标签归档：吡唑

1-叔丁基-3-(1-萘基)-1H-吡唑并[3,4-d]嘧啶-4-胺盐酸盐,1-Naphthyl PP1 (hydrochloride),CAS：956025-47-1,货号：IN0290-10mg

发表于由

1-叔丁基-3-(1-萘基)-1H-吡唑并[3,4-d]嘧啶-4-胺盐酸盐,1-Naphthyl PP1 (hydrochloride),CAS：956025-47-1,货号：IN0290-10mg

市场价： ￥2000.0
价格：
￥1600.00
品牌： solarbio
规格： 10mg
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参考文献

AZD4547

发表于由

AZD4547

货号：
IA2440

品牌：
Jinpan

AZD4547

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产品简介
别名 rel-N-[5-[2-(3,5-二甲氧基苯基)乙基]-1H-吡唑-3-基]-4-[(3R,5S)-3,5-二甲基-1-哌嗪基]苯甲酰胺
CAS 1035270-39-3
分子式 C26H33N5O3
分子量 463.57
储存条件 -20℃
纯度 ≥98%
单位 瓶
生物活性 AZD4547 是一种有效的 FGFR 家族抑制剂，作用于 FGFR1，FGFR2，FGFR3 和 FGFR4，IC50 分别为 0.2 nM，2.5 nM，1.8 nM 和 165 nM。[1]
IC50 FGFR1:0.2 nM ; FGFR2:2.5 nM ; FGFR3:1.8 nM ; FGFR4:165 nM[1]
In Vitro AZD4547还抑制重组VEGFR2（KDR）激酶活性，IC50为24 nM。在KG1a，Sum52-PE，MCF7和KMS11细胞系中，AZD4547有效抑制FGFR1,2和3酪氨酸激酶的自身磷酸化（IC50值分别为12,2和40 nM），并显示较弱的FGFR4细胞激酶活性抑制（IC50 = 142 nM）。与细胞KDR和IGFR配体诱导的磷酸化相比，观察到显著较弱的抑制活性（分别为258和828nM的IC 50值），代表相对于细胞FGFR1的约20和70倍选择性。此外，AZD4547在细胞水平上有效抑制通过FRS2，PLCγ和MAPK影响的FGFR磷酸化和下游信号传导[1]。
In Vivo 携带KMS11肿瘤的雌性SCID小鼠随机化并用一系列耐受良好剂量的AZD4547长期治疗。口服AZD4547治疗导致剂量依赖性肿瘤生长抑制。与载体治疗的对照组相比，每日两次施用3mg / kg的AZD4547可使统计学上显著的肿瘤生长抑制率为53％（单尾t检验P <0.0005），而剂量为12.5 mg / kg，每日一次，6.25 mg每天两次/ kg导致完全肿瘤停滞（P <0.0001）。进一步的功效研究在KG1a模型中使用12.5 mg / kg每日一次AZD4547导致65％的肿瘤生长抑制（P = 0.002）[1]。
激酶实验 将细胞用AZD4547或对照在37℃处理3小时，然后用10ng / mL aFGF / bFGF和10μg/ mL肝素刺激20分钟。用标准SDS-PAGE程序进行蛋白质印迹，并在4℃下进行抗体孵育过夜。抗体来自以下来源：FGFR1，FGFR2和FRS2，FGFR3蛋白，α-微管蛋白-B512和Bcl2（C2）和BIM [1]。
靶点 FGFR
动物实验 使用小鼠[1]瑞士衍生的裸（nu / nu）和严重联合免疫缺陷小鼠（SCID）。通过皮下注射0.1mL肿瘤细胞（对于LoVo为1×106，对于HCT-15为1×107，对于Calu-6为1×107）或0.2mL（对于KMS11和2×107）来建立肿瘤异种移植物。 KG1a）与基质胶1：1混合，但LoVo和HCT-15除外，其中不含Matrigel。当肿瘤达到超过0.2cm 3的确定大小时，将小鼠随机分入对照组和治疗组（AZD4547,1.5-50mg / kg，每日一次或通过口服强饲法每日两次）。在研究期间每周两次记录肿瘤体积（通过厚度测量），动物体重和肿瘤状况。计算肿瘤体积。
细胞实验 将细胞系与固定浓度的AZD4547一起温育72小时。对于荧光激活细胞分选（FACS），将细胞用70％乙醇固定，然后与碘化丙锭/ RNase A标记溶液一起孵育。用FACSCalibur仪器和CellQuest分析软件评估细胞周期谱。对于细胞凋亡分析，轻轻收获细胞和培养基并离心，然后洗涤细胞沉淀。然后处理细胞用于膜联蛋白V-异硫氰酸荧光素（FITC）染色和碘化丙锭摄取。然后用FACSCalibur仪器评估膜联蛋白V染色阳性细胞的比例，并通过CellQuest分析软件[1]进行象限分选。
数据来源文献 [1]. Gavine PR, et al. AZD4547: an orally bioavailable, potent, and selective inhibitor of the fibroblast growth factor receptor tyrosine kinase family. Cancer Res, 2012, 72(8), 2045-2056
规格 5mg 10mM*1mL in DMSO 10mg 50mg

