DDMS

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DDMS

本产品不向个人销售，仅用作科学研究，不用于任何人体实验及非科研性质的动物实验。

CAS NO:

206052-03-1

包装与价格：

包装	价格(元)
1mg (solution)	电议
5mg (solution)	电议
10mg (solution)	电议

产品介绍

化学性质

Physical Appearance	A solution in ethanol. To change the solvent, simply evaporate the ethanol under a gentle stream of nitrogen and immediately add the solvent of choice.
Storage	Store at -20°C
M.Wt	433.2
Cas No.	206052-03-1
Formula	C₁₃H₂₃Br₂NO₃S
Synonyms	Dibromo-dodecenyl-methylsulfimide
Solubility	≤20mg/ml in DMSO;30mg/ml in dimethyl formamide
Chemical Name	12,12-dibromo-N-(methylsulfonyl)-11-dodecenamide
Canonical SMILES	BrC(=CCCCCCCCCCC(=O)NS(=O)(=O)C)Br
运输条件	蓝冰运输或根据您的需求运输。
一般建议	为了使其更好的溶解，请用37℃加热试管并在超声波水浴中震动片刻。不同厂家不同批次产品溶解度各有差异，仅做参考。若实验所需浓度过大至产品溶解极限，请添加助溶剂助溶或自行调整浓度。溶液形式一般不宜长期储存，请尽快用完。

资料参考

DDMS is a CYP4A2 enzyme inhibitor.

Biosynthesis of 20-HETE from arachidonic acid by the cytochrome P450 4A (CYP450 4A) isoforms is a key component of vascular homeostasis, especially in renal circulation.

In vitro: To determine whether inhibition of 20-HETE contributes to the vasodilatory effects of NO, the effects of DDMS on the response to SNP were examined in rat renal arterioles preconstricted with phenylephrine). Results showed that after DDMS treatment, SNP could increase vascular diameter by only 17% [1].

In vivo: The effects of DDMS on the mean arterial pressure and renal blood flow responses to infusion of an NO donor and a synthase inhibitor were also examined. It was found that infusion of MAHMA NONOate at 1, 3, 5, and 10 nmol/min was able to reduce mean arterial pressure by 16, 30, 40, and 48 mm Hg and lowered renal vascular resistance by 15 %, 26 %, 30%, and 34% of control. In addition, after DDMS treatment at 10 mg/kg, the mean arterial pressure and renal vascular resistance responsed to 1-hexamine, 6-(2-hydroxy-1-methyl-2-nitrohydrazino)N-methyl averaged only 20% of those seen during control [1].

Clinical trial: So far, no clinical study has been conducted.

Reference:
[1] Alonso-Galicia, M. ,Drummond, H.A.,Reddy, K.K., et al. Inhibition of 20-HETE production contributes to the vascular responses to nitric oxide. Hypertension 29, 320-325 (1997).