中文 
SB 431542 GLPBIO
基本售价：578.00元
产品描述 SB-431542, a small molecule inhibitor of the type I TGF-β receptor, blocks intracellular mediators of TGF-1 signaling, which leads to decreased TGF-β1–mediated proliferation, cytokines and collagen expression. In clinical settings, SB-431542 is widely used to treat respiratory asthma, and inhibits proliferation and synthesis of adventitial fibro in the process of pulmonary vascular remodeling.[1]In vitro study indicated that SB-431542 is able to inhibit ALK5 with an IC50 of 94 nM and other type I receptors, such as ALK4. Although SB-431542 inhibited ALK4 with an IC50 of 140 nM. Moreover, SB-431542 inhibited TGF-β1–induced collagen Iα1 and PAI-1 mRNA with IC50 values of 60 and 50 nM, respectively. In addition, SB-431542 inhibited TGF-β1–induced fibronectin mRNA and protein with IC50 values of 62 and 22 nM, respectively. These data demonstrate for the first time that ALK5 activity is required for TGF-β1 regulation of extracellular matrix markers FN, collagen Iα1, and PAI-1 mRNA.[1]In vivo study demonstrated that SB-431542 has the capacity to inhibit TGF-β1-induced gene expression. SB-431542 is recognized as a important inhibitor of the TGF-β1 receptors in blocking TGF-β1/Smads signal pathways in vascular remodeling. Moreover, hypoxia-induced vascular remodeling can significantly increase the amount of cytokines and collagen in vascular adventitia. However, after the treatment of SB-431542, attenuation of the fibrosis promoting effects of TGF-β1, including TGF-β1-induced cell proliferation, cell motility, cell migration and cell synthesis were observed. Therefore, it is significant to the identify the potential of SB-431542 for the treatment of hypoxia-induced pulmonary hypertension.[2]References:[1]. Laping NJ, et al. Inhibition of transforming growth factor (TGF)-beta1-induced extracellular matrix with a novel inhibitor of the TGF-beta type I receptor kinase activity: SB-431542. Mol Pharmacol. 2002 Jul;62(1):58-64.[2]. Yuan W, et al. SB-431542, a specific inhibitor of the TGF-β type I receptor inhibits hypoxia-induced proliferation of pulmonary artery adventitial fibroblasts. Pharmazie. 2016 Feb;71(2):94-100.SB-431542 是 I 型 TGF-β 受体的小分子抑制剂，可阻断 TGF-1 信号转导的细胞内介质，从而导致 TGF-β1 介导的增殖、细胞因子和胶原蛋白表达减少。在临床上，SB-431542被广泛用于治疗呼吸性哮喘，抑制肺血管重构过程中外膜纤维的增殖和合成。[1]体外研究表明，SB-431542 能够以 94 nM 的 IC50 抑制 ALK5 和其他 I 型受体，例如 ALK4。尽管 SB-431542 以 140 nM 的 IC50 抑制 ALK4。此外，SB-431542 抑制 TGF-β1 诱导的胶原蛋白 Iα1 和 PAI-1 mRNA，IC50 值分别为 60 和 50 nM。此外，SB-431542 抑制 TGF-β1 诱导的纤连蛋白 mRNA 和蛋白质，IC50 值分别为 62 和 22 nM。这些数据首次表明，TGF-β1 对细胞外基质标志物 FN、胶原蛋白 Iα1 和 PAI-1 mRNA 的调节需要 ALK5 活性。[1]体内研究表明，SB-431542 具有抑制 TGF-β1 诱导的基因表达的能力。 SB-431542 被认为是 TGF-β1 受体的重要抑制剂，可阻断血管重塑中的 TGF-β1/Smads 信号通路。此外，缺氧诱导的血管重塑可以显着增加血管外膜中细胞因子和胶原蛋白的数量。然而，在 SB-431542 处理后，观察到 TGF-β1 的纤维化促进作用减弱，包括 TGF-β1 诱导的细胞增殖、细胞运动、细胞迁移和细胞合成。因此，鉴定SB-431542治疗缺氧性肺动脉高压的潜力具有重要意义。