MethazolamideCarbonic anhydrase inhibitor CAS# 554-57-4 |
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Quality Control & MSDS
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| Cas No. | 554-57-4 | SDF | Download SDF |
| PubChem ID | 4100 | Appearance | Powder |
| Formula | C5H8N4O3S2 | M.Wt | 236.27 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Synonyms | L584601 | ||
| Solubility | DMSO : ≥ 50 mg/mL (211.62 mM) *"≥" means soluble, but saturation unknown. | ||
| Chemical Name | N-(3-methyl-5-sulfamoyl-1,3,4-thiadiazol-2-ylidene)acetamide | ||
| SMILES | CC(=O)N=C1N(N=C(S1)S(=O)(=O)N)C | ||
| Standard InChIKey | FLOSMHQXBMRNHR-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C5H8N4O3S2/c1-3(10)7-4-9(2)8-5(13-4)14(6,11)12/h1-2H3,(H2,6,11,12) | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | Methazolamide is a carbonic anhydrase inhibitor used to treat glaucoma.
Target: Carbonic Anhydrase
Methazolamide is a carbonic anhydrase inhibitor with Ki of 50 nM, 14 nM and 36 nM for hCA I, hCA II and bCA IV isoforms, respectively [1]. Methazolamide is of strength equal to acetazolamide, another carbonic anhydrase inhibitor used to treat irregular breathing disorders. However, methazolamide differs from acetazolamide in that it fails to activate Ca2+-dependent potassium channels in skeletal muscles. Methazolamide does not impair respiratory work performance in anesthetized rabbits [2]. Oral administration of methazolamide decreases IOPs and AHFRs in clinically normal dogs, with effectiveness diminishing in the evening [3]. References: | |||||
Methazolamide Dilution Calculator
Methazolamide Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 4.2324 mL | 21.1622 mL | 42.3245 mL | 84.6489 mL | 105.8111 mL |
| 5 mM | 0.8465 mL | 4.2324 mL | 8.4649 mL | 16.9298 mL | 21.1622 mL |
| 10 mM | 0.4232 mL | 2.1162 mL | 4.2324 mL | 8.4649 mL | 10.5811 mL |
| 50 mM | 0.0846 mL | 0.4232 mL | 0.8465 mL | 1.693 mL | 2.1162 mL |
| 100 mM | 0.0423 mL | 0.2116 mL | 0.4232 mL | 0.8465 mL | 1.0581 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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Methazolamide, a derivative of sulfonamide, is an inhibitor of carbonic anhydrase (CA) that potently inhibits isoenzymes of CA, CA II and CA IV with values of 50% inhibition concentration IC50 of 8.1 nM and 80.3 nM respectively. Methazolamide has been widely used to treat glaucoma for its ability to reduce the rate of fluid formation in the inner eye through slowing the formation of bicarbonate ions and subsequently resulting in reduction in sodium and fluid transport. Recent studies have revealed that methazolamide, while other CA inhibitos are not, also acts as an insulin sensitizer to suppress hepatic glucose production in vivo.
Reference
Konstantopoulos N, Molero JC, McGee SL, Spolding B, Connor T, de Vries M, Wanyonyi S, Fahey R, Morrison S, Swinton C, Jones S, Cooper A, Garcia-Guerra L, Foletta VC, Krippner G, Andrikopoulos S, Walder KR. Methazolamide is a new hepatic insulin sensitizer that lowers blood glucose in vivo. Diabetes. 2012;61(8):2146-2154
Chang X, Yan X, Zhang Y. Treat ankylosing spondylitis with methazolamide. Int J Med Sci;8(5):413-419
Gudmundsdóttir E, Stefánsson E, Bjarnadóttir G, Sigurjónsdóttir JF, Gudmundsdóttir G, Masson M, Loftsson T. Methazolamide 1% in cyclodextrin solution lowers IOP in human ocular hypertension. Invest Ophthalmol Vis Sci. 2000;41(11):3552-3554.
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Methazolamide Plus Aminophylline Abrogates Hypoxia-Mediated Endurance Exercise Impairment.[Pubmed:26680684]
High Alt Med Biol. 2015 Dec;16(4):331-42.