AZD4547是一种新型选择性的FGFR抑制剂。

西地那非 标准品

发表于由

西地那非 标准品

货号：
YZ-510068

品牌：
中检所

西地那非 标准品

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产品简介
英文名称 Sildenafil
CAS 139755-83-2
分子式 C22H30N6O4S
分子量 474.58
储存条件 2-8℃
规格 100mg
别名：1-[4-乙氧基-3-[5-(6,7-二氢-1-甲基-7-氧代-3-丙基-1H-吡唑并[4,3d]嘧啶)]苯磺酰]-4-甲基哌嗪;5-[2-乙氧基-5-(4-甲基哌嗪-1-基磺基)苯基]-1-甲基-3-正丙基-1,6-二氢-7H-吡唑并[4,3-D]嘧啶-;5-[2-Ethoxy-5-(4-Methylpiperazin-1-yl-Sulphonyl)Phenyl]-1-Methyl-3-n-Pr

熔点：187-189°C

3-甲基吡唑

发表于由

3-甲基吡唑

货号：
IM2750

品牌：
Jinpan

3-甲基吡唑

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产品简介
有效期 2年
MDL MFCD00005240
EC EINECS 215-925-7
InChIKey XKVUYEYANWFIJX-UHFFFAOYSA-N
InChI InChI=1S/C4H6N2/c1-4-2-3-5-6-4/h2-3H,1H3,(H,5,6)
PubChem CID 15073
别名 3-甲基-2H-吡唑
英文名称 3-Methylpyrazole
CAS 1453-58-3
分子式 C4H6N2
分子量 82.1
储存条件 2-8℃
纯度 ≥98%
外观（性状） Light yellow to reddish brown Powder
单位 瓶
生物活性 3-Methylpyrazole （3-MeP）, a very weak inhibitor of ADH，could inhibit the metabolism of MAM by rat liver microsomes[1].
In Vitro The addition of varying amounts of 3-MeP or 4-IP to liver microsomal incubations resulted in the inhibition of MAM metabolism. significant inhibition (approximately 20% with respect to control incubations without inhibitor) was obtained with a concentration of 4-IP of 0.001 raM. At the same concentration, little inhibition by 3-MeP was evident; however, a 25% inhibition of the metabolism resulted when the concentration of 3-MeP was in_x005fcreased to 0.01 mM.[1]
In Vivo Pretreatment of rats with either 4-IP or 3-MeP 15 min prior to treatment with 25 mg/kg MAMOAc produced a dose-dependent inhibition of liver DNA methylation, assayed 6 h after administration of the carcinogen. In the case of pretreatment with 3-MeP, the means of decreases in the levels of the methylated guanines were 25%, 31% (P < 0.05), and 49 % (P < 0.0 J), for respective do ses of 0.1, 0.3, and 1.0 mmol/kg of the inhibitor. In the colon mucosa, pretreatment with 3-MeP produced no inhibition of DNA methylation in the colon mucosa, rather an increase was observed. Thus, with pretreatments of 3-MeP of 0.1, 0.3, and 1.0 mmol/kg, the percent increases in colon mucosa levels of O6-MeG and 7-MEG were 37%, 56% (P< 0.03), and 52% (P < 0.01), respectively.[1]
激酶实验 Rats were sacrificed by decapitation, and livers quickly excised, rinsed with ice-cold 0.9% NaC1 (saline), and homogenized in 3 weight volumes of ice-cold 0.25 M sucrose, 0.01 M potassium phosphate buffer, pH 7.5. The homogenate was centrifuged at 9000 g for 20 rain, and the microsomal fraction was obtained by centrifuging the resulting supernatant at 100000 g for 1 h. Microsomes were washed by resuspension in the same medium used for homogenization, followed by recentrifugation. The sediment from this step was weighed and resuspended in 3 weight-volumes of 0.1 M potassium phosphate buffer, pH 7.0. Following assay of protein content (Lowry et al. 1951), aliquots of resuspended microsomes (approximately 1 mg protein) were incubated, in a total volume of 0.5 ml, with 50 nmol MAM(1,2-14C), 3.5 mM glucose-6-phosphate, 5 units glucose-6- phosphate dehydrogenase, 1.5 mM NADP, 3.5 mM MgC12, and various concentrations of 3-MeP or 4-IP, in 