CA IX/carbonic anhydrase (IC50 = 30 nM)
Carbonic anhydrases (CAs), including CAIX (pan-CA inhibitor) [2]

Acetazolamide also inhibits hCA II with an IC50 of 130 nM[1]. As a tiny heteroaromatic sulfonamide, acetazolamide (Ace) binds to several carbonic anhydrases with great affinity and inhibits the activity of carbonic anhydrases (CAs)[2]. The treatments with high Acetazolamide concentration (AceH, 50 nM), Cisplatin (Cis; 1 μg/mL), and Cis in combination with low Acetazolamide concentration (AceL, 10 nM) greatly decreased the viability of Hep-2 cells in comparison to the control group[2]. P53 expression levels are markedly elevated upon treatment with the Acetazolamide/Cis combination, as seen by the significantly higher P53 protein expression levels following both AceL+Cis and AceH+Cis treatments in comparison to the control group. Comparing the Ace/Cis combo treatment to the control group, it reduces the bcl-2/bax expression ratio considerably and enhances the expression of the caspase-3 protein. When compared to the control group, the AceL, AceH, Cis, and AceL+Cis therapies dramatically lower the bcl-2/bax ratio[2]. Hep-2 cell apoptosis is efficiently promoted by combined Ace and Cis treatment[2]. The expression of AQP1 mRNA in Hep-2 cells is significantly reduced by combined Ace/Cis therapy. In Hep-2 cells, the AceH and AceL+Cis treatments both reduce the expression of aquaporin-1 (AQP1) mRNA in comparison to the control group[2].

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Acetazolamide (AZ) , MS-275 and AZ + MS-275 treatments inhibit growth of NB SH-SY5Y cells.
AZ, MS-275 and AZ + MS-275 treatments reduced migration capacity in NB SH-SY5Y cells.
Results: We evaluated the antitumor potential of the HDAC inhibitor (HDACi), pyridylmethyl-N-{4-[(2-aminophenyl)-carbamoyl]-benzyl}-carbamate (MS-275) in combination with a pan CA inhibitor, acetazolamide (AZ) on NB SH-SY5Y, SK-N-SH and SK-N-BE(2) cells. The key observation was that the combination AZ + MS-275 significantly inhibited growth, induced cell cycle arrest and apoptosis, and reduced migration capacity of NB cell line SH-SY5Y. [2]

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The aim of the present study was to determine whether acetazolamide (Ace) treatment enhances the chemosensitivity of Hep-2 laryngeal cells to cisplatin (Cis). At the logarithmic growth phase, Hep-2 cells were treated with Ace, Cis or both, and cell viability was detected using an MTT assay. The degree of apoptosis was detected using flow cytometry. Expression levels of apoptosis-related proteins, including BCL2 apoptosis regulator (bcl-2), BCL2 associated X (bax) and caspase-3, and of proliferation-related proteins, including proliferating cell nuclear antigen (PCNA) and tumor protein p53 (P53), were detected using western blotting. mRNA expression levels of aquaporin-1 (AQP1) in each group were detected using reverse transcription-polymerase chain reaction. Compared with the drugs used alone, treatment with both Ace and Cis displayed synergistic effects on the growth inhibition and apoptosis induction in Hep-2 cells. The Ace/Cis combination decreased the expression of PCNA but increased the expression of p53. In addition, the combination treatment decreased the ratio of bcl-2/bax and increased the expression of caspase-3, as well as decreased the expression of AQP1. These results demonstrated that the combined use of Ace and Cis enhanced the chemosensitivity of laryngeal carcinoma cells.[3]

