing gout attacks and kidney stone formation. Oxypurinol inhibits the enzyme xanthine oxidase, which is responsible for the production of uric acid, thereby reducing the risk of gout and kidney stones.

Gout suppressants are a type of medication used to treat acute gout attacks and reduce the risk of future episodes. They work by decreasing the production of uric acid in the body or improving its elimination, thereby reducing the formation of uric acid crystals that cause inflammation and pain in the joints. Common examples of gout suppressants include:

1. Colchicine: This medication is often used to treat acute gout attacks by reducing inflammation and swelling in the affected joint. It should be taken as soon as possible after the onset of symptoms for best results.

2. Nonsteroidal anti-inflammatory drugs (NSAIDs): These medications, such as ibuprofen, naproxen, and celecoxib, can help alleviate pain and inflammation during an acute gout attack. They are usually more effective when taken at the first sign of an attack.

3. Corticosteroids: In some cases, corticosteroid medications like prednisone may be prescribed to treat severe gout attacks that do not respond to other treatments. These drugs can be administered orally or injected directly into the affected joint.

4. Allopurinol and febuxostat: These medications are called xanthine oxidase inhibitors, which reduce uric acid production in the body. They are typically used for chronic gout management to prevent future attacks and lower the risk of complications such as kidney stones and joint damage.

It is important to note that some gout suppressants may have side effects or interact with other medications, so it is crucial to discuss any concerns with a healthcare provider before starting treatment. Additionally, lifestyle changes such as maintaining a healthy weight, following a low-purine diet, and staying hydrated can help manage gout symptoms and lower the risk of future attacks.

Uric acid is a chemical compound that is formed when the body breaks down purines, which are substances that are found naturally in certain foods such as steak, organ meats and seafood, as well as in our own cells. After purines are broken down, they turn into uric acid and then get excreted from the body in the urine.

However, if there is too much uric acid in the body, it can lead to a condition called hyperuricemia. High levels of uric acid can cause gout, which is a type of arthritis that causes painful swelling and inflammation in the joints, especially in the big toe. Uric acid can also form crystals that can collect in the kidneys and lead to kidney stones.

It's important for individuals with gout or recurrent kidney stones to monitor their uric acid levels and follow a treatment plan prescribed by their healthcare provider, which may include medications to lower uric acid levels and dietary modifications.

Sulfinpyrazone is a medication that belongs to the class of drugs known as uricosurics. It works by increasing the amount of uric acid that is removed from the body through urine, which helps to lower the levels of uric acid in the blood. This makes it useful for the treatment of conditions such as gout and kidney stones that are caused by high levels of uric acid.

In addition to its uricosuric effects, sulfinpyrazone also has antiplatelet properties, which means that it can help to prevent blood clots from forming. This makes it useful for the prevention of heart attacks and strokes in people who are at risk.

Sulfinpyrazone is available by prescription and is typically taken by mouth in the form of tablets. It may be used alone or in combination with other medications, depending on the individual patient's needs and medical condition. As with any medication, sulfinpyrazone should be used under the supervision of a healthcare provider, and patients should follow their provider's instructions carefully to ensure safe and effective use.

Gout is a type of inflammatory arthritis that occurs when urate crystals accumulate in and around the joints, causing sudden attacks of severe pain, swelling, redness, and tenderness. Urate crystals can form when there are high levels of uric acid in the blood. Uric acid is a waste product that is produced when the body breaks down purines, substances that are found naturally in certain foods, such as steak, organ meats, and seafood. Other foods also promote higher levels of uric acid, such as alcoholic beverages, especially beer, and drinks sweetened with fruit sugar (fructose).

Normally, uric acid dissolves in the blood and passes through the kidneys and out of the body in urine. But sometimes either the body produces too much uric acid or the kidneys excrete too little uric acid. When this happens, uric acid can build up, forming sharp, needle-like urate crystals in a joint or surrounding tissue that cause pain, inflammation and swelling.

Gout most commonly affects the big toe but can also occur in any joint in the body. The symptoms of gout are often acute, occurring suddenly without warning and frequently at night. The attacks are characterized by a rapid onset of pain, swelling, warmth, and redness in the affected joint. An attack of gout can be so painful that it wakes you up from sleep.

Over time, gout can cause permanent damage to the joints and surrounding tissue, resulting in chronic arthritis. If left untreated, gout also can lead to an accumulation of uric acid crystals in the kidneys, which can result in kidney stones.

Flurbiprofen is a non-steroidal anti-inflammatory drug (NSAID) that is commonly used to treat pain, inflammation, and fever. It works by inhibiting the activity of cyclooxygenase (COX) enzymes, which are involved in the production of prostaglandins, chemicals that contribute to inflammation and pain.

Flurbiprofen is available in various forms, including tablets, capsules, and topical creams or gels. It is used to treat a variety of conditions, such as arthritis, menstrual cramps, dental pain, and migraines.

Like other NSAIDs, flurbiprofen can cause side effects, such as stomach ulcers, bleeding, and kidney problems, especially when taken in high doses or for long periods of time. It is important to follow the recommended dosage and consult with a healthcare provider before taking this medication.

Hyperuricemia is a medical condition characterized by an excessively high level of uric acid in the blood. Uric acid is a waste product that's produced when the body breaks down purines, which are substances found in certain foods and drinks, such as red meat, seafood, and alcoholic beverages. Normally, uric acid is dissolved in the blood and then excreted by the kidneys through urine. However, if there's too much uric acid in the body or if the kidneys can't eliminate it efficiently, it can build up in the blood, leading to hyperuricemia.