[2]Chemical Properties Cas No.301836-41-9SDF化学名4-[4-(1,3-benzodioxol-5-yl)-5-pyridin-2-yl-1H-imidazol-2-yl]benzamideCanonical SMILESC1OC2=C(O1)C=C(C=C2)C3=C(NC(=N3)C4=CC=C(C=C4)C(=O)N)C5=CC=CC=N5分子式C22H16N4O3 分子量384.39 溶解度≥ 19.2mg/mL in DMSO, ≥ 10.06 mg/mL in EtOH with ultrasonic储存条件Store at -20°CGeneral tipsFor obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Shipping ConditionEvaluation sample solution : ship with blue iceAll other available size: ship with RT , or blue ice upon request溶解性数据 制备储备液1 mg5 mg10 mg1 mM2.6015 mL13.0076 mL26.0152 mL5 mM0.5203 mL2.6015 mL5.203 mL10 mM0.2602 mL1.3008 mL2.6015 mL
(Z)-PUGNAc试剂 GLPBIO
基本售价：431.00元
(1Z)-2-(乙酰基氨基)-2-脱氧-N-[[(苯基氨基)羰基]氧基]-D-葡萄糖酸肟DELTA-内酯) 产品描述 Proteins can be modified post-translationally by the addition of O-linked N-acetylglucosamine (O-GlcNAc). Nuclear cytoplasmic O-GlcNAcase and acetyltransferase (NCOAT) is a β-N-acetylglucosaminidase that removes GlcNAc from O-glycosylated proteins. PUGNAc is a (phenylcarbamoyl)oxime analog of GlcNAc that reversibly inhibits NCOAT (Ki = 40-110 nM).[1],[2] It also less potently inhibits other hexosaminidases and exochitinases.[2],[3],[4] (Z)-PUGNAc is a stereoisomer of PUGNAc that is a more potent inhibitor of NCOAT than the (E) isomer, both in vitro and in cells.[5]Reference:[1]. Horsch, M., Hoesch, L., Vasella, A., et al. N-Acetylglucosaminono-1,5-lactone oxime and the corresponding (phenylcarbamoyl)oxime. Novel and potent inhibitors of β-N-acetylglucosaminidase. European Journal of Biochemistry 197(3), 815-818 (1991).[2]. Dong, D.L.Y., and Hart, G.W. Purification and characterization of an O-GlcNAc selective N-acetyl-β-D-glucosaminidase from rat spleen cytosol. The Journal of Biological Chemisty 269(30), 19321-19330 (1994).[3]. Hodge, A., Gooday, G.W., and Alexander, I.J. Inhibition of chitinolytic activities from tree species and associated fungi. Phytochemistry 41, 77-84 (1996).[4]. Macauley, M.S., Bubb, A.K., Martinez-Fleites, C., et al. Elevation of global O-GlcNAc levels in 3T3-L1 adipocytes by selective inhibition of O-GlcNAcase does not induce insulin resistance. The Journal of Biological Chemisty 283(50), 34687-34695 (2008).[5]. Perreira, M., Kim, E.J., Thomas, C.J., et al. Inhibition of O-GlcNAcase by PUGNAc is dependent upon the oxime stereochemistry. Bioorganic & Medicinal Chemistry 14, 837-846 (2006).Chemical Properties Cas No. 132489-69-1 SDF 别名 (1Z)-2-(乙酰基氨基)-2-脱氧-N-[[(苯基氨基)羰基]氧基]-D-葡萄糖酸肟DELTA-内酯 化学名 [(Z)-[(3R,4R,5S,6R)-3-Acetamido-4,5-dihydroxy-6-(hydroxymethyl)oxan-2-ylidene]amino] N-phenylcarbamate Canonical SMILES O=C(C)N[C@@H]1[C@@H](O)[C@H](O)[C@@H](CO)O/C1=N\OC(NC2=CC=CC=C2)=O 分子式 C15H19N3O7 分子量 353.33 溶解度 1mg/ml in DMSO， 10mg/mL in DMF 储存条件 Store at -20°C, stored under nitrogen General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while. Shipping Condition Evaluation sample solution : ship with blue iceAll other available size: ship with RT , or blue ice upon request 溶解性数据 制备储备液 1 mg 5 mg 10 mg 1 mM 2.8302 mL 14.1511 mL 28.3022 mL 5 mM 0.566 mL 2.8302 mL 5.6604 mL 10 mM 0.283 mL 1.4151 mL 2.8302 mL
