Dexamethasone Phosphate disodium

别名: Dexamethasone 21-phosphate disodium EGP-437 EGP 437 EGP437 Dex-Phos. 地塞米松磷酸钠;16alpha-甲基-11beta,17alpha,21-三羟基-9alpha-氟孕甾-1,4-二烯-3,20-二酮-21-磷酸酯二钠盐;21-磷酸地塞米松二钠盐;21-磷酸地塞米松;地塞米松磷酸钠原粉;地塞米松21-磷酸二钠盐水合物;Dexamethasone 21-Phosphate Disodium Salt Hydrate 地塞米松21-磷酸二钠盐水合物;地塞美松磷酸钠
目录号: V6227 纯度: ≥98%
地塞米松磷酸二钠,地塞米松的水溶性盐形式,通过 i 给药。
Dexamethasone Phosphate disodium CAS号: 2392-39-4
产品类别: Glucocorticoid Receptor
产品仅用于科学研究,不针对患者销售
规格 价格 库存 数量
100mg
250mg
500mg
1g
2g
5g
10g
Other Sizes

Other Forms of Dexamethasone Phosphate disodium:

  • 地塞米松
  • 醋酸地塞米松
  • 地塞米松磷酸酯
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InvivoChem产品被CNS等顶刊论文引用
顾客使用InvivoChem 产品地塞米松磷酸钠发表2篇科研文献
纯度/质量控制文件

