Triiodothyronine;三碘甲状腺氨酸产品简介CAS6893-02-3中文名称三碘甲状腺氨酸英文名称Triiodothyronine别名T3;O-(4-Hydroxy-3-iodophenyl)-3,5-diiodo-L-tyrosine;L-3,3,5-Tresitope;3,3,5-Triiodo-L-thyronine;Lyothyronine;碘噻罗宁纯度≥98%分子式C15H12I3NO4分子量650.97外观(性状)White to brown Solid储存条件Powder : -20℃, 2 years;In solvent(母液): -20℃, 1 month; -80℃, 6 months溶解性Soluble in DMSO ≥10mg/mLECEINECS 229-999-3MDLMFCD00002593InChIKeyAUYYCJSJGJYCDS-LBPRGKRZSA-NInChIInChI=1S/C15H12I3NO4/c16-9-6-8(1-2-13(9)20)23-14-10(17)3-7(4-11(14)18)5-12(19)15(21)22/h1-4,6,12,20H,5,19H2,(H,21,22)/t12-/m0/s1PubChem CID5920SMILESOC1=C(I)C=C(OC2=C(I)C=C(C[C@H](N)C(O)=O)C=C2I)C=C1描述是有效的甲状腺激素受体 TRα 和 TRβ 的激动剂。(It is a potent agonist of thyroid hormone receptors TRα and TRβ.)靶点Thyroid Hormone Receptor通路Endocrinology & Hormones生物活性3,3',5-Triiodo-L-thyronine是有效的甲状腺激素受体 TRα 和 TRβ 的激动剂,Ki 值为2.3 nM。[1-2]In Vitro3, 3', 5-三碘-L-甲状腺素 (T3, 100nM) 刺激TRβ1过表达的肝细胞增殖[1]。 3, 3', 5-三碘-L-甲状腺素与人β1甲状腺激素受体 (hTRβ1) 结合, 并改变其构象。 3, 3', 5-三碘-L-甲状腺素促进生长, 诱导分化并调节代谢作用[2]。细胞实验制备甲状腺激素耗尽 (Td) 血清。进行甲基纤维素中肝癌细胞的生长。为了确定3, 3', 5-三碘-L-甲状腺素 (T3) 对细胞生长的影响, 在第0天将细胞以3×10 4个细胞/ 60mm培养皿的密度接种, 并在含有培养基的培养基中培养。 5%常规血清, 5%Td或5%Td和100nM T3。初始接种后3周, 甲基纤维素中的集落形成评分[1]。数据来源文献[1]. Lin KH, et al. Stimulation of proliferation by 3, 3', 5-triiodo-L-thyronine in poorly differentiated human hepatocarcinoma cells overexpressing beta 1 thyroid hormone receptor. Cancer Lett. 1994 Oct 14; 85 (2) :189-94.[2]. Bhat MK, et al. Conformational changes of human beta 1 thyroid hormone receptor induced by binding of 3, 3', 5-triiodo-L-thyronine. Biochem Biophys Res Commun. 1993 Aug 31; 195 (1) :385-92.Note以上数据均来自公开文献, Solarbio暂未进行独立验证, 仅供参考。These protocols are for reference only. Solarbio does not independently validate these methods.规格50mg 10mM*1mL in DMSO 100mg 500mg单位支
Pinocembrin;乔松素产品简介CAS480-39-7中文名称乔松素英文名称Pinocembrin别名Dihydrochrysin;Galangin flavanone;5,7-Dihydroxyflavanone;松属素纯度HPLC≥98%分子式C15H12O4分子量256.25外观(性状)White to off-white Solid储存条件Powder : 2-8℃, 2 years; In solvent(母液): -20℃, 1 month; -80℃, 6 months溶解性Soluble in DMSOMDLMFCD06858345SMILESO=C1C[C@@H](C2=CC=CC=C2)OC3=CC(O)=CC(O)=C13描述为竞争性的组氨酸脱羧酶 (histidine decarboxylase) 抑制剂。(It is a competitive histidine decarboxylase inhibitor.)靶点Histidine decarboxylase通路Metabolic Enzyme&Protease生物活性Pinocembrin ((+)-Pinocoembrin) 是从蜂胶中得到的黄酮类物质,为竞争性的组氨酸脱羧酶 (histidine decarboxylase) 抑制剂,同时为有效的抗过敏剂,具有抗氧化、抗菌、抗炎作用。