0.1 M potassium phosphate buffer, pH 7.0. After incubation in a shaker bath at 37 ~ for 30 min, the reaction was stopped by plunging the incubation vessels into an ice bath. The suspensions were clarified and deproteinized by centrifugal ultrafiltration 600g, 30rain, 0-4~ using Centrifree Micropartition System tubes. Aliquots of the ultrafiltrates were submitted to HPLC using two Whatman ODS-3 (0.46 x 25 cm) columns in series, preceded by a 0.7 x 5 em column packed with Aminex A-29 anion exchange resin in the phosphate form. The system was eluted with 0.2 M ammonium phosphate buffer, pH 3.1, at a flow rate of 0.5 ml/min for the first 28 rain, and at 1 ml/min thereafter. The function of the Aminex A-29 precolumn was to retard the elution of formic acid (pK~ = 3.77) which would otherwise coelute with formaldehyde, very near the void volume. The absorbance of the effluent was monitored at 215 nm, and fractions were collected at 1 rain intervals for determination of radioactivity by scintillation counting. The extent of metabolism was determined by summing the radioactivity in the formaldehyde, methanol, and formic acid peaks, and subtracting from this the radioactivity found in the formaldehyde and methanol peaks which resulted when identical incubations were carried out in the absence of microsomes. Under these conditions, 2.4 nmol MAM was metabolized to prod_x005fucts in 30 min.[1]
SMILES CC1=NNC=C1
靶点 Others
动物实验 Determination of methylated guanines in rat liver and colon mucosa DNA. Rats were injected i.p. with saline or with various concentra_x005ftions of 3-MeP or 4-IP in saline. After 15 min, the animals were injected s.c. with 25 mg/kg of nonradioactive MAMOAc dissolved in saline. The rats were sacrificed 6 h later and the livers and colons rinsed with ice-cold 0.14 M KC1 and stored at -70 ~ DNA from livers and colon mucosae was isolated by the method of Daoud and Irving (1977). Purified DNA was hydrolyzed in 0.1 N HC1 at 37 ~ for 18 h. After determination of absorbance at 266 nm, portions of the hydrolyzates were submitted to HPLC using a Whatman Partisil SCX column (0.46 x 25 cm) with an Aquapore CX-300 guard column. The system was eluted with 0.1 M ammonium phosphate buffer, pH 2.0, at a rate of 2 ml/min. The effluent was sequentially monitored for absorbance at 276 nm for the quantitation of guanine, and for fluorescence at 370 nm (excitation, 295 nm) for the quantitation of O6-MeG and 7- MeG (Herron and Shank 1981).[1]
数据来源文献 [1]. Fiala ES, et al. Differential effects of 4-iodopyrazole and 3-methylpyrazole on the metabolic activation of methylazoxymethanol to a DNA methylating species by rat liver and rat colon mucosa in vivo. J Cancer Res Clin Oncol. 1987;113(2):145-50.
规格 200mg 500mg 1g

是酒精脱氢酶的弱抑制剂。

安乃近 标准品

发表于由

安乃近 标准品

货号：
YZ-100002

品牌：
中检所

安乃近 标准品

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产品简介
英文名称 Analgin
CAS 5907-38-0
分子式 C13H16N3O4S.Na
分子量 333.34
储存条件 2-8℃
规格 200mg
别名：二吡喃酮;安乃近水合物;[(1,5-二甲基-2-苯基-3-氧代-2,3-二氢-1H-吡唑-4-基)甲氨基]甲烷磺酸钠盐;安乃近;(Antipyrinylmethylamino)MethanesulfonicacidSodiumsaltMonohydrate;DipyroneMonohydrate;MetamizolMonohydrate;Methanesulfonicacid,(Antipyrin）