纯度: ≥98%

产品描述
地塞米松磷酸二钠是地塞米松的水溶性盐形式,通过静脉注射给药,是一种强效合成糖皮质激素类类固醇药物,也是一种具有抗炎和免疫抑制活性的白细胞介素受体调节剂。地塞米松具有抗炎和免疫抑制作用。它的糖皮质激素作用比皮质醇强 25 倍,同时具有最小的盐皮质激素作用。地塞米松用于治疗多种疾病,包括:风湿病、多种皮肤病,如多形红斑、严重过敏、哮喘。
生物活性&实验参考方法
靶点
Glucocorticoid receptor
体外研究 (In Vitro)
地塞米松磷酸二钠通过调节许多调节因子(例如激活蛋白-1、核因子-AT 和核因子-kB)来促进参与调节反应的重要基因的激活和抑制[1]。地塞米松磷酸二钠的 EC50 为 2.2 nM,可有效控制 A549 细胞释放粒细胞-巨噬细胞集落刺激因子 (GM-CSF)。在浓度提高 10-100 倍时,地塞米松磷酸二钠 (EC50=36 nM) 通过感应 β2 红外受体并附着在葡萄糖信号接收激素 (GR) 的 DNA 上,抑制 GM-CSF 的释放。 GM-CSF 释放的抑制与地塞米松磷酸二钠 (IC50=0.5 nM) 对 3×κB(NF-κB、IκBα 和 I-κBβ)的抑制有关 [2]。
体内研究 (In Vivo)
用 2 × 5 mg/kg 剂量的地塞米松磷酸二钠治疗成功抑制了脂多糖 (LPS) 诱导的受体。当小鼠暴露于脂多糖(LPS)并单次注射地塞米松磷酸二钠(10 mg/kg(ip))时,我们的实验系统中粒细胞募集和氧自由度均显着下降。革命者自发地涌现。吸入 LPS 前一小时和吸入后一小时,效果具有统计学意义。当向健康动物施用水雾剂时,BALF 中的粒细胞数量下降至与这些动物相似的值 [3]。与图表相比,用地塞米松磷酸二钠治疗的老鼠吃的食物更少,体重也更轻。尽管地塞米松磷酸二钠注射液的剂量在食品指南范围内,但五天的注射期导致肝脏质量(+42%)和肝脏相对体重(+65%)显着增加。治疗5天后,腓肠肌的肌肉是相同的,但与喂食的动物相比,动物的体重也有所减轻。湿重下降了 20%,但相对重量保持完全相同(克/100 克体重),表明手术后体重减轻与体重减轻相协调[4]。
酶活实验
1.糖皮质激素在控制哮喘和类风湿性关节炎等慢性炎症性疾病方面非常有效,但其抗炎作用的确切分子机制尚不清楚。它们通过与细胞质受体(GR)结合来激活或抑制基因表达。这可能是通过GR与DNA的直接结合(反式激活)或通过抑制AP-1和NF-kappaB等转录因子的活性(反式抑制)发生的。2.局部活性类固醇丙酸氟替卡松(EC50=1.8 x 10(-11)M)和布地奈德(EC50=5.0 x 10(-11)M)在抑制A549细胞释放GM-CSF方面比替普瑞定(EC50=8.3 x 10(-10)M)、布替西科特(EC50=3.7 x 10(-8)M)以及地塞米松(EC50=2.2 x 10(-9)M)更有效。抗糖皮质激素RU486还抑制了这些细胞中GM-CSF的释放(IC50=1.8 x 10(-10)M)。3.发现丙酸氟替卡松(EC50=9.8 x 10(-10)M)、布地奈德(EC50=1.1 x 10(-9)M)和地塞米松(EC50=3.6 x 10(-8)M)诱导β2受体转录的浓度依赖性能力与GR DNA结合有关,其浓度比抑制GM-CSF释放高10-100倍。24小时后,未观察到NF-kappaB、IkappaBalpha或I-kappaBbeta内源性抑制剂的诱导,糖皮质激素未改变IL-1β降解并随后诱导IkappaB的能力。4.丙酸氟替卡松(IC50=0.5 x 10(-11)M)、布地奈德(IC50=2.7 x 10(-11M))、地塞米松(IC50=0.5 x 10(-9)M)和RU486(IC50=2.7 x 10-11)抑制3 xκB的能力与抑制GM-CSF释放有关。5.这些数据表明,一系列糖皮质激素的抗炎特性与其反式加压而非反式激活基因的能力有关[2]。
细胞实验
糖皮质激素是一种广泛应用于临床实践的抗炎药。越来越多的证据表明外泌体是炎症的重要介质,但糖皮质激素是否调节外泌体的分泌和功能尚不清楚。在本研究中,我们观察到经地塞米松处理后,脂多糖(LPS)诱导的RAW264.7巨噬细胞的外泌体分泌减少。重要的是,从LPS诱导的RAW264.7巨噬细胞中分离的外泌体增加了RAW264.6细胞中TNF-α和IL-6的产生。然而,在用从地塞米松处理的细胞中分离的外泌体治疗后,这种增加不太明显。此外,地塞米松降低了LPS诱导的RAW264.7巨噬细胞外泌体中促炎微小RNA-155的表达。我们假设外泌体是糖皮质激素在LPS诱导的巨噬细胞炎症反应中抗炎作用的新靶点。这些发现将有利于抗炎治疗新方法的开发[5]。
动物实验
We investigated the role that mitochondrial proton leak may play in the glucocorticoid-induced hypermetabolic state. Sprague-Dawley rats were injected with dexamethasone over a period of 5 days. Liver mitochondria and gastrocnemius subsarcolemmal and intermyofibrillar mitochondria were isolated from dexamethasone-treated, pair-fed and control rats. Respiration and membrane potential were measured simultaneously using electrodes sensitive to oxygen and to the potential-dependent probe triphenylmethylphosphonium, respectively. Five days of dexamethasone injection resulted in a marked increase in the basal proton conductance of liver mitochondria, but not in the muscle mitochondrial populations. This effect would have a modest impact on energy expenditure in rats.[4]
参考文献
