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製品番号: HY-B0718

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Methoxyflurane

Name: Methoxyflurane
Brand: MedChemExpress
SKU: HY-B0718
Price: 25.00 USD
Availability: InStock
Rating: 5 (1 reviews)

(別名: DA-759)

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Methoxyflurane (DA-759) is a volatile anesthetic and nephrotoxic agent. Methoxyflurane undergoes defluorination to generate inorganic fluoride and oxalic acid, leading to polyuric renal insufficiency, proximal tubular necrosis, mitochondrial swelling, and ADH-resistant polyuria. Methoxyflurane inhibits Na⁺/K⁺ ATPase sodium transport. Methoxyflurane is used in research on neurological diseases and kidney diseases.

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研究用途以外に使用した場合、当社は一切の責任を負いかねます。

純度 : 98.0%
CAS 番号: 76-38-0
分子式: C₃H₄Cl₂F₂O
分子量:164.97

保管条件:

Pure form -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month

Methoxyflurane 構造式

CAS 番号: 76-38-0

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Top Publications Citing

Use of MCE Products

Fluorescent Dye

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

生物活性

製品説明

体外実験

Methoxyflurane (90-270 μM) enhances 5-HT₃ receptor-mediated currents in N1E-115 mouse neuroblastoma cells, shifting the 5-HT EC₅₀ from 1.86 μM to 1.07 μM at 270 μM^[5].
Methoxyflurane inhibits Carbamoylcholine chloride (HY-B1208)-evoked catecholamine secretion in bovine adrenal chromaffin cells with an IC₅₀ of 230-250 μM, and inhibits high K⁺-evoked secretion with an IC₅₀ of approximately 1200 μM, without affecting basal secretion^[6].
Methoxyflurane reduces Carbamoylcholine chloride- and high K⁺-evoked ⁴⁵Ca²⁺ influx in bovine adrenal chromaffin cells, and for K⁺ stimulation, this reduction is sufficient to account for the inhibition of catecholamine secretion^[6].
Methoxyflurane inhibits Carbamoylcholine chloride-evoked ²²Na⁺ influx in bovine adrenal chromaffin cells, and this inhibition is sufficient to account for the reduction in catecholamine secretion^[6].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

体内実験

Renal RegulationOthers

Renal Regulation

Methoxyflurane (0.5-0.75%; inhalation; 180-360 min) anesthesia produces dose-dependent, ADH-resistant polyuric renal insufficiency in Fischer 344 rats, accompanied by proximal tubular mitochondrial injury and inorganic fluoride-mediated nephrotoxicity^[1].

Others

Methoxyflurane (0.13%; inhalation; 7 h/day; 1-15 consecutive days) exposure at subanesthetic concentrations shortens sleep time and reduces mortality following lethal-concentration Methoxyflurane (0.5%; inhalation; 5 h; 96 h after previous exposure) in healthy male Sprague-Dawley rats, consistent with nonspecific stimulation of xenobiotic metabolism^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:

Fischer 344 (principal model) and Buffalo (strain comparison)^[1]
Dosage:

0.5% for 180 min; 0.75% for 360 min
Administration:

inhalation; 180 min; 360 min
Result:

Fischer 344 and Buffalo rats metabolized Methoxyflurane to a greater extent than the other three rat strains, with higher serum and urine inorganic fluoride activity.
Only Fischer 344 rats developed functional and pathological evidence of a renal lesion after Methoxyflurane.
Renal functional and morphological changes were proportional to Methoxyflurane dose; polyuria after Methoxyflurane anesthesia or direct inorganic fluoride injection was ADH-resistant.
At 24 hr after 0.5% Methoxyflurane for 180 min, proximal convoluted tubular cells showed swollen mitochondria and some indentation of the nucleus.
At 24 hr after 0.75% Methoxyflurane for 360 min, there was pronounced mitochondrial swelling, degeneration, and rupture.
Injection of inorganic fluoride (NaF) produced a much greater degree of renal insufficiency in Fischer 344 rats than in Buffalo rats, and sodium fluoride injection in Fischer 344 rats resulted in dose-related polyuric renal insufficiency and pathological abnormalities similar to those after Methoxyflurane anesthesia.
Enzyme induction increased defluorination and nephrotoxicity, whereas SKF 525A (Proadifen hydrochloride) (HY-B1311) resulted in decreased defluorination and an attenuated renal lesion.
Gentamicin (HY-A0276A) and Methoxyflurane adverse renal functional and pathological effects were additive in Fischer 344 rats.

Animal Model:

Sprague-Dawley (male, initial body weight 40-50 g)^[3]
Dosage:

0.13% (sleeping time); 0.13% followed 96 h later by 0.5% (tolerance experiment)
Administration:

inhalation; 7 h/day for 1, 2, 3, 4, 5, 10, and 15 consecutive days; inhalation; 7 h/day for 10 consecutive days; then inhalation for 5 h 96 h later
Result:

Sleeping time after Methoxyflurane 0.13% was 96 minutes on day 1, 68 minutes on day 2, 43 minutes on day 3, 43 minutes on day 4, 34 minutes on day 5, 22 minutes on day 10, and 21 minutes on day 15.
Sleeping time decreased 79% between the first and fifteenth day of Methoxyflurane exposure.
After prior exposure to 0.13% Methoxyflurane 7 h/day for 10 days, exposure to 0.5% Methoxyflurane for 5 h resulted in 43% mortality (n=21).

Related Protocols :

Nephrotoxicity Study

臨床実験

NCT Number	Sponsor	Condition	Start Date	Phase A549
NCT01329991			2011-05	PHASE1

化学情報

CAS 番号 76-38-0
性状 Liquid
分子量 164.97
分子式 C₃H₄Cl₂F₂O
Color Colorless to light yellow
SMILES

COC(F)(F)C(Cl)Cl
別名

DA-759
輸送条件

Room temperature in continental US; may vary elsewhere.

保管条件

Pure form	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

純度とドキュメンテーション

バッチを選択:

純度: 99.98%

Assay: 99.98%

ee.: 99.98%

データシート (288 KB)
SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
COA (2659 KB)
元素分析報告書 (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
取扱説明書 (2659 KB)

参考文献

[1]. Mazze RI. Methoxyflurane nephropathy. Environmental Health Perspectives. 1976 Jun;15:111.

[2]. Kharasch ED, et al. Human kidney methoxyflurane and sevoflurane metabolism: intrarenal fluoride production as a possible mechanism of methoxyflurane nephrotoxicity. Anesthesiology. 1995 Mar 1;82(3):689-99.

[3]. Berman ML, et al. Nonspecific stimulation of drug metabolism in rats by methoxyflurane. Anesthesiology. 1970 Jun 1;32(6):500-6.

[4]. Kharasch ED, et al. New insights into the mechanism of methoxyflurane nephrotoxicity and implications for anesthetic development (part 2): Identification of nephrotoxic metabolites. Anesthesiology. 2006 Oct 1;105(4):737-45.

[5]. Jenkins A, et al. Actions of general anaesthetics on 5-HT3 receptors in N1E-115 neuroblastoma cells. British journal of pharmacology. 1996 Apr;117(7):1507-15.

[6]. Pocock G, et al. The action of volatile anaesthetics on stimulus-secretion coupling in bovine adrenal chromaffin cells. British journal of pharmacology. 1988 Sep;95(1):209-17.

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