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Acetazolamide (AZ), at concentrations of 10-160 μM, reduced the viability of neuroblastoma (NB) cell lines SH-SY5Y, SK-N-SH, and SK-N-BE(2) in a dose-dependent manner. The IC50 values for AZ alone were: SH-SY5Y = 45 μM, SK-N-SH = 42 μM, SK-N-BE(2) = 49 μM. When combined with MS-275, the IC50 values for the combination were lower: SH-SY5Y = 17.5 μM, SK-N-SH = 16.5 μM, SK-N-BE(2) = 19.2 μM. [2]
Acetazolamide treatment (40 μM) increased the proportion of SH-SY5Y cells in SubG0 phase (0.6%) and decreased cells in S phase (13%) and G2/M phase (6%). It also reduced the expression of cyclin D1 and CDK4. [2]
Acetazolamide (40 μM) inhibited the migration of SH-SY5Y cells by 10% at 48 h and 12% at 72 h in a wound healing assay. [2]
Acetazolamide reduced the clonogenic potential of SH-SY5Y cells in methylcellulose assays. [2]
Acetazolamide treatment reduced the expression of HIF-1α and CAIX in NB xenografts, as shown by immunohistochemistry. [2]

In neuroblastoma (NB) SH-SY5Y xenografts, acetazolamide (40 mg/kg) greatly amplifies the inhibitory effect of MS-275 on tumorigenesis[3]. ? In NB SH-SY5Y xenografts, acetazolamide (40 mg/kg) and/or MS-275 therapy decrease HIF1-α and CAIX expression[3]. ? In NB SH-SY5Y xenografts, the expression of mitotic and proliferative markers is decreased by acetazolamide (40 mg/kg), MS-275, and acetazolamide+MS-275[3]. ? The gonococcal load in the vagina of infected mice is dramatically reduced by 90% when acetazolamide (50 mg/kg; PO) is administered for three days[6].

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Gonococcal infections represent an urgent public health threat worldwide due to the increasing incidence of infections that has been accompanied by an increase in bacterial resistance to most antibiotics. This has resulted in a dwindling number of effective treatment options. Undoubtedly, there is a critical need to develop new, effective anti-gonococcal agents. In an effort to discover new anti-gonococcal therapeutics, we previously identified Acetazolamide, a carbonic anhydrase inhibitor, as a novel inhibitor of Neisseria gonorrhoeae. Acetazolamide exhibited potent anti-gonococcal activity in vitro as it inhibited growth of strains of N. gonorrhoeae at concentrations that ranged from 0.5 to 4 μg/mL. The aim of this study was to investigate the in vivo efficacy of acetazolamide in a mouse model of N. gonorrhoeae genital tract infection. Compared to vehicle-treated mice, acetazolamide significantly reduced the gonococcal burden by 90% in the vagina of infected mice after three days of treatment. These results indicate that acetazolamide warrants further investigation as a promising treatment option to supplement the limited pipeline of anti-gonococcal therapeutics.[6]

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In a mouse model of N. gonorrhoeae genital tract infection, oral administration of acetazolamide (50 mg/kg) for three consecutive days significantly reduced the gonococcal burden in the vagina by approximately 90% (1.0-log10 reduction) compared to vehicle-treated mice [6]

AlamarBlue cytotoxicity assay [2]
Standard protocol was performed as describe. Percent survival vs. control (DMSO- 0.2x10−4μM) of cells when treated with Acetazolamide (AZ) , MS-275 and AZ + MS-275 were observed using AlamarBlue agent agent (10% of total volume) was added to each well for 4 h before fluorometric detection. Fluorescence was measured using the SPECTRAmax Gemini Spectrophotometer (excitation 540 nm; emission 590 nm).

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Propidium Iodide cell cycle assay [2]
Briefly, 2 × 106 cells treated with Acetazolamide (AZ) and/or MS-275 were lifted by citrate saline and fixed in 80% ice-cold ethanol for 48 h. Cells were then pelleted and re-suspended in 2 mg/mL RNase A for 5 min. A 0.1 mg/mL propidium iodide solution was added, incubated for 30 min at RT, and cells filtered through a cell-strainer into a 5 mL polystyrene tube. Labeled cells were analyzed on a BD FACSCAN flow cytometer. Data was fitted by the Watson-Pragmatic model on FlowJo Software.