[1]In VitroPinocembrin(5,10,25,50,100或200μM,24小时)显著降低RBL-2H3细胞的细胞活力[1]。 Pinocembrin(25或50μM)抑制iNOS,PGE-2和COX-2水平,增加p38-Mapk和IкB-α,并抑制IкB-α的磷酸化[1]。细胞活力测定[1]细胞系:RBL-2H3细胞浓度:5,10,25,50,100或200μM孵育时间:24小时结果:在≥100μM时细胞活力降低~50%。在较低浓度下显示75%的细胞活力。[1]数据来源文献[1]. Hanieh H, et al. Pinocembrin, a novel histidine decarboxylase inhibitor with anti-allergic potential in in vitro. Eur J Pharmacol. 2017 Nov 5;814:178-186.规格5mg 10mM*1mL in DMSO 10mg 20mg单位瓶为竞争性的组氨酸脱羧酶 (histidine decarboxylase) 抑制剂。
可泮利塞产品简介CAS1032568-63-0中文名称可泮利塞英文名称Copanlisib别名库潘尼西纯度≥98%分子式C23H28N8O4分子量480.52外观(性状)Off-white to brown Solid储存条件Powder : 2-8℃, 2 years; In solvent(母液): -20℃, 1 month; -80℃, 6 months溶解性Soluble in Water ≥1mg/mL(Need to add HCl dropwise to help dissolve)MDLMFCD18633201InChIKeyMWYDSXOGIBMAET-UHFFFAOYSA-NInChIInChI=1S/C23H28N8O4/c1-33-19-17(35-10-2-6-30-8-11-34-12-9-30)4-3-16-18(19)28-23(31-7-5-25-20(16)31)29-21(32)15-13-26-22(24)27-14-15/h3-4,13-14,25H,2,5-12H2,1H3,(H2,24,26,27)PubChem CID135565596SMILESO=C(C1=CN=C(N)N=C1)NC2=NC3=C(OC)C(OCCCN4CCOCC4)=CC=C3C5=NCCN25描述是一种 ATP竞争,选择性 I 型 PI3K 抑制剂。(It is an ATP-competitive, selective type I PI3K inhibitor.)靶点PI3K通路PI3K/Akt/mTOR生物活性Copanlisib (BAY 80-6946) is a potent, selective and ATP-competitive pan-class I PI3K inhibitor, with IC50s of 0.5 nM, 0.7 nM, 3.7 nM and 6.4 nM for PI3Kα, PI3Kδ, PI3Kβ and PI3Kγ, respectively. Copanlisib has more than 2,000-fold selectivity against other lipid and protein kinases, except for mTOR. Copanlisib has superior antitumor activity[1].In VitroCopanlisib (BAY 80-6946; 20-200 nM; 24 hours; BT20 breast cancer cells) treatmemnt induces apoptosis in a subset of tumor cell lines that are resistant to Lapatinib and Trastuzumab[1].In VivoCopanlisib (BAY 80-6946; 0.5-6 mg/kg; intravenous injection; every second day, every third day; for 60 days; athymic nude rats) treatment displays robust antitumor activity in the rat KPL4 tumor xenograft model[1].数据来源文献[1]. Liu N, et al. BAY 80-6946 is a highly selective intravenous PI3K inhibitor with potent p110α and p110δ activities in tumor cell lines and xenograft models. Mol Cancer Ther. 2013 Nov;12(11):2319-30.规格2mg 5mg单位瓶