[1]. LaLone CA, et al. Effects of a glucocorticoid receptor agonist, Dexamethasone, on fathead minnow reproduction, growth, and development. Environ Toxicol Chem. 2012 Mar;31(3):611-22.
[2]. Adcock IM, et al. Ligand-induced differentiation of glucocorticoid receptor (GR) trans-repression and transactivation: preferential targetting of NF-kappaB and lack of I-kappaB involvement. Br J Pharmacol. 1999 Jun;127(4):1003-11.
[3]. Rocksén D, et al. Differential anti-inflammatory and anti-oxidative effects of Dexamethasone and N-acetylcysteine in endotoxin-induced lung inflammation. Clin Exp Immunol. 2000 Nov;122(2):249-56.
[4]. Roussel D, et al. Dexamethasone treatment specifically increases the basal proton conductance of rat liver mitochondria. FEBS Lett. 2003 Apr 24;541(1-3):75-9.
[5]. Yun Chen, et al. Glucocorticoids inhibit production of exosomes containing inflammatory microRNA-155 in lipopolysaccharide-induced macrophage inflammatory responses. Int J Clin Exp Pathol 2018;11(7):3391-3397.
其他信息
Dexamethasone sodium phosphate is an organic sodium salt which is the disodium salt of dexamethasone phosphate. It has a role as a glucocorticoid receptor agonist. It contains a dexamethasone phosphate(2-).
Dexamethasone Sodium Phosphate is a sodium phosphate salt form of Dexamethasone, a synthetic adrenal corticosteroid with potent anti-inflammatory properties. In addition to binding to specific nuclear steroid receptors, dexamethasone also interferes with NF-kB activation and apoptotic pathways. This agent lacks the salt-retaining properties of other related adrenal hormones. (NCI04)
See also: Dexamethasone (broader); Dexamethasone sodium phosphate; neomycin sulfate (component of) ... View More ...
*注: 文献方法仅供参考, InvivoChem并未独立验证这些方法的准确性
化学信息 & 存储运输条件
精确质量
516.13
元素分析
C, 51.17; H, 5.47; F, 3.68; Na, 8.90; O, 24.78; P, 6.00
CAS号
2392-39-4
相关CAS号
Dexamethasone;50-02-2;Dexamethasone acetate;1177-87-3;Dexamethasone phosphate;312-93-6
PubChem CID
16961
外观&性状
Typically exists as white to off-white solids at room temperature
密度
1.32g/cm3
沸点
669.6ºC at 760 mmHg
熔点
233-235 °C
闪点
358.7ºC
蒸汽压
2.81E-15mmHg at 25°C
折射率
1.591
LogP
2.889
tPSA
156.83
氢键供体(HBD)数目
2
氢键受体(HBA)数目
9
可旋转键数目(RBC)
3
重原子数目
34
分子复杂度/Complexity
962
定义原子立体中心数目
8
SMILES
C[C@@H]1C[C@H]2[C@@H]3CCC4=CC(=O)C=C[C@@]4([C@]3([C@H](C[C@@]2([C@]1(C(=O)COP(=O)([O-])[O-])O)C)O)F)C.[Na+].[Na+]
InChi Key
PLCQGRYPOISRTQ-FCJDYXGNSA-L
InChi Code
InChI=1S/C22H30FO8P.2Na/c1-12-8-16-15-5-4-13-9-14(24)6-7-19(13,2)21(15,23)17(25)10-20(16,3)22(12,27)18(26)11-31-32(28,29)30/h6-7,9,12,15-17,25,27H,4-5,8,10-11H2,1-3H3,(H2,28,29,30)/q2*+1/p-2/t12-,15+,16+,17+,19+,20+,21+,22+/m1../s1
化学名
sodium 2-((8S,9R,10S,11S,13S,14S,16R,17R)-9-fluoro-11,17-dihydroxy-10,13,16-trimethyl-3-oxo-6,7,8,9,10,11,12,13,14,15,16,17-dodecahydro-3H-cyclopenta[a]phenanthren-17-yl)-2-oxoethyl phosphate
别名
Dexamethasone 21-phosphate disodium EGP-437 EGP 437 EGP437 Dex-Phos.
HS Tariff Code
2934.99.9001
存储方式