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Wound healing assay [2]
SH-SY5Y cells were seeded in a 48-well plate on glass cover slips and allowed to adhere overnight at a density of 105 cells/well in 500 μl culture medium in triplicate. Wells were marked with a straight black line on the bottom for orientation. At the time of 90% confluence, cell monolayers were scratched with a 200 μl pipette tip using the marker guide. Loosened non-adherent cells were washed off with medium. Fresh medium was added to the cultures with additions of Acetazolamide (AZ) (10 μM, 20 μM, 40 μM) and MS-275 (0.75 μM, 1.5 μM and 3 μM) and cultured for 48 h. After the 48 h period cells were washed with PBS and fixed in 4% paraformaldehyde. After three washes in PBS, cells were stained with 1% Crystal violet in 20% methanol. Phase contrast light microscopic images (10x original magnification) were taken at time points of 0, 48 and 72 h of treatment. Migrated cells were counted manually to quantify numbers of cells migrated to wound area using NIH Image J program. Each experiment was conducted three times in triplicate and one representative assay is shown.

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For the drug treatments, Hep-2 cells were treated with Acetazolamide (ACE) (a low concentration of 1×10−8 mol/l, termed here Acetazolamide (ACE)L; or a high concentration of 5×10−8 mol/l, termed here AceH), Cis (1 µg/ml) alone, or Cis in combination with Ace (AceL+Cis, or AceH+Cis) for 48 h. Cells that were treated with equal volumes of vehicle were used as control. Ace was used at 1×10−8 or 5×10−8 mol/l in all experiments. Cis was used at 1 µg/ml in all experiments. Both Cis and Ace were dissolved in dimethyl sulfoxide (DMSO) and then added to PBS to dilute to the final working concentrations. The final concentration of DMSO in cultures did not exceed 0.5%. HUVECs were treated with AceH alone, Cis alone or in combination (AceH+Cis) or control (vehicle) for 48 h.[3]

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Annexin V apoptosis assay [3]
Quantification of apoptotic cells was performed by Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) double staining using a FITC-Annexin V Apoptosis Detection kit. At the logarithmic growth phase, Hep-2 cells were placed in 6-well plates. The cells were treated with Acetazolamide (ACE)L, AceH, Cis, AceL+Cis, AceH+Cis, or vehicle for 48 h. Then, cells were washed in PBS, digested with trypsin, and resuspended in calcium-enriched HEPES buffer. This suspension was stained with Annexin V-FITC and PI for 15 min, as per the manufacturer's instructions. Finally, the cells were analyzed by FlowJo software.

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Cell viability was assessed using MTT assay. Hep-2 cells were plated in 96-well plates and treated with Acetazolamide (AceL: 1×10⁻⁸ mol/L, AceH: 5×10⁻⁸ mol/L), cisplatin (1 µg/ml), or their combinations for 48 h. MTT solution (5 mg/ml) was added and incubated for 4 h, followed by DMSO addition. Optical density was measured at 490 nm. [3]
Apoptosis was assessed by Annexin V-FITC/PI staining using flow cytometry. Hep-2 cells were treated with drugs for 48 h, then stained with Annexin V-FITC and PI for 15 min and analyzed by flow cytometry. [3]
Western blotting was performed to detect protein expression. After drug treatment for 48 h, cells were lysed, proteins were separated by SDS-PAGE, transferred to membranes, and probed with antibodies against p53, PCNA, bcl-2, bax, caspase-3, and β-actin. Signals were detected using enhanced chemiluminescence. [3]
mRNA expression of AQP1 was analyzed by RT-PCR. Total RNA was extracted, reverse transcribed, and amplified by PCR. Products were separated by agarose gel electrophoresis and quantified. [3]