脂质多糖（Lipopolysaccharides from Escherichia coli O111:B4 LPS试剂）GLPBIO
基本售价：1981.00元
Lipopolysaccharides from Escherichia coli O111:B4(Synonyms: LPS, 脂多糖) 脂质多糖（Lipopolysaccharides from Escherichia coli O111:B4 LPS）通过凝胶过滤色谱法纯化。产品描述 This product is extracted from E. coli serotype O111:B4 and purified by gel filtration. The source strain is from a private collection. This LPS serotype has been used to stimulate B-cells and induce NOS in human hepatocytes.Lipopolysaccharides (LPSs) are characteristic components of the cell wall of Gram-negative bacteria. LPS and its lipid A moiety stimulate cells of the innate immune system by the Toll-like receptor 4 (TLR4), a member of the Toll-like receptor protein family, which recognizes common pathogen-associated molecular-patterns (PAMPs).Lipopolysaccharide (LPS) is vital to both the structural and functional integrity of the Gram-negative bacterial outer membrane. Ubiquitously expressed by all Gram-negative bacteria, and containing several well-conserved domains, lipopolysaccharide also serves as one of the primary targets of the innate arm of the mammalian immune system. The lipopolysaccharides have a profound effect on the mammalian immune system and are of great significance in the pathophysiology of many disease processes.[1]In vitro study indicated that the bone resorption and the inhibition of collagen synthesis caused by lipopolysaccharide could be prevented by PB effectively. Lipopolysaccharide at a concentration of 10μg /ml inhibited bone collagen synthesis by 43% and PB reversed this inhibition in a dose-dependent manner. Even at concentrations as low as 5 μg/ml (PB: LPS =1:2) it reduced the bone-resorbing activity of the lipopolysaccharide by 85%. This effect was specific for resorption stimulated by lipopolysaccharide.[2]Lipopolysaccharide preconditioning to mice obviously reduced coelenterazine-Induced fluorescent lesions of Colon26 cells at 7 and 14 days after the intraportal inoculation of Colon26 cells, which expressed Nano-lantern, in comparison to control mice. Moreover, lipopolysaccharide preconditioning significantly reduced the fluorescence intensity of tumors than that of the control mice at both 7 and 14 days after tumor inoculation as well as reduced the liver weight in comparison to control mice at 14 days. Results showed that tumor metastasis was exclusively found in the lungs but not liver. Lipopolysaccharide preconditioning also tended to reduce lung metastasis in vivo.[3]References:[1]. Erridge C, et al. Structure and function of lipopolysaccharides. Microbes Infect. 2002 Jul;4(8):837-51.[2]. Harvey W, et al. In vitro inhibition of lipopolysaccharide-induced bone resorption by polymyxin B. Br J Exp Pathol. 1986 Oct;67(5):699-705.