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

注意: 请将本产品存放在密封且受保护的环境中,避免吸湿/受潮。
运输条件
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
溶解度数据
溶解度 (体外实验)
H2O : ≥ 100 mg/mL (~193.65 mM)
DMSO : ~1 mg/mL (~1.94 mM)
溶解度 (体内实验)
配方 1 中的溶解度: 100 mg/mL (193.65 mM) in PBS (这些助溶剂从左到右依次添加,逐一添加), 澄清溶液; 超声助溶。

请根据您的实验动物和给药方式选择适当的溶解配方/方案:
1、请先配制澄清的储备液(如:用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液,按从左到右的顺序依次添加助溶剂,澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明,并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中,混合均匀/澄清;向上述体系中加入50 μL Tween-80,混合均匀/澄清;然后继续加入450 μL ddH2O (或 saline)定容至 1 mL;

3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出,可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果,工作液请现配现用!
6、如不确定怎么将母液配置成体内动物实验的工作液,请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。
计算器

摩尔浓度计算器可计算特定溶液所需的质量、体积/浓度,具体如下:

  • 计算制备已知体积和浓度的溶液所需的化合物的质量
  • 计算将已知质量的化合物溶解到所需浓度所需的溶液体积
  • 计算特定体积中已知质量的化合物产生的溶液的浓度
使用摩尔浓度计算器计算摩尔浓度的示例如下所示:
假如化合物的分子量为350.26 g/mol,在5mL DMSO中制备10mM储备液所需的化合物的质量是多少?
  • 在分子量(MW)框中输入350.26
  • 在“浓度”框中输入10,然后选择正确的单位(mM)
  • 在“体积”框中输入5,然后选择正确的单位(mL)
  • 单击“计算”按钮
  • 答案17.513 mg出现在“质量”框中。以类似的方式,您可以计算体积和浓度。

稀释计算器可计算如何稀释已知浓度的储备液。例如,可以输入C1、C2和V2来计算V1,具体如下:

制备25毫升25μM溶液需要多少体积的10 mM储备溶液?
使用方程式C1V1=C2V2,其中C1=10mM,C2=25μM,V2=25 ml,V1未知:
  • 在C1框中输入10,然后选择正确的单位(mM)
  • 在C2框中输入25,然后选择正确的单位(μM)
  • 在V2框中输入25,然后选择正确的单位(mL)
  • 单击“计算”按钮
  • 答案62.5μL(0.1 ml)出现在V1框中
g/mol

分子量计算器可计算化合物的分子量 (摩尔质量)和元素组成,具体如下:

注:化学分子式大小写敏感:C12H18N3O4  c12h18n3o4
计算化合物摩尔质量(分子量)的说明:
  • 要计算化合物的分子量 (摩尔质量),请输入化学/分子式,然后单击“计算”按钮。
分子质量、分子量、摩尔质量和摩尔量的定义:
  • 分子质量(或分子量)是一种物质的一个分子的质量,用统一的原子质量单位(u)表示。(1u等于碳-12中一个原子质量的1/12)
  • 摩尔质量(摩尔重量)是一摩尔物质的质量,以g/mol表示。
/

配液计算器可计算将特定质量的产品配成特定浓度所需的溶剂体积 (配液体积)

  • 输入试剂的质量、所需的配液浓度以及正确的单位
  • 单击“计算”按钮
  • 答案显示在体积框中
动物体内实验配方计算器(澄清溶液)
第一步:请输入基本实验信息(考虑到实验过程中的损耗,建议多配一只动物的药量)
第二步:请输入动物体内配方组成(配方适用于不溶/难溶于水的化合物),不同的产品和批次配方组成不同,如对配方有疑问,可先联系我们提供正确的体内实验配方。此外,请注意这只是一个配方计算器,而不是特定产品的确切配方。
+
+
+

计算结果:

工作液浓度 mg/mL;

DMSO母液配制方法 mg 药物溶于 μL DMSO溶液(母液浓度 mg/mL)。如该浓度超过该批次药物DMSO溶解度,请首先与我们联系。

体内配方配制方法μL DMSO母液,加入 μL PEG300,混匀澄清后加入μL Tween 80,混匀澄清后加入 μL ddH2O,混匀澄清。

(1) 请确保溶液澄清之后,再加入下一种溶剂 (助溶剂) 。可利用涡旋、超声或水浴加热等方法助溶;
            (2) 一定要按顺序加入溶剂 (助溶剂) 。