Xenograft studies for determining the in vivo efficacy of Acetazolamide (AZ) , MS-275, and Acetazolamide (AZ)  + MS-275 combination [2]
For the in vivo xenograft study, 4–6 weeks-old female NOD/SCID mice were obtained from the animal facility. Subcutaneous xenograft tumors were developed by injecting SH-SY5Y cells (2 × 106) into the inguinal fat pad of NOD/SCID mice. When tumor diameter reached 0.5 cm, the mice were randomized into four groups (5 mice per group). The control and treatment groups received intraperitoneal injections of vehicle (PBS) or Acetazolamide (AZ) (40 mg/kg), MS-275 (20 mg/kg) or the combination, respectively, every day for 2 weeks. Experiments were terminated when tumor sizes exceeded 2 cm3 in volume or animals showed signs of morbidity. Tumor diameters were measured on a daily basis until termination. The long (D) and short diameters (d) were measured with calipers. Tumor volume (cm3) was calculated as V = 0.5 × D × d2. After euthanizing the mice, tumors were resected, weighed and fixed in 10% neutral-buffered formalin at room temperature and processed for histopathology. For the in vivo serial heterotransplantation analysis, 2x106 untreated and pretreated Acetazolamide (AZ)  + MS-275 cells, manually and enzymatically dissociated from treated tumors, were injected subcutaneously to NOD/SCID mice. Growth rates were measured 2–3 times per week. On the 38th day, the animals were sacrificed, after which tumors were removed and weighed.

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Mice infection and treatment [6]
Two days after pellet implantation (Day 0), the vagina of each mouse was rinsed with 50 mM HEPES (pH = 7.4), and each mouse was inoculated intravaginally with 20 μL of the prepared bacterial suspension of N. gonorrhoeae FA1090 (1.2 × 108 CFU/mL). Two days post-infection (Day +2), mice were randomly allocated into groups (n=10) and administered either Acetazolamide (50 mg/kg) or the vehicle (DMSO-Tween 80-PBS, 1:1:8) orally for three consecutive days. As a positive control, one group of mice was administered a single intraperitoneal dose of ceftriaxone (15 mg/kg in water).

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Female ovariectomized BALB/c mice were implanted with a controlled-release estradiol pellet two days before infection. Mice were infected intravaginally with N. gonorrhoeae FA1090 (approximately 1.2×10^8 CFU/mL). Two days post-infection, mice were treated orally with acetazolamide (50 mg/kg) or vehicle (DMSO-Tween 80-PBS, 1:1:8) for three consecutive days. Vaginal swabs were collected daily and cultured on selective agar to quantify bacterial load. Ceftriaxone (15 mg/kg, single intraperitoneal dose) served as a positive control [6]

Absorption, Distribution and Excretion
Carbonic anhydrase inhibitors bind tightly to carbonic anhydrase; therefore, after systemic administration, the concentration of carbonic anhydrase inhibitors in tissues rich in this enzyme will be higher. /Carbonic Anhydrase Inhibitors/
Carbonic anhydrase inhibitors. Drug: Acetazolamide; Oral absorption: Almost complete; Plasma half-life: 6–9 hours; Elimination route: Complete renal excretion. /Excerpt from Table/
Acetazolamide is associated with rabbit response; renal response was measured by monitoring urine flow and sodium excretion, which occurred immediately after injection and were logarithmically related to the dose.
Intravenous bolus injection of (14)C-labeled acetazolamide was performed in rabbits. Drug concentrations in plasma, urine, and washed erythrocytes were determined, with washed erythrocyte concentration indicating bound drug.
For more data on the absorption, distribution, and excretion (complete) of acetazolamides (6 in total), please visit the HSDB record page.

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Metabolism/Metabolites
Acetazolamide dose does not alter metabolism.