[3]. Nishikawa M, et al. Lipopolysaccharide preconditioning reduces liver metastasis of Colon26 cells by enhancing antitumor activity of natural killer cells and natural killer T cells in murine liver. J Gastroenterol Hepatol. 2021 Jul;36(7):1889-1898.该产品从大肠杆菌血清型 O111:B4 中提取，并通过凝胶过滤进行纯化。源菌株来自私人收藏。这种 LPS 血清型已被用于刺激 B 细胞并在人肝细胞中诱导 NOS。脂多糖 (LPS) 是革兰氏阴性菌细胞壁的特征成分。 LPS 及其脂质 A 部分通过 Toll 样受体 4 (TLR4) 刺激先天免疫系统的细胞，TLR4 是 Toll 样受体蛋白家族的一员，可识别常见的病原体相关分子模式 (PAMP)。\n脂多糖 (LPS) 对于革兰氏阴性细菌外膜的结构和功能完整性至关重要。脂多糖由所有革兰氏阴性菌普遍表达，并包含几个保存完好的结构域，也是哺乳动物免疫系统先天性臂的主要靶标之一。脂多糖对哺乳动物的免疫系统具有深远的影响，在许多疾病过程的病理生理学中具有重要意义。[1]体外研究表明，PB可有效阻止脂多糖引起的骨吸收和胶原合成抑制。浓度为 10μg/ml 的脂多糖抑制骨胶原合成达 43%，PB 以剂量依赖的方式逆转这种抑制作用。即使浓度低至 5 μg/ml（PB: LPS =1:2），它也会将脂多糖的骨吸收活性降低 85%。这种效应对脂多糖刺激的再吸收具有特异性。[2]与对照小鼠相比，在门静脉内接种表达 Nano-lantern 的 Colon26 细胞后 7 天和 14 天，对小鼠进行脂多糖预处理明显减少了腔肠素诱导的 Colon26 细胞荧光损伤。此外，在肿瘤接种后 7 天和 14 天，脂多糖预处理显着降低了肿瘤的荧光强度，与对照小鼠相比，在 14 天时，与对照小鼠相比，肝脏重量也有所减轻。结果表明，肿瘤转移仅发生在肺部，而不是肝脏。脂多糖预处理也倾向于减少体内肺转移。[3]Chemical Properties Cas No.SDF别名LPS, 脂多糖分子式分子量溶解度Soluble in water (5 mg/ml) or cell culture medium (1 mg/ml)储存条件Store at 2-8°CGeneral tipsFor obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Shipping ConditionEvaluation sample solution : ship with blue iceAll other available size: ship with RT , or blue ice upon request
TBTU 试剂 GLPBIO
基本售价：126.00元
TBTU(Synonyms: 2-(1H-苯并三偶氮L-1-基)-1,1,3,3-四甲基脲四氟硼酸酯) 肽偶联剂 产品描述 IC50: Not available.The utilization of new peptide coupling reagents in organic synthesis has greatly flourished the development of peptide synthesis. TBTU, 2-(1H-Benzotriazol-1-yl)-1,1,3,3-tetramethyluronoium hexafluorphosphate, serves as a typical peptide coupling reagent which has a relatively lower racemization. In normal condition, coupling reactions mediated by TETU take only six minutes to complete when HOBt is added. Moreover, racemization in this reaction could be reduced to insignificant levels. Due to these features, TBTU is regarded as one of the key reagents of choice in both manufactory and lab. [1]In vitro: It was reported that during synthesis of the macrocyclic peptide cyclotheonamide B, TBTU played an important role in coupling steps. Studies showed that TBTU had been successfully used in several coupling reactions, for instance, this reagent was suitable for couplings involving proline nitrogen, and therefore served as a crucial reagent for the macrolactamization. Although TBTU normally proceeded with little racemization, to suppress the racemization completely, HOBt was also required. Thus, in a typical reaction system, TBTU was added into 0.5 mM solution of CH2Cl2, followed by addition of HOBt and pyridine. Finally, cyclopentapeptide was obtained with a yield of 61%. [1]In vivo: So far, no in vivo data has been reported.Clinical trial: So far, no clinical trial has been conducted.Reference:[1]Bastiaans HM, van der Baan JL and Ottenheijm HC. Flexible and convergent total synthesis of cyclotheonamide B. J. Org. Chem. 1997; 62: 3880-9.Chemical Properties Cas