磺胺苯吡唑

磺胺苯吡唑

货号:
IS2360

品牌:
Jinpan

磺胺苯吡唑

暂无详情
产品简介
有效期 2年
MDL MFCD00057226
EC EINECS 208-384-3
InChIKey QWCJHSGMANYXCW-UHFFFAOYSA-N
InChI InChI=1S/C15H14N4O2S/c16-12-6-8-14(9-7-12)22(20,21)18-15-10-11-17-19(15)13-4-2-1-3-5-13/h1-11,18H,16H2
PubChem CID 5335
别名 苯磺酰胺
英文名称 Sulfaphenazole
CAS 526-08-9
分子式 C15H14N4O2S
分子量 314.36
储存条件 2-8℃
纯度 ≥98%
外观(性状) White to pale yellow Powder
单位
生物活性 Sulfaphenazole (Depocid, Depotsulfonamide, Plisulfan, Raziosulfa) is an inhibitor of CYP2C9 with Ki value of 0.3 μM and demonstrates at least 100-fold selectivity over other CYP450 isoforms (Ki values of 63 and 29 μM for CYP2C8 and CYP2C18, respectively, and no activity at CYP1A1, CYP1A2, CYP3A4, CYP2C19).[1-2]
In Vitro Cystamine is a transglutaminase (TGase) inhibitor. In addition to TGase inhibition, cystamine is able to replenish glutathione and to inhibit caspase activity. The inhibitory capacity of cystamine in vitro is largely affected by the extent of the reduced form of the molecule. Nonetheless, cystamine inhibits in situ TGase activity decidedly stronger than cysteamine[1].
In Vivo Treatment with cystamine results in prolonged survival and decreased abnormal movements in a murine model of HD(Huntington’s disease). Cystamine does not cross the blood brain barrier[1]. Cystamine treatment normalizes transglutaminase and GGEL levels in R6/2 mice. cystamine has significant efficacy in improving the neurological and neuropathological phenotype observed in the R6/2 transgenic model of HD and strongly suggests that Tgase plays a role in HD[2].
SMILES O=S(C1=CC=C(N)C=C1)(NC2=CC=NN2C3=CC=CC=C3)=O
靶点 CYP2C9
动物实验 The cells (2×106) are labeled with BP at 1 mM or amine compounds (0 to 1.0 mM) in serum-free medium for 1h prior to harvesting. After washing twice with PBS, the cells are suspended in PBS containing protease inhibitors and sonicated (2 s pulse/2 s pause×5, 20% amplitude). The homogenate is centrifuged for 10 min at 20,000g at 4℃. The cell extract(0.2 mg/ml, 50 μl/well) is coated in the wells of a 96-well microtiter plate for 12 h at 4℃. The wells are then overcoated with 5% BSA in PBS for 1 h at room temperature. After washing three times with PBST, BP incorporated into the cellular proteins is assessed as performed in microtiter plate assays.[1]
细胞实验 Animal Models: wild-type (Wt) and R6/2 mice; Dosages: 112, 225, and 400 mg/kg; Administration: i.p.[2]
数据来源文献 [1] Jeon JH, et al. Exp Mol Med. 2004, 36(6):576-81.
[2] Dedeoglu A, et al. J Neurosci. 2002, 22(20):8942-50.
规格 50mg 100mg