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Biological half-life
3 to 9 hours
Plasma half-life: 6-9 hours (see table)

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Acetazolamideis rapidly and almost completely absorbed from the gastrointestinal tract. After a single oral dose of 400 mg, serum concentrations reach 20-40 μg/mL.It is excreted by the kidneys in its unmetabolized form[6]

Toxicity Summary
Identification: Acetazolamide is a synthetic drug. Acetazolamide is a white to pale yellowish-white odorless crystalline powder. Acetazolamide is slightly soluble in water and slightly soluble in ethanol (approximately 750 g/L); practically insoluble in ether and chloroform. Uses: Preoperative management of angle-closure glaucoma or as an adjunct to the treatment of open-angle glaucoma. Abnormal Fluid Retention: Drug-induced edema, obesity, and congestive heart failure. Epilepsy. Metabolic alkalosis. Periodic paralysis. Human Exposure: Acute or chronic acetazolamide overdose may cause dehydration symptoms such as thirst, drowsiness, confusion, poor skin turgor, and prolonged capillary refill time, but paradoxical persistent diuresis may also occur. Electrolyte disturbances, including hyponatremia, hypokalemia, and non-anion intermittent hyperchloremic metabolic acidosis, especially at moderate to high doses, may lead to further deterioration of mental status, seizures, ECG abnormalities, and arrhythmias. Pre-existing renal insufficiency increases toxicity at the same dose. Specific reactions exist, leading to bone marrow suppression and hepatic and renal insufficiency. Acetazolamide may also precipitate in the renal tubules, forming stones and causing renal colic. Hypokalemia may cause muscle weakness, decreased reflexes, and hypochloremic metabolic alkalosis. In elderly patients, chronic metabolic acidosis may lead to chronic compensatory hyperventilation, increasing pulmonary vascular resistance and reducing left ventricular function. This is particularly important in patients taking beta-blockers or calcium channel blockers concurrently. The ventricular fibrillation threshold may be lowered. Potassium deficiency may cause arrhythmias. Abuse or overdose may cause pancreatitis. Acute overdose or prolonged use or abuse may cause hyperglycemia, hyperuricemia, and hyperlipidemia. Hypersensitivity reactions such as rash, photosensitivity, thrombocytopenia, and pancreatitis are rare. Contraindications: Renal hyperchloremic acidosis. Addison's disease and all types of adrenal insufficiency. Known sodium and potassium deficiency (at least before treatment). Long-term use is contraindicated in patients with chronic angle-closure glaucoma. It is also contraindicated in patients with known hypersensitivity to sulfonamides. Acetazolamide should not be used to alkalinize urine after a salicylate overdose, as it may exacerbate metabolic acidosis. Acetazolamide is readily absorbed from the gastrointestinal tract. It is distributed throughout the body; primarily concentrated in erythrocytes, plasma, and kidneys, with smaller amounts concentrated in the liver, muscles, eyes, and central nervous system. Acetazolamide does not accumulate in tissues. This drug can cross the placenta in unknown amounts. Acetazolamide binds tightly to carbonic anhydrase, resulting in higher concentrations in tissues containing this enzyme, such as erythrocytes and the renal cortex. Small amounts of acetazolamide undergo irreversible binding to erythrocytes. Its binding to plasma proteins is 70% to 90%. Acetazolamide is not metabolized. It is primarily excreted unchanged via the kidneys through renal tubular secretion and passive reabsorption. Although small amounts