No.125700-67-6SDF别名2-(1H-苯并三偶氮L-1-基)-1,1,3,3-四甲基脲四氟硼酸酯化学名[benzotriazol-1-yloxy(dimethylamino)methylidene]-dimethylazanium;tetrafluoroborateCanonical SMILES[B-](F)(F)(F)F.CN(C)C(=[N+](C)C)ON1C2=CC=CC=C2N=N1分子式C11H16BF4N5O 分子量321.1 溶解度≥ 106mg/mL in DMSO, ≥ 50.2mg/mL in Water, <5.11mg/mL in EtOH储存条件Desiccate at -20°CGeneral tipsFor obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Shipping ConditionEvaluation sample solution : ship with blue iceAll other available size: ship with RT , or blue ice upon request溶解性数据 制备储备液1 mg5 mg10 mg1 mM3.1143 mL15.5715 mL31.1429 mL5 mM0.6229 mL3.1143 mL6.2286 mL10 mM0.3114 mL1.5571 mL3.1143 mL
Ultra High Sensitivity ECL Kit (ECL超敏化学发光试剂盒) GLPBIO
基本售价：350.00元
Ultra High Sensitivity ECL Kit (ECL超敏化学发光试剂盒) 实验参考方法 1. 将HRP标记的抗体孵育结束后的蛋白印迹膜漂洗干净。2. 将ECL-A液和ECL-B液按等体积的比例混匀，即得到ECL工作液（现配现用），每5cm x 8cm的印迹膜约需要3-5 ml ECL工作液。注：吸取A液和B液的吸头一定要分开。3. 将印迹膜表面的液体在吸水纸上吸干，平铺在塑料膜上。4. 将配好的ECL工作液均匀的滴在印迹膜表面，反应2分钟左右后，去除ECL工作液。5. 将印迹膜夹在两层塑料膜之间，进行X光压片或者放入发光成像仪内拍照。注意事项:1.勿将超敏ECL化学发光工作液暴露在阳光或强光下,否则会导致其失活。建议将工作液保存在棕色瓶中,并避免长时间暴露在阳光下,实验室光照对工作液影响不大。2.使用生物素/亲和素体系时,避免使用脱脂奶粉作为封闭液,因为脱脂奶粉中含有多种内源性生物素,容易产生非特异性信号。3.使用充足的洗涤缓冲液、封闭液、抗体稀释液和底物工作液去覆盖印迹膜,以确保印迹膜处于湿润状态。使用大量的封闭液和洗涤液能减少非特异性信号的产生。4.叠氮钠是HRP酶的抑制剂,会对反应体系产生干扰,因此缓冲液中应避免使用叠氮钠做为防腐剂。5.印迹膜与ECL化学发光工作液孵育后5-30min内的发出的荧光是最强的,随后荧光会随着时间的延长减弱。蛋白点荧光较弱时可以适当延长曝光时间。 产品描述ECL试剂检测的核心原理为氧化反应发光：鲁米诺(lumino)作为发光底物的主要成分，在碱性条件下，通过辣根过氧化酶(HRP)催化，被H2O2氧化生成3-氨基邻苯二酸的激发态中间体，当其回到基态时发出光子，最大发射波长为425 nm。光子信号可通过X射线胶片或CCD成像仪被捕获。GlpBio超高灵敏度ECL试剂盒可在HRP和过氧化物存在下氧化鲁米诺，从而在飞克级抗原范围内进行检测。 该反应产生延长的化学发光，可以在X射线胶片或数字成像系统上看到该化学发光。GlpBio超高灵敏度ECL试剂盒可产生强效，长寿命的信号，再加上极低的背景水平，可延长曝光时间，从而检测低丰度蛋白质。 产品组成 Components 200ml 1000ml Solution A 100 mL 100 mL × 5 Solution B 100 mL 100 mL × 5 功能属性 应用&特点 卓越的灵敏度——皮克至低飞克级的抗原检测更高的信噪比——精准发光底物，降低背景更利节省抗体——优化底物系统，更高抗体结合力优异的性价比——更高的性能，更低的价格极佳的稳定性——新型氧化剂，常温下稳定保存1年运输方式 蓝冰运输. 储存条件 储存于4°C避光, 稳定保存1年。 用途 仅供研究使用!不能用于人体。
Nystatin (Fungicidin)试剂 GLPBIO
基本售价：450.00元
Nystatin (Fungicidin)(Synonyms: 制霉菌素) Nystatin (Fungicidin) 是一种口服活性多烯抗真菌抗生素，对酵母菌和支原体有效。 产品描述 Nystatin (Fungicidin) is a polyene antifungal antibiotic [1].Antifungal antibiotic is a pharmaceutical fungicide used to treat and prevent mycoses.Nystatin is a polyene antifungal antibiotic that is effective against yeast and mycoplasma [1]. In liquid media, Nystatin inhibited C. albicans at concentrations of 5-20 U/ml[2].In a 200 clinical isolates, which comprised of 113 Candida albicans, 54 Candida glabrata, 11 Candida parapsilosis, 11 Candida tropicalis and 11 Candida krusei. Nystatin exhibited MIC90 value of 4 mg/L against C. albicans isolates and all non-albicans Candida species tested. The results confirmed C. Albicans was most frequently susceptible and Nystatin could be used to treat vulvovaginal candidiasis caused by non-albicans Candida species. Nystatin would be an important choice for women affected by non-albicans Candida species which present higher resistance to the imidazole-based treatments [3].