是CYP2C9的特异性抑制剂。

吡唑蒽酮

吡唑蒽酮

货号:
IS1270

品牌:
Jinpan

吡唑蒽酮

暂无详情
产品简介
EC EINECS 204-955-6
MDL MFCD00022289
InChIKey ACPOUJIDANTYHO-UHFFFAOYSA-N
InChI InChI=1S/C14H8N2O/c17-14-9-5-2-1-4-8(9)13-12-10(14)6-3-7-11(12)15-16-13/h1-7H,(H,15,16)
PubChem CID 8515
别名 1,9-吡唑并蒽酮;吡唑蒽酮
英文名称 SP600125
CAS 129-56-6
分子式 C14H8N2O
分子量 220.23
纯度 Purity≥98%
单位
生物活性 SP600125是一种可逆,ATP竞争性的 JNK 抑制剂,抑制 JNK1, JNK2 和 JNK3 的 IC50 分别为 40, 40, 90 nM。[1-5]
In Vitro 在小鼠β细胞中,MIN6,SP600125(20μM)诱导p38 MAPK的磷酸化及其下游CREB依赖性启动子激活[2]。在HCT116细胞中,SP600125(20μM)阻断G2期至有丝分裂转变并诱导核内复制。 SP600125的这种能力与JNK抑制无关,但由于其抑制Aurora A和Polo样激酶1上游的CDK1-细胞周期蛋白B激活[3]。SP600125是一种ATP竞争性JNK2抑制剂,Ki值为0.19±0.06μM。SP600125抑制c-Jun的磷酸化,在Jurkat T细胞中IC50为5μM至10μM。在CD4 +细胞中,例如从人脐带或外周血中分离的Th0细胞,SP600125阻断细胞活化和分化,并抑制炎症基因COX-2,IL-2,IL-10,IFN-γ和TNF-α的表达。 ,IC50为5μM至12μM[1]。
In Vivo 以15或30mg/kg静脉内施用SP600125显著抑制TNF-α血清水平,而口服施用剂量依赖性地阻断TNF-α表达,在口服30mg/kg时观察到显著抑制[1]。 SP600125在体内减轻LPS诱导的大鼠ALI。 SP600125组大鼠BALF中TNF-α和IL-6的表达水平显著降低[4]。
SMILES O=C1C2=C3C(NN=C3C4=C1C=CC=C4)=CC=C2
靶点 Ferroptosis;JNK
动物实验 小鼠[1]雌性CD-1小鼠(8-10周龄)在PPCES载体中静脉注射或口服SP600125(30%PEG-400/20%聚丙二醇/ 15%Cremophor EL/5%乙醇/ 30%)在用盐水(0.5mg/kg)中的LPS静脉注射之前15分钟,最终体积为5mL/kg。在90分钟时,从腹腔静脉获得末端出血,并回收血清。通过使用ELISA分析样品的小鼠TNF-α。大鼠[4]将40只雄性Wistar大鼠随机分为4组(n = 10):对照组,LPS组,生理盐水组(NS)和SP600125组。通过气管内注射LPS诱导急性肺损伤(ALI)。简而言之,用戊巴比妥钠麻醉大鼠,然后气管内注射5mg/kg LPS。然后将大鼠置于垂直位置并旋转1分钟以将LPS分布在肺中。在LPS注射后10分钟通过腹膜内注射(15mg/kg)给予生理盐水或SP600125。
细胞实验 基本上进行mRNA半衰期的测定,除了在加入放线菌素D(5μg/ mL)之前用(细菌)脂多糖(LPS; 50ng/mL)刺激CD14 +细胞2小时。在放线菌素D之后立即加入SP600125(25μM)或载体(0.5%DMSO vol/vol)。通过使用实时逆转录(RT)-PCR进行分析。用RNeasy Mini试剂盒提取总RNA。使用TNF Taqman探针通过实时RT-PCR测量TNF mRNA。通过使用甘油醛-3-磷酸脱氢酶(GAPDH)表达将所有数据标准化。 TNF-α正向引物是5-CTGGCCCAGGCAGTCAGAT-3,反向引物是5-TATCTCTCAGCTCCACGCCATT-3。 Taqman探针序列是5-FAM-CCTGTAGCCCATGTTGTAGCAAACCCTCA-TAMRA-3[1]。
数据来源文献 [1]. Bennett BL, et al. SP600125, an anthrapyrazolone inhibitor of Jun N-terminal kinase. Proc Natl Acad Sci U S A, 2001, 98(24), 13681-13686.
[2]. Vaishnav D, et al. SP600125, an inhibitor of c-jun N-terminal kinase, activates CREB by a p38 MAPK-mediated pathway. Biochem Biophys Res Commun, 2003, 307(4), 855-860.
[3]. Kim JA, et al. SP600125 suppresses Cdk1 and induces endoreplication directly from G2 phase, independent of JNK inhibition. Oncogene, 2010, 29(11), 1702-1716.
[4]. Zheng Y, et al. JNK inhibitor SP600125 protects against lipopolysaccharide-induced acute lung injury via upregulation ofclaudin-4. Exp Ther Med. 2014 Jul;8(1):153-158.
[5]. Zhang H, et al. SP600125 Suppresses Keap1 Expression and Results in NRF2-mediated Prevention of Diabetic Nephropathy. J Mol Endocrinol. J Mol Endocrinol. 2018 Feb;60(2):145-157.
规格 10mg 10mM*1mL in DMSO 50mg

SP600125是一种可逆,ATP竞争性的 JNK 抑制剂。

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:IN0290-5mg

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:IN0290-5mg

市场价: 1120.0
价格:
896.00
品牌: solarbio
规格: 5mg
产品详情

说明书下载

参考文献

瑞加德松

瑞加德松

货号:
IR0830

品牌:
Jinpan

瑞加德松

暂无详情
产品简介
有效期 2年
MDL MFCD09832544
别名 类伽腺苷;2-[4-[(甲基氨基)羰基]-1H-吡唑-1-基]腺苷酸
英文名称 Regadenoson
CAS 313348-27-5
分子式 C15H18N8O5
分子量 390.35
储存条件 -20°C
纯度 ≥98%
外观(性状) White to beige Powder
单位
SMILES OC[C@@H]1[C@H]([C@H]([C@H](N2C=NC3=C2N=C(N4N=CC(C(NC)=O)=C4)N=C3N)O1)O)O
靶点 Adenosine Receptor
规格 5mg 10mg 25mg
Regadenoson是一种A 2A腺苷受体激动剂。

3-甲基吡唑

3-甲基吡唑

货号:
IM2750

品牌:
Jinpan

3-甲基吡唑

暂无详情
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
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。

AZD4547

AZD4547

货号:
IA2440

品牌:
Jinpan

AZD4547

暂无详情
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
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。

1-叔丁基-3-(1-萘基)-1H-吡唑并3,4-d嘧啶-4-胺盐酸盐

1-叔丁基-3-(1-萘基)-1H-吡唑并[3,4-d]嘧啶-4-胺盐酸盐

货号:
IN0290

品牌:
Jinpan

1-叔丁基-3-(1-萘基)-1H-吡唑并3,4-d嘧啶-4-胺盐酸盐

暂无详情
产品简介
MDL MFCD28142637
别名 1-NA-PP1hydrochloride
英文名称 1-Naphthyl PP1 (hydrochloride)
CAS 956025-47-1
分子式 C19H20ClN5
分子量 353.85
纯度 ≥98%
外观(性状)
单位
货期 1-2天
SMILES CC(N1N=C(C2=C3C=CC=CC3=CC=C2)C4=C(N)N=CN=C41)(C)C.[H]Cl
靶点 Bcr-Abl;Src;CDK2;CAMK II;c-Fyn
规格 5mg 10mM*1mL (in DMSO) 10mg

是一种选择性的 src 家族激酶抑制剂,能够抑制 v-Src 和 c-Fyn,c-Abl,CDK2 和CAMK II。