of the unchanged drug are excreted in bile, there is no evidence of enterohepatic circulation. Acetazolamide is a carbonic anhydrase inhibitor. Acetazolamide reduces the availability of these ions for active transport to secretions by non-competitive, reversible inhibition of carbonic anhydrase, decreasing the process by which carbon dioxide and water generate hydrogen and bicarbonate ions. One patient died of cholestatic jaundice after taking 13 grams of acetazolamide over 26 days. Another patient developed fatal bone marrow suppression with leukopenia, thrombocytopenia, and anemia after 14 weeks of acetazolamide treatment. Yet another patient developed renal failure (anuria) after 2 weeks of acetazolamide use. Despite its widespread use, no birth defects have been reported with acetazolamide. However, a woman who took 750 mg/day of acetazolamide for glaucoma during early and mid-pregnancy gave birth to an infant with a sacrococcygeal teratoma, but a causal relationship could not be established. Teratogenicity studies in rats and mice showed that the offspring of rats and mice were missing the fourth and fifth toes on the right forelimb. No obvious lesions were observed in newborn rabbits and monkeys. The drug can cross the placenta in unknown amounts. Potentially dangerous interactions: Acetazolamide may enhance the effects of folic acid antagonists, oral hypoglycemic agents, and oral anticoagulants. Acetazolamide can inhibit the urinary disinfectant effect of methylamine by maintaining urine alkalinity. Acetazolamide alkalinizes urine, reducing the urinary excretion of many weak bases (including amphetamine, quinine, quinidine, and ethamazol), thereby enhancing their pharmacological effects. Drug-induced osteomalacia has been reported in a patient taking phenytoin sodium and acetazolamide. More serious side effects include blood disorders, skin toxicity, and kidney stone formation. There have been no reports of Stevens-Johnson syndrome. Symptomatic adverse reactions: Flushing, thirst, headache, somnolence, dizziness, fatigue, irritability, excitement, paresthesia, ataxia, tachypnea, and gastrointestinal disturbances (dollery) have been reported. Oral administration is the common route of administration. No significant skin absorption. No significant absorption or local irritation. Animal/Plant Studies: Numerous animal studies have shown that acetazolamide has extremely low toxicity in the studied species (mice, dogs, rats, monkeys).
Interactions
Acetazolamide may enhance the effects of mercury diuretics in animals.
Concomitant use of glucocorticoids, especially those with significant mineralocorticoid activity; mineralocorticoid glucocorticoids; amphotericin B for injection; and corticotropin, especially with long-term use, may lead to severe hypokalemia when combined with carbonic anhydrase inhibitors and should be used with caution; serum potassium levels and cardiac function should be monitored during concomitant use. /Carbonic Anhydrase Inhibitors/
Concomitant use of glucocorticoids or corticotropin with acetazolamide sodium may increase the risk of hypernatremia and/or edema because these drugs cause sodium and fluid retention; the risk of glucocorticoids or corticotropin may depend on the patient's sodium requirements, which are determined by the disease being treated. /Acetazolamide Sodium/
The long-term co-use of glucocorticoids or corticotropin with carbonic anhydrase inhibitors may increase the risk of hypocalcemia and osteoporosis because these drugs increase calcium excretion. /Carbonic Anhydrase Inhibitors/
For more (complete) data on the interactions of acetazolamides (16 in total), please visit the HSDB record page.