制霉菌素（Fungicidin）是一种多烯类抗真菌抗生素[1]。抗真菌抗生素是一种用于治疗和预防真菌病的药物真菌剂。制霉菌素是一种多烯类抗真菌抗生素，对酵母菌和支原体有有效的抗菌作用[1]。在液体培养基中，制霉菌素以5-20 U/ml的浓度抑制了白色念珠菌（Candida albicans）[2]。在200个临床分离株中，包括113个白色念珠菌、54个光滑念珠菌、11个副银白念珠菌、11个热带银白念珠菌和11个克鲁氏念珠菌。制霉菌素对C. albicans分离株和所有检测的非白色念珠菌菌株的MIC90值均为4 mg/L。结果证实C. albicans最常易感，制霉菌素可用于治疗由非白色念珠菌菌株引起的阴道念珠菌病。对于对咪唑类药物治疗具有较高抗药性的女性患者，制霉菌素是一种重要选择[3]。References:[1]. Childs AJ. Effect of Nystatin on Growth of Candida albicans During Antibiotic Therapy. Br Med J, 1956, 1(4968): 660-662.[2]. Stewart GT. Laboratory and Clinical Studies with Nystatin in Post-antibiotic Mycotic Infections. Br Med J, 1956, 1(4968): 658-660.[3]. Choukri F, Benderdouche M, Sednaoui P. In vitro susceptibility profile of 200 recent clinical isolates of Candida spp. to topical antifungal treatments of vulvovaginal candidiasis, the imidazoles and nystatin agents. J Mycol Med, 2014, 24(4): 303-307.
D-Luciferin (sodium salt) D-荧光素（钠盐）GLPBIO
基本售价：3328.00元
D-荧光素（钠盐）（别名：D-萤光素钠；D-(-)-萤光素钠；萤火虫萤光素钠；甲壳虫萤光素钠） 萤火虫荧光素酶的化学发光底物产品描述 D-荧光素钠盐是荧光素酶的底物，可催化生物发光昆虫产生光。D-Luciferin 是荧光素酶的常见底物，经常用于整个生物技术领域，尤其是体内成像技术。成像的作用机制是D-荧光素（底物）在ATP和荧光素酶的作用下被氧化发光。当D-荧光素过量时，产生的光子数与荧光素酶的浓度呈正相关。将携带荧光素酶编码基因 (Luc) 的质粒转染到细胞中后，将带有 Luc 的细胞植入研究动物体内，然后注射 D-荧光素，通过生物发光成像 (BLI) 检测光强变化。ATP 对该反应系统的影响也可用于根据生物发光强度的变化来指示能量或生命体征。[1][2]D-萤光素与萤光素酶、ATP和氧发生反应并发光，光被感光胶片检测到。[3]所有体外 D-荧光素测量均在 37°C 下 1 分钟后使用 30 秒的采集时间使用一系列 520 至 800 nm 的滤光片获得。体外分析表明，在相对较低但具有生物学相关性（体内）的底物浓度 (0.1 mM) 下，四种荧光素酶中的三种在与 D-荧光素结合时会产生最大信号。[4]体内分析表明，就信号强度而言，Luc2、CBG99 和 CBR2 的最佳底物是 D-荧光素。CBR2 使用近红外底物 NH2-NpLH2 给出最亮的信号。当与 CycLuc1 或 Akalumine-HCl 配对时，Akaluc 更亮。此外，还推荐了具有不同颜色的荧光素酶的新组合，这些荧光素酶具有在浅表组织中与单一底物进行复用的潜力，例如 CBG99/ D-荧光素 (540 nm) 和 CBR2/ D-荧光素 (620 nm)；CBG99/ D-荧光素 (540 nm) 和 Luc2/ D-荧光素 (610 nm)。[4]D-Luciferin (sodium salt)，D-蒿光素镶盐是蒿光素发酵的底物，可催化生物产生光昆虫产光。D-Luciferin 是蒿光素的常见底物，常用于整个生物技术领域，特别是体内合成技术。成象的作用机制是D-荧光素素（底物）在ATP和草光素发酵下的作用下被氧化发光。当D-禾光素过量时，生成的光子数与禾光素的浓度相当相关。将携带禾光素酶编码基因 (Luc) 的质粒转染到细胞中后，将带上Luc的细胞植入研究运动物体内，然后注射D-草光素，通过生物发射像(BLI)检测光强变化。ATP对应反应系统的影响也可用于根据生物发光强度的变化来指示能量或生命体征[1][ 2 ]。D-腐光素与腐光素、ATP和氧化反应并发，光被感光胶片检测到[3]。所有体外D-褐光素测定量在37°C下1分钟后使用30秒的采集时间使用一系列520至800 nm的滤光片获得。体外分析表示，在相对较低但具有生物相关性（体内）的底物浓度（0.1 mM )下，四种草光素发酵中的三种在与D-橄榄光素结合时会生产最大信号[4]。体内分析表明，就信号强度而言，Luc2、CBG99 和 CBR2 的最佳底物是 D-橄榄光素。CBR2 使用近红外底物 NH2-NpLH2 给出最亮的信号。当与CycLuc1或Akalumine-HCl配比这时，Akaluc更亮了。另外，还推荐了具有不同颜色的草光素发酵剂的组合，这些草光素发酵剂在浅表组中与单底物进进行复用的潜能，例如CBG99/ D-蒿光素( 540 nm) 和 CBR2/ D-荧光素 (620 nm)；CBG99/ D-荥光素 (540 nm) 和 Luc2/ D-荥光素 (610 nm) [4 ]。参考文献：[1] McElroy WD。隔离系统中生物发光的能源。Proc Natl Acad Sci US A. 1947 年 11 月；33(11):342-5。内政部：10.1073/pnas.33.11.342。[2] 格林 A，麦克罗伊 WD。三磷酸腺苷在荧光素激活中的作用。Arch Biochem Biophys。1956 年 10 月；64(2):257-71。内政部：10.1016/0003-9861(56)90268-5。[3] Hauber R. 一种用于蛋白质印迹的新型、非常灵敏的生物发光增强检测系统。J. 临床。化学。临床。生化。1987,25, 第 511-514 页。doi:10.1515/cclm.1987.25.8.511。[4] Zambito G. 使用荧光素类似物评估点击甲虫和萤火虫荧光素酶的亮度和光谱特性：鉴定用于体内生物发光成像的荧光素酶和底物的首选配对。分子成像生物学。2020 年 12 月；22(6):1523-1531。内政部：10.1007/s11307-020-01523-7。