临床试验信息
NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT02955641 UNKNOWN STATUSV Drug: Dexamethasone Disodium Phosphate 0.1%
Drug: Nepafenac 0.1%
Drug: Hydroxyethylcellulose 0.19%
Glaucoma, Angle-Closure
Glaucoma, Closed-Angle
Glaucoma, Narrow-Angle
Sheba Medical Center 2016-11-01 Not Applicable
NCT01004497 COMPLETED Drug: Dasatinib
Drug: Cyclophosphamide
Drug: Vincristine
Acute Lymphoblastic Leukemia The Catholic University of Korea 2010-03 Phase 2
NCT06437054 NOT YET RECRUITING Drug: Dexamethasone
Drug: Hyaluronic acid
Other: Indocyanine green(ICG)
Hearing Loss, Sensorineural
Hearing Loss, Sudden
Intratympanic Injection
Seoul National University Hospital 2025-02-15 Phase 1
Phase 2
NCT03580473 COMPLETED Drug: SATURNO II association
Drug: Vigadexa®
Cataract
Ocular Inflammation
EMS 2020-02-27 Phase 2
NCT02973880 COMPLETED Drug: NETILDEX™ ophthalmic gel
Drug: NETILDEX™ eye drops solution
Cataract
Cataract Extraction
SIFI SpA 2017-10-15 Phase 3
生物数据图片
  • (a) Concentration-dependent inhibition of interleukin (IL)-1β (1 ng ml−1)-stimulated granulocyte-macrophage colony stimulating factor (GM-CSF) release into the media from A549 cells at 24 h following fluticasone propionate (FP), budesonide (Bud) and dexamethasone (Dex) treatment. (b) Concentration-dependent inhibition of IL-1β (1 ng ml−1)-stimulated GM-CSF release from A549 cells at 24 h following treatment with the anti-glucocorticoid RU486. (c) The effect of low concentration (10−9 m) RU486 (RU) treatment on the inhibition of IL-1β-stimulated GM-CSF release by 10−10 m FP, Bud and Dex. (d) The effects of increasing concentrations of phenylarsine oxide (PAO) on IL-1β (1 ng ml−1)-stimulated induction of GM-CSF release into culture medium at 24 h. Results are plotted as the means±s.e.means of the percentage of maximal IL-1β-stimulated GM-CSF release in the absence any drug. n=4–7 for each data point except in (c) where results are the mean of two independent experiments.[1].[2]. Adcock IM, et al. Ligand-induced differentiation of glucocorticoid receptor (GR) trans-repression and transactivation: preferential targetting of NF-kappaB and lack of I-kappaB involvement. Br J Pharmacol. 1999 Jun;127(4):1003-11.
  • (a) Representative electrophoretic mobility shift assay showing the concentration-dependent effect of fluticasone propionate (FP), Budesonide (Bud) and dexamethasone (Dex) on glucocorticoid receptor (GR)-induced activation as represented by increased DNA binding (GRE binding) (arrowed) within the nucleus after 2 h incubation. (b) Supershift assay of dexamethasone (10−6 m)-stimulated GR DNA binding. Increased DNA binding is seen following dexamethasone treatment (lane 2). Pre-incubation of retarded complexes with an anti-GR antibody (lane 3) shows specific enhanced retardation of GR/GRE band. Specificity of binding was indicated by the addition of 100 fold excess unlabelled oligonucleotide (lane 4). Unbound oligonucleotide is indicated by an arrow at the bottom of the gel. (c) Densitometric analysis of the retarded bands in (a) and corrected for maximal band intensity showing the concentration-dependent increase in GRE binding following 2 h incubation with FP, Bud and Dex within the nucleus as a percentage of the maximal increase observed.[2]. Adcock IM, et al. Ligand-induced differentiation of glucocorticoid receptor (GR) trans-repression and transactivation: preferential targetting of NF-kappaB and lack of I-kappaB involvement. Br J Pharmacol. 1999 Jun;127(4):1003-11.
  • (a) Western blot analysis of β2-receptor (β2R) expression at 24 h following increasing concentrations of fluticasone propionate (FP), budesonide (Bud), dexamethasone (dex) or RU486. The single 47 kD band representing the β2-receptor is indicated by the arrow. Incubation with control media does not affect β2-receptor expression. (b) Graphical representation of the results shown in (a). Results are shown as the percentage change in β2-receptor band density compared to control untreated cells and are representative of four individual experiments and are reported as the means±s.e.means.[2]. Adcock IM, et al. Ligand-induced differentiation of glucocorticoid receptor (GR) trans-repression and transactivation: preferential targetting of NF-kappaB and lack of I-kappaB involvement. Br J Pharmacol. 1999 Jun;127(4):1003-11.
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