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Acetazolamide, alone or in combination with cisplatin, has not shown significant cytotoxicity in normal human umbilical vein endothelial cells (HUVECs) in vitro. [3]

[1]. Dual-tail approach to discovery of novel carbonic anhydrase IX inhibitors by simultaneously matching the hydrophobic and hydrophilic halves of the active site. Eur J Med Chem. 2017 May 26;132:1-10.

[2]. Acetazolamide potentiates the anti-tumor potential of HDACi, MS-275, in neuroblastoma. BMC Cancer. 2017 Feb 24;17(1):156.

[3]. Combined treatment with acetazolamide and cisplatin enhances chemosensitivity in laryngeal carcinoma Hep-2 cells. Oncol Lett. 2018 Jun;15(6):9299-9306.

[4]. Acetazolamide: a forgotten diuretic agent. Cardiol Rev. 2011 Nov-Dec;19(6):276-8.

[5]. Interaction of antihypertensive acetazolamide with nonsteroidal anti-inflammatory drugs. J Photochem Photobiol B. 2013 Aug 5;125:155-63.

[6]. In vivo efficacy of acetazolamide in a mouse model of Neisseria gonorrhoeae infection. Microb Pathog. 2022 Mar;164:105454.

Therapeutic Uses

Antidote; Carbonic anhydrase inhibitor; Diuretic
Veterinary Use: Used to treat laminitis, mammary edema, enterotoxemia, ascites, and glaucoma in various animals.
Carbonic anhydrase inhibitors are primarily used as adjunctive therapy for open-angle (chronic simple) glaucoma and secondary glaucoma, and to lower intraocular pressure before surgery for certain types of glaucoma. /Carbonic anhydrase inhibitor; included on the US product label/
Acetazolamide is used to lower intraocular pressure in malignant (ciliary body obstructive) glaucoma, which may occur after inflammatory surgery, trauma, or use of miotics. /Not included on the US product label/
For more complete data on the therapeutic uses of acetazolamide (13 in total), please visit the HSDB record page.

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Drug Warnings
Veterinary Use: Contraindicated in adrenal insufficiency or hypokalemic hyponatremia.
The safety of using these drugs during pregnancy has not been established. These medications are contraindicated in patients with idiopathic renal hyperchloremic acidosis, renal failure, known sodium and potassium deficiency, Addison's disease, or known sensitivity to these medications. Carbonic anhydrase inhibitors. Diuretics, such as acetazolamide and thiazide diuretics, alkalize urine, thus theoretically limiting the use of methylamine and its mandelate and hippurate as anti-infective agents for the urinary tract. Maternal use generally compatible with breastfeeding: Acetazolamide: Signs or symptoms reported by the infant or effects on lactation: None. /Excerpt from Table 6/ For more complete data on drug warnings for acetazolamide (13 in total), please visit the HSDB record page.

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Pharmacodynamics Acetazolamide is a potent carbonic anhydrase inhibitor that effectively controls fluid secretion, treats certain seizure disorders, and promotes diuresis in cases of abnormal fluid retention. Acetazolamide is not a mercury diuretic. Conversely, it is a non-bacterial sulfonamide, with a chemical structure and pharmacological activity quite different from those of bacterial sulfonamides. Acetazolamide is a small-molecule heteroaromatic sulfonamide that can act as a carbonic anhydrase inhibitor. [3] Studies have shown that acetazolamide may inhibit tumor metastasis by downregulating AQP1 expression. [3] This study shows that acetazolamide enhances the chemosensitivity of laryngeal cancer Hep-2 cells to cisplatin, suggesting it may be a potential combination therapy for laryngeal cancer. [3]

C4H6N4O3S2

222.237

221.988

C, 21.62; H, 2.72; N, 25.21; O, 21.60; S, 28.85

59-66-5

Acetazolamide;59-66-5; 1424-27-7 (sodium)

1986

White to off-white solid powder

1.7±0.1 g/cm3

256-261°C

1.641

-0.26

2

7

2

13

297

0

BZKPWHYZMXOIDC-UHFFFAOYSA-N

InChI=1S/C4H6N4O3S2/c1-2(9)6-3-7-8-4(12-3)13(5,10)11/h1H3,(H2,5,10,11)(H,6,7,9)

N-(5-sulfamoyl-1,3,4-thiadiazol-2-yl)acetamide

Acetazolamide; Diluran; Diamox; Defiltran; 59-66-5; Diamox; Acetamox; Nephramide; Glaupax; N-(5-Sulfamoyl-1,3,4-thiadiazol-2-yl)acetamide; Acetazolamid; PIM005; Glaupax

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~50 mg/mL (~224.97 mM)
H2O : < 0.1 mg/mL

Solubility in Formulation 1: ≥ 2.5 mg/mL (11.25 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (11.25 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (11.25 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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Solubility in Formulation 4: 1.96 mg/mL (8.82 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication (<60°C).

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 (Please use freshly prepared in vivo formulations for optimal results.)