化学性质 编号 103404-75-7 自卫队 别名 D-卤光素镶盐; D-(-)-萤光素钠；萤火虫荧光素钠；甲虫萤光素钠 典型的微笑 O=C([O-])[C@H]1CSC(C(S2)=NC3=C2C=C(O)C=C3)=N1.[Na+] 分子式 C 11 H 7 N 2 O 3 S 2 •Na 份量 302.3 溶解度 DMSO：100 mg/mL (330.80 mM) 水：33.33 mg/mL (110.25 mM) 存储条件 -20°C避光保存 一般提示 为获得更高的溶解度，请将管子在 37 ℃ 下加热并在超声波浴中摇晃一会儿。 运输条件 评估样品溶液：随附 blue ice所有其他可用尺寸：按要求随 RT 或 blue ice 一起装运 溶解性数据 制备储备液 1毫克 5毫克 10毫克 1毫米 3.308 毫升 16.5399 毫升 33.0797 毫升 5毫米 0.6616 毫升 3.308 毫升 6.6159 毫升 10毫米 0.3308 毫升 1.654 毫升 3.308 毫升
3-硝基丙酸 | 3-Nitropropionic acid GLPBIO
基本售价：378.00元
3-硝基丙酸(Synonyms: 3-硝基丙酸; β-Nitropropionic acid; Bovinocidin) 复合物 II 的抑制剂 产品描述3-Nitropropanoic acid 是琥珀酸脱氢酶的不可逆抑制剂。 参考文献：[1]。黄 LS 等。3-硝基丙酸是线粒体呼吸的自杀抑制剂，在被复合物 II 氧化后，与酶活性位点的催化碱基精氨酸形成共价加合物。J 生物化学。2006 年 3 月 3 日；281(9)：5965-72。 化学性质编号 504-88-1 自卫队 别名 3-硝基丙酸; β-硝基丙酸；杀牛素 化学名 3-硝基丙酸 典型的微笑 OC(CC[N+]([O-])=O)=O 分子式 C 3 H 5 NO 4 份量 119.08 溶解度 ≥ 6mg/mL 在 DMSO 中 存储条件 4°C，远离潮湿和光线 一般提示 为获得更高的溶解度，请将管子在 37 ℃ 下加热并在超声波浴中摇晃一会儿。 运输条件 评估样品溶液：随附 blue ice所有其他可用尺寸：按要求随 RT 或 blue ice 一起装运 溶解性数据制备储备液 1毫克 5毫克 10毫克 1毫米 8.3977 毫升 41.9886 毫升 83.9772 毫升 5毫米 1.6795 毫升 8.3977 毫升 16.7954 毫升 10毫米 0.8398 毫升 4.1989 毫升 8.3977 毫升
Erastin | 埃拉斯汀 GLPBIO
基本售价：350.00元
埃拉斯汀 铁死亡诱导剂 化学性质 卡斯号571203-78-6.SDF别名不适用化学名2-[1-[4-[2-（4-氯苯氧基）乙酰基]哌嗪-1-基]乙基]-3-（2-乙氧基苯基）喹唑啉-4-酮规范的微笑O=C1N（C2=CC=CC=C2OCC）C（C（N3CCN（C（COC4=CC=C（Cl）C=C4）=O）CC3）C）=NC5=C1C=CC=C5分子式C30H31ClN 4 O4 分子量547.04 溶解度≥ 10.92mg/mL 的 DMSO 溶液，温和加热储存条件储存在-20°C，溶液中不稳定，即用型。一般提示为了获得更高的溶解度，请在37°C下加热管子并在超声波浴中摇晃一会儿。运输条件评估样品解决方案：随附蓝冰 所有其他可用尺寸：随附 RT 或蓝冰（根据要求）产品描述Erastin是一种细胞渗透性铁死亡激活剂，对表达癌基因RAS的细胞具有选择性的抗肿瘤剂。Erastin通过直接与VDAC2 / 3结合来诱导铁死亡以改变线粒体外膜的通透性，从而降低NADH氧化速率。除了发挥靶向作用外，厄拉斯汀还增强了某些癌细胞的化疗、靶向治疗和免疫治疗，这表明厄拉斯汀在癌细胞治疗中的潜在作用。[3]Erastin及其类似物特异性地通过系统xc−抑制胱氨酸摄取，并在各种细胞环境中触发铁死亡，并且比SAS更有效。此外，Erastin 作为 HT-2500 和 Calu-1080 细胞中系统 xc− 功能的抑制剂，其效力比 SAS 高 1 倍（HT-1080：erastin IC50 = 0.20 μM，SAS IC 50 =450 μM;Calu-1：erastin IC50 = 0.14 μM，SAS IC50 = 460 μM）。[1]Erastin是SLC7A11的抑制剂，通过体外和体内实验被发现对结直肠CSC具有显着更强的细胞毒性作用。此外，Erastin减弱了结直肠CSC（结直肠癌干细胞）的化学抗性。对于体内实验，每两天将Erastin（10mg / kg）静脉注射到患有结直肠癌的小鼠中。结果发现，埃拉斯汀抑制了ALDH1活性，并减少了结直肠癌细胞的球体大小和数量。[2]参考文献：[1]. 迪克森 SJ， et al.胱氨酸 - 谷氨酸交换的药理学抑制诱导内质网应激和铁死亡。生活。2014 五月 20;3：e02523.[2]. 徐旭， 等.靶向SLC7A11通过诱导铁死亡特异性地抑制结直肠癌干细胞的进展。欧洲药学杂志 2020 1 月 152;105450：3。[4]. 杨莹， 等.Nedd2泛素化VDAC3/2020以抑制erastin诱导的黑色素瘤铁死亡。纳特公社。23 11 月 1;433（<>）：<>.Erastin是一种可渗透细胞的铁下垂激活剂和抗肿瘤剂，对表达癌基因RAS的细胞有选择性。Erastin通过直接与VDAC2/3结合来改变线粒体外膜的通透性，从而降低NADH氧化的速率，诱导铁下垂。除了发挥靶向作用外，erastin还增强了某些癌细胞的化疗、靶向治疗和免疫治疗的效果，这表明erastin在癌细胞治疗中的潜在作用。Erastin及其类似物通过系统xc-特异性地抑制胱氨酸的摄取，并在多种细胞环境中引发铁下垂，其作用比SAS更强。此外，Erastin在HT-1080和Calu-1细胞中作为系统xc功能抑制剂的效力是SAS的2500倍（HT-1080：Erastin IC50=0.20μM，SAS IC50=450μM;Calu-1：Erastin IC 50=0.14μM，SASIC50=460μM）。通过体外和体内实验，发现SLC7A11抑制剂Erastin对结肠直肠癌CSC具有更强的细胞毒性作用。此外，Erastin降低了结肠直肠癌干细胞的化学耐药性。对于体内实验，每两天向患有结直肠癌的小鼠静脉注射Erastin（10mg/kg）。发现Erastin抑制ALDH1活性，并减少结直肠癌细胞中的球体大小和数量。实验参考方法 细胞实验 [1]： 细胞系143B/BJeHLT/BJeLR/Calu-1/HT-1080制备方法溶于DMSO至20 mM。反应条件10 μM， 72 小时应用Erastin通过系统xc−抑制胱氨酸摄取，并在各种细胞环境中触发铁死亡。（HT-1080：埃拉斯汀IC50 = 0.20μM;Calu-1：埃拉斯汀 IC50 = 0.14 μM）动物实验[2]： 动物模型BALB/c 裸鼠（结直肠癌）制备方法溶于DMSO至20 mM剂型10毫克/千克，静脉注射应用埃拉斯汀抑制 ALDH1 活性，并减少结直肠癌细胞的球体大小和数量。引用：[1]. 迪克森 SJ， 等.胱氨酸 - 谷氨酸交换的药理学抑制诱导内质网应激和铁死亡。生活。2014 五月 20;3：e02523.[2]. 徐旭， 等.靶向SLC7A11通过诱导铁死亡特异性地抑制结直肠癌干细胞的进展。欧洲药学杂志 2020 1 月 152;105450：<>。