In hypoxia, endurance exercise performance is diminished; pharmacotherapy may abrogate this performance deficit. Based on positive outcomes in preclinical trials, we hypothesized that oral administration of Methazolamide, a carbonic anhydrase inhibitor, aminophylline, a nonselective adenosine receptor antagonist and phosphodiesterase inhibitor, and/or Methazolamide combined with aminophylline would attenuate hypoxia-mediated decrements in endurance exercise performance in humans. Fifteen healthy males (26 +/- 5 years, body-mass index: 24.9 +/- 1.6 kg/m(2); mean +/- SD) were randomly assigned to one of four treatments: placebo (n = 9), Methazolamide (250 mg; n = 10), aminophylline (400 mg; n = 9), or Methazolamide (250 mg) with aminophylline (400 mg; n = 8). On two separate occasions, the first in normoxia (FIO2 = 0.21) and the second in hypoxia (FIO2 = 0.15), participants sat for 4.5 hours before completing a standardized exercise bout (30 minutes, stationary cycling, 100 W), followed by a 12.5-km time trial. The magnitude of time trial performance decrement in hypoxia versus normoxia did not differ between placebo (+3.0 +/- 2.7 minutes), Methazolamide (+1.4 +/- 1.7 minutes), and aminophylline (+1.8 +/- 1.2 minutes), all with p > 0.09; however, the performance decrement in hypoxia versus normoxia with Methazolamide combined with aminophylline was less than placebo (+0.6 +/- 1.5 minutes; p = 0.01). This improvement may have been partially mediated by increased SpO2 in hypoxia with Methazolamide combined with aminophylline compared with placebo (73% +/- 3% vs. 79% +/- 6%; p < 0.02). In conclusion, coadministration of Methazolamide and aminophylline may promote endurance exercise performance during a sojourn at high altitude.
Methazolamide improves neurological behavior by inhibition of neuron apoptosis in subarachnoid hemorrhage mice.[Pubmed:27731352]
Sci Rep. 2016 Oct 12;6:35055.
Subarachnoid hemorrhage (SAH) results in significant nerve dysfunction, such as hemiplegia, mood disorders, cognitive and memory impairment. Currently, no clear measures can reduce brain nerve damage. The study of brain nerve protection after SAH is of great significance. We aim to evaluate the protective effects and the possible mechanism of Methazolamide in C57BL/6J SAH animal model in vivo and in blood-induced primary cortical neuron (PCNs) cellular model of SAH in vitro. We demonstrate that Methazolamide accelerates the recovery of neurological damage, effectively relieves cerebral edema, and improves cognitive function in SAH mice as well as offers neuroprotection in blood- or hemoglobin-treated PCNs and partially restores normal neuronal morphology. In addition, western blot analyses show obviously decreased expression of active caspase-3 in Methazolamide-treated SAH mice comparing with vehicle-treated SAH animals. Furthermore, Methazolamide effectively inhibits ROS production in PCNs induced by blood exposure or hemoglobin insult. However, Methazolamide has no protective effects in morality, fluctuation of cerebral blood flow, SAH grade, and cerebral vasospasm of SAH mice. Given Methazolamide, a potent carbonic anhydrase inhibitor, can penetrate the blood-brain barrier and has been used in clinic in the treatment of ocular conditions, it provides potential as a novel therapy for SAH.
The Metabolism of Methazolamide in Immortalized Human Keratinocytes, HaCaT Cells.[Pubmed:28137210]
Drug Metab Lett. 2017;10(4):295-305.
OBJECTIVE: Drug therapy is occasionally accompanied by an idiosyncratic severe toxicity, which occurs very rarely, but can lead to patient mortality. Methazolamide, an anti-glaucomatous agent, could cause severe skin eruptions called Stevens-Johnson syndrome/toxic epidermal necrolyis (SJS/TEN). Its precise etiology is still uncertain. In this study, the metabolism of Methazolamide was investigated in immortalized human keratinocytes to reveal the possible mechanism which causes SJS/TEN. METHODS: The metabolism of Methazolamide was studied using immortalized human keratinocytes, HaCaT cells. HPLC was used to isolate a metabolite from the culture medium. Mass spectrometry (LCMS/ MS) was employed for its characterization. Three typical chemical inducers were assessed for the inducibility of cytochrome P450, and methimazole was used as the inhibitor of flavin-containing monooxygenase (FMO). RESULTS: A sulfonic acid, N-[3-methyl-5-sulfo-1,3,4-thiadiazol-2(3H)-ylidene]acetamide (MSO) was identified as the final metabolite. Dexamethasone and beta-naphthoflavone behaved as an inducer of cytochrome P450 in the metabolism, but isoniazid did not. The effect of methimazole was not consistent. We did not detect any glucuronide nor any mercapturic acid (N-acetylcysteine conjugate). CONCLUSION: N-[3-methyl-5-sulfo-1,3,4-thiadiazol-2(3H)-ylidene]acetamide (MSO) is not considered to be a direct product of an enzymatic reaction, but rather an auto-oxidation product of N-[3-methyl-5- sulfe-1,3,4-thiadiazol-2(3H)-ylidene]acetamide, a chemically unstable sulfenic acid, which is produced by cytochrome P450 from the beta-lyase product of cysteine conjugate of Methazolamide. MSO is considered to be susceptible to glutathione and to return to glutathione conjugate of Methazolamide, forming a futile cycle. A hypothetical scenario is presented as to the onset of the disease.