7H-吡唑并4,3-E1,2,4三氮唑并1,5-C嘧啶-5-胺

发表于由

7H-吡唑并[4,3-E][1,2,4]三氮唑并[1,5-C]嘧啶-5-胺

货号：
IS0410

品牌：
Jinpan

7H-吡唑并4,3-E1,2,4三氮唑并1,5-C嘧啶-5-胺

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产品简介
MDL MFCD00933778
别名 2-(2-furanyl)-7-(2-phenylethyl)-7H-pyrazolo[4,3-e][1,2,4]triazolo[1,5-c]pyrimidin-5-amine
英文名称 SCH 58261
CAS 160098-96-4
分子式 C18H15N7O
分子量 345.36
纯度 ≥98%
单位 瓶
货期 1-2天
SMILES NC1=NC(N(CCC2=CC=CC=C2)N=C3)=C3C4=NC(C5=CC=CO5)=NN14
靶点 Adenosine Receptor
规格 5mg 10mM*1mL (in DMSO) 10mg
SCH 58261 是一种强效、选择性的竞争性腺苷 A2A 受体拮抗剂。

AM 251；1-(2,4-二氯苯基)-5-(4-碘苯基)-4-甲基-N-(哌啶-1-基)-1H-吡唑-3-甲酰胺

发表于由

AM 251；1-(2,4-二氯苯基)-5-(4-碘苯基)-4-甲基-N-(哌啶-1-基)-1H-吡唑-3-甲酰胺

货号：
IA3760

品牌：
Jinpan

AM 251；1-(2,4-二氯苯基)-5-(4-碘苯基)-4-甲基-N-(哌啶-1-基)-1H-吡唑-3-甲酰胺

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产品简介
MDL MFCD01861181
InChIKey BUZAJRPLUGXRAB-UHFFFAOYSA-N
InChI InChI=1S/C22H21Cl2IN4O/c1-14-20(22(30)27-28-11-3-2-4-12-28)26-29(19-10-7-16(23)13-18(19)24)21(14)15-5-8-17(25)9-6-15/h5-10,13H,2-4,11-12H2,1H3,(H,27,30)
PubChem CID 2125
别名 1-(2,4-二氯苯基)-5-(4-碘苯基)-4-甲基-N-(哌啶-1-基)-1H-吡唑-3-甲酰胺
CAS 183232-66-8
分子式 C22H21Cl2IN4O
分子量 555.24
储存条件 2-8℃
纯度 ≥98%
单位 瓶
生物活性 AM251是选择性大麻素1 (CB1) 受体拮抗剂，IC50 为8 nM。AM251也是 GPR55 的激动剂，EC50为39 nM[1-7]。
IC50 8 nM (CB1 receptor)[1]
In Vitro AM251在HEK293细胞中产生激动剂反应，类似于在酵母表达系统中发现的[2]。 AM-251在未受刺激和乙酰化的LDL刺激的Raw 264.7巨噬细胞，CB2 +/+和CB2 – / – 腹膜巨噬细胞中减少胆固醇酯的合成[3]。
In Vivo CB1拮抗剂AM251（3mg/kg，ip）降低辣椒素诱发的夜间行为（F1,18 = 28.45，p <0.0001）。这种抑制作用是基因型依赖的（F1,18 = 14.83，p <0.01），基因型和AM251的作用之间的相互作用接近显著性（F1,18 = 4.704，p = 0.0587）。计划的比较显示，AM251减少了脂肪酸酰胺水解酶（FAAH）KO小鼠中的抗抑郁行为（p <0.01），但相对于它们各自的载体对照，未能改变WT小鼠中的抗抑郁行为（p> 0.2）。 AM251（3mg/kg，ip）减少FAAH KO（F1,9 = 21.43，p <0.01）但不是WT小鼠（p> 0.3）的热超敏反应的持续时间。 AM251在FAAH KO中以时间依赖性方式抑制辣椒素诱发的热超敏反应（F5,9 = 4.349，p <0.01），但在WT小鼠中没有（p> 0.3）。事后分析显示，与FAAH KO动物相比，接受载体（ip）的FAAH KO小鼠在辣椒素后30（p <0.05），60（p <0.05）和90（p <0.001）分钟时显示出增强的热超敏反应。收到AM251）[4]。单向ANOVA显示，与对照相比，注射到大鼠中的AM251（AM-251）显著降低了张开臂中的进入百分比和在张开臂中花费的时间。 Tukey-Kramer测试分析显示，与开放臂中花费的时间相比，对照大鼠的剂量为1mg/kg（P <0.05）和5mg/kg（P <0.01）显著降低。此外，AM251显著降低了开放臂中1和5 mg/kg剂量的百分比（P <0.05）[5]。