Mitomycin C | 丝裂霉素C GLPBIO
基本售价：504.00元
Mitomycin C(Synonyms: 丝裂霉素 C,Ametycine)A potent DNA crosslinker产品描述Mitomycin C, a kind of antibiotic isolated from Streptomyces caespitosus or Streptomyces lavendulae, inhibits DNA synthesis through covalent mitomycin C-DNA adduct with EC50 values of 0.14μM in PC3 cells.Mitomycin C is an antibiotic that has demonstrated antitumor activity in preclinical and clinical studies and is widely used to treat various cancers. Mitomycin C is known to act synergistically with capecitabine and irinotecan. Some studies suggested that the combination of 5-FU plus Mitomycin C is more active in vitro than mono-therapy in colorectal cancer. The efficacy of the combination of Mitomycin C with other cytotoxic agents such as capecitabine and raltiterxed for colorectal cancer has been reported.[1]Mitomycin C not only potentiates TRAIL-induced apoptosis in HCT116 (p53−/−) colon cancer cells but also sensitizes TRAIL-resistant colon cancer cells HT-29 to the cytokine. At a mechanistic level, Mitomycin C downregulates cell survival proteins, including Bcl2, Mcl-1 and Bcl-XL, and upregulates pro-apoptotic proteins including Bax, Bim and the cell surface expression of TRAIL death receptors DR4 and DR5. Besides, the result of cell experiment indicates that Mitomycin C inhibits HT-29 with IC50 of 40 nM. [1,2]Mitomycin C also plays an effective role in antitumor in vivo. For in vivo experiment, Mitomycin C suppressed tumor growth significantly and did not impact the weight of the mice with TRAIL, indicating that the therapeutic combination of Mitomycin C and TRAIL is well-tolerated and has anti-tumor activity in vivo. [1]References:[1]. Cheng H, et al. Mitomycin C potentiates TRAIL-induced apoptosis through p53-independent upregulation of death receptors: evidence for the role of c-Jun N-terminal kinase activation. Cell Cycle. 2012 Sep 1;11(17):3312-23.[2]. Hodgkinson TJ, et al. Chemical synthesis and cytotoxicity of some azinomycin analogues devoid of the 1-azabicyclo[3.1.0]hexane subunit. Bioorg Med Chem Lett. 2000 Feb 7;10(3):239-41.丝裂霉素C（Mitomycin C）是一种从凯撒链霉菌或紫菜链霉菌中分离出来的抗生素，通过共价丝裂霉素C-DNA抑制PC3细胞中的DNA合成，EC50值为0.14μM。丝裂霉素C是一种抗生素，在临床前和临床研究中显示出抗肿瘤活性，广泛用于治疗各种癌症。研究结果表明，5-FU联合丝裂霉素C在结直肠癌的体外治疗中比单一疗法更有效。丝裂霉素C与其他细胞毒性药物如卡培他滨和雷立泰联合治疗结直肠癌的效果更好。丝裂霉素C不仅增强了TRAIL诱导的HCT116（p53-/-）结肠癌细胞凋亡，而且使结肠癌细胞HT-29对细胞因子敏感。丝裂霉素C下调细胞存活蛋白，包括Bcl2、Mcl-1和Bcl-XL，并上调促凋亡蛋白，包括Bax、Bim和TRAIL死亡受体DR4和DR5。此外，细胞实验结果表明，丝裂霉素C抑制HT-29细胞的IC50是40nM。丝裂霉素C在体内抗肿瘤中也发挥了重要作用。在体内实验中，丝裂霉素C显著抑制肿瘤生长，且不会影响TRAIL小鼠的体重，表明丝裂霉素C和TRAIL的治疗组合耐受性良好，在体内具有抗肿瘤活性。
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赛国生物为您提供10个 GLPBIO ，如在选择 GLPBIO产品 有疑问可以联系在线客服。