Mild cases of hyperuricemia may not cause any symptoms and may not require treatment. However, high levels of uric acid can lead to the formation of uric acid crystals, which can accumulate in the joints and tissues, causing inflammation and pain. This condition is known as gout. Hyperuricemia can also increase the risk of developing kidney stones and kidney disease.

Hyperuricemia can be caused by several factors, including a diet high in purines, genetic factors, kidney disease, certain medications, and conditions that cause rapid cell turnover, such as cancer or psoriasis. Treatment for hyperuricemia typically involves lifestyle changes, such as reducing the intake of purine-rich foods and beverages, maintaining a healthy weight, and staying hydrated. Medications may also be prescribed to lower uric acid levels in the blood and prevent gout attacks.

Allopurinol is a medication used to treat chronic gout and certain types of kidney stones. It works by reducing the production of uric acid in the body, which is the substance that can cause these conditions when it builds up in high levels. Allopurinol is a xanthine oxidase inhibitor, meaning it blocks an enzyme called xanthine oxidase from converting purines into uric acid. By doing this, allopurinol helps to lower the levels of uric acid in the body and prevent the formation of new kidney stones or gout attacks.

It is important to note that allopurinol can have side effects, including rash, stomach upset, and liver or kidney problems. It may also interact with other medications, so it is essential to inform your healthcare provider of any other drugs you are taking before starting allopurinol. Your healthcare provider will determine the appropriate dosage and monitoring schedule based on your individual needs and medical history.

Probenecid is a medication that is primarily used to treat gout and hyperuricemia (high levels of uric acid in the blood). It works by decreasing the production of uric acid in the body and increasing its excretion through the kidneys.

In medical terms, probenecid is a uricosuric agent, which means it increases the urinary excretion of urate, the salt form of uric acid. It does this by inhibiting the reabsorption of urate in the proximal tubules of the kidneys, thereby promoting its elimination in the urine.

Probenecid is also used in conjunction with certain antibiotics, such as penicillin and cephalosporins, to increase their concentration in the body by reducing their excretion by the kidneys. This is known as probenecid-antibiotic interaction.

It's important to note that probenecid should be used under the supervision of a healthcare provider, and its use may be contraindicated in certain medical conditions or in combination with specific medications.

Pyrazinamide is an antituberculosis agent, a type of medication used to treat tuberculosis (TB) caused by Mycobacterium tuberculosis. It is an antimicrobial drug that works by inhibiting the growth of the bacterium. Pyrazinamide is often used in combination with other TB drugs such as isoniazid, rifampin, and ethambutol.

The medical definition of Pyrazinamide is: a synthetic antituberculosis agent, C6H5N3O (a pyridine derivative), used in the treatment of tuberculosis, especially in combination with isoniazid and rifampin. It is converted in the body to its active form, pyrazinoic acid, which inhibits the growth of Mycobacterium tuberculosis by interfering with bacterial cell wall synthesis.

It's important to note that Pyrazinamide should be used under the supervision of a healthcare professional and is usually prescribed for several months to ensure complete eradication of the TB bacteria. As with any medication, it can cause side effects, and individuals should report any unusual symptoms to their healthcare provider.

Organic cation transport proteins (OCTs) are a group of membrane transporters that facilitate the movement of organic cations across biological membranes. These transporters play an essential role in the absorption, distribution, and elimination of various endogenous and exogenous substances, including drugs and toxins.

There are four main types of OCTs, namely OCT1, OCT2, OCT3, and OCTN1 (also known as novel organic cation transporter 1 or OCT6). These proteins belong to the solute carrier (SLC) family, specifically SLC22A.

OCTs have a broad substrate specificity and can transport various organic cations, such as neurotransmitters (e.g., serotonin, dopamine, histamine), endogenous compounds (e.g., creatinine, choline), and drugs (e.g., metformin, quinidine, morphine). The transport process is typically sodium-independent and can occur in both directions, depending on the concentration gradient of the substrate.

OCTs are widely expressed in various tissues, including the liver, kidney, intestine, brain, heart, and placenta. Their expression patterns and functions vary among different OCT types, contributing to their diverse roles in physiology and pharmacology. Dysfunction of OCTs has been implicated in several diseases, such as drug toxicity, neurodegenerative disorders, and cancer.

In summary, organic cation transport proteins are membrane transporters that facilitate the movement of organic cations across biological membranes, playing crucial roles in the absorption, distribution, and elimination of various substances, including drugs and toxins.

Organic anion transporters (OATs) are membrane transport proteins that are responsible for the cellular uptake and excretion of various organic anions, such as drugs, toxins, and endogenous metabolites. They are found in various tissues, including the kidney, liver, and brain, where they play important roles in the elimination and detoxification of xenobiotics and endogenous compounds.

In the kidney, OATs are located in the basolateral membrane of renal tubular epithelial cells and mediate the uptake of organic anions from the blood into the cells. From there, the anions can be further transported into the urine by other transporters located in the apical membrane. In the liver, OATs are expressed in the sinusoidal membrane of hepatocytes and facilitate the uptake of organic anions from the blood into the liver cells for metabolism and excretion.

There are several isoforms of OATs that have been identified, each with distinct substrate specificities and tissue distributions. Mutations in OAT genes can lead to various diseases, including renal tubular acidosis, hypercalciuria, and drug toxicity. Therefore, understanding the function and regulation of OATs is important for developing strategies to improve drug delivery and reduce adverse drug reactions.

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