激酶实验 在12孔培养板中接种巨噬细胞（2×106 /孔）。在从2mg/mL乙醇储备溶液中加入7-酮胆固醇（7KC）之前1小时，从在DMSO中制备的4mM储备溶液中加入AM-251或SR144528。调节对照以接受等体积的DMSO和乙醇。 16小时后，测定胱天蛋白酶-3活性。所有治疗均一式三份进行，数据以平均RFLU/mg蛋白±SD表示[3]。
SMILES O=C(C1=NN(C2=CC=C(Cl)C=C2Cl)C(C3=CC=C(I)C=C3)=C1C)NN4CCCCC4
靶点 Cannabinoid Receptor antagonist
动物实验 小鼠[4]在这些实验中使用总共246只体重为17-48g的小鼠。确定基线反应后，小鼠接受单次ip注射（5 mL/kg）AMG9810（3 mg/kg，每组n = 5），AM251（3 mg/kg，每组n = 5）或载体（每组n = 6）。在i.pl.之前30分钟进行Ip注射。辣椒素或载体给药。在皮内注射辣椒素或载体之前和之后10,30,60,90和120分钟评估缩爪潜伏期。在每个时间点在每只爪中一式两份地测量爪撤回潜伏期，并且报告为来自每只动物的两次重复测定的平均值，对受试者进行平均。大鼠[5]使用重量为250-350的雄性Wistar大鼠。使用以下试剂：CB1受体激动剂，Win-55212（0.3,1和5mg/kg，ip）; CB1受体拮抗剂，AM251（0.3,1和5mg/kg，ip）;在该研究中，内源性大麻素分解抑制剂URB-597（0.03,0.1和0.3mg/kg，ip）。生理盐水（0.9％氯化钠）用作载体。所有药物都是新鲜制备的，并以每10g体重大鼠0.1mL的体积腹膜内（ip）给药。将所有物质溶解在生理盐水中并在升高的迷宫测试前30分钟施用。
数据来源文献 [1]. Bruno A, et al. Beyond radio-displacement techniques for identification of CB1 ligands: the first application of afluorescence-quenching assay. Sci Rep. 2014 Jan 20;4:3757.
[2]. Sharir H, et al. Pharmacological characterization of GPR55, a putative cannabinoid receptor. Pharmacol Ther. 2010 Jun;126(3):301-13.
[3]. Thewke D, et al. AM-251 and SR144528 are acyl CoA:cholesterol acyltransferase inhibitors. Biochem Biophys Res Commun. 2009 Apr 3;381(2):181-6.
[4]. Carey LM, et al. A pro-nociceptive phenotype unmasked in mice lacking fatty-acid amide hydrolase. Mol Pain. 2016 May 13;12. pii: 1744806916649192.
[5]. Komaki A, et al. Study the Effect of Endocannabinoid System on Rat Behavior in Elevated Plus-Maze. Basic Clin Neurosci. 2015 Jul;6(3):147-53.
[6]. Jiang X, et al. Role of cannabinoid receptor type 1 in tibial and pudendal neuromodulation of bladder overactivity in cats. Am J Physiol Renal Physiol. 2017 Mar 1;312(3):F482-F488.
[7]. Sun L, et al. Endocannabinoid activation of CB1 receptors contributes to long-lasting reversal of neuropathic pain by repetitive spinal cord stimulation. Eur J Pain. 2017 May;21(5):804-814.
规格 5mg 10mg 50mg

AM251是选择性CB1受体拮抗剂。