刀豆蛋白A IV ConA产品简介英文名称ConA Type A IVCAS11028-71-0来源From Canavalia ensiformis(Jack bean)别名刀豆素A;刀豆球蛋白A分子式C15H24外观(性状)白色冻干粉储存条件-20℃有效期3年溶解性10 mg/mL in water规格25mg 100mg 1g单位瓶ConA促细胞有丝分裂,主要对T淋巴细胞有激发作用,凝集红细胞和动物精子,抑制肿瘤细胞运动,以及延长异源移植存活时间等作用。一种重要的生化和免疫研究试剂。ConA物理性状:白色至类白色粉末;溶于水,溶解后变浑浊,参考浓度为10mg/ml。ConA溶解性:10 mg/ml溶于水会形成略带黄色的透明的溶液,具体的使用浓度因具体的试验而定。ConA应用:刀豆蛋白(Concanavalin A,Con A)是从刀豆(Jack bean)中提取出来的凝集素,能沉淀多种糖类,葡聚糖和果聚糖等很多其它多糖,以及免疫球蛋白和血型物质等多种糖蛋白,还沉淀肺炎球菌多糖,并能凝集多种红细胞。Con A 能和很多细菌和动物细胞反应,能区分某些正常和肿瘤细胞,能促进细胞分裂(促有丝分裂作用)。Con A IV 用于淋巴下拨转化实验,也被用来刺激T细胞产生IL-1 样因子,还用于脾细胞增生,研究激活所必需的配体/受体作用。此外,尚区分正常分泌ACTH 的垂体细胞和分泌ACTH 的腺肿瘤细胞、用于研究糖基化在离子通道调节中的作用、用于糖蛋白的分离纯化和多糖、糖蛋白糖链结构的研究等。1992 年,Tiegs 等成功地应用刀豆蛋自A( ConA)诱发了小鼠特异性肝损伤,这一实验模型是近年来新发展起来的由T 淋巴细胞介导的肝损害,它的建立和应用为深入研究肝细胞损害的细胞学与分子学机制以及进行治疗药物筛选提供了更为方便和理想的实验动物模型。 备注:产品信息可能会有优化升级。请以实际标签信息为准。
WST-8产品简介CAS193149-74-5英文名称WST-8纯度≥98%分子式C20H14N6NaO11S2分子量601.48外观(性状)White to yellow Solid储存条件Powder : 2-8℃, 2 years; In solvent(母液): -20℃, 1 month; -80℃, 6 months溶解性Soluble in Water ≥50mg/mLMDLMFCD09264687InChIKeyVSIVTUIKYVGDCX-UHFFFAOYSA-MInChIInChI=1S/C20H14N6O11S2.Na/c1-37-18-10-14(26(29)30)6-9-17(18)24-22-20(21-23(24)12-2-4-13(5-3-12)25(27)28)16-8-7-15(38(31,32)33)11-19(16)39(34,35)36;/h2-11H,1H3,(H-,31,32,33,34,35,36);/q;+1/p-1PubChem CID9894947SMILESCOC1=CC([N+]([O-])=O)=CC=C1[N+]2=NC(C3=CC=C(S(=O)(O)=O)C=C3S(=O)([O-])=O)=NN2C4=CC=C([N+]([O-])=O)C=C4.[Na]描述是一种水溶性的四唑染料,用于比色测定细胞增殖或细胞毒性。(It is a water-Soluble tetrazolium dye used for colorimetric determination of cell proliferation or cytotoxicity.)规格20mg 50mg单位瓶
Vismodegib;维莫德吉产品简介CAS879085-55-9中文名称维莫德吉英文名称Vismodegib别名GDC-0449;GDC0449纯度HPLC≥98%分子式C19H14Cl2N2O3S分子量421.3外观(性状)Off-white to yellow Solid储存条件Powder : 2-8℃, 2 years; In solvent(母液): -20℃, 1 month; -80℃, 6 months溶解性Soluble in DMSOMDLMFCD12407408ECEINECS 806-752-3SMILESO=C(C1=CC=C(C=C1Cl)S(=O)(C)=O)NC2=CC=C(C(C3=NC=CC=C3)=C2)Cl描述Vismodegib 是一种 hedgehog 抑制剂;同时可抑制 P-gp 和 ABCG2 的活性。(Vismodegib is a hedgehog inhibitor; simultaneously inhibits the activity of P-gp and ABCG2.)靶点Hedgehog通路Hedgehog;Stem Cells生物活性Vismodegib 是一种可口服的 hedgehog 抑制剂,IC50 值为 3 nM;同时可抑制 P-gp 和 ABCG2 的活性,IC50 值分别为 3.0 μM 和 1.4 μM。Vismodegib是一种新型小分子HPI。Vismodegib是一种ABCG2抑制剂 [1-6]In VitroVismodegib是一种ABCG2抑制剂,通过阻断其在HEK293细胞中的输出,可以增加另一种ABCG2底物米托蒽醌的有效细胞内浓度。 Vismodegib(10μM)将MDCKII/Pgp细胞和MDCKII/MRP1细胞重新敏化为秋水仙碱治疗[2]。 Vismodegib(25μM或50μM)浓度依赖性地抑制HCC和H1339细胞[3]。In VivoVismodegib(0.3至75 mg/kg,po)在成神经管细胞瘤同种异体移植肿瘤中非常有效。 Vismodegib(> 46 mg/kg,po)导致患者来源的结肠直肠异种移植物的生长延迟[4]。动物实验当肿瘤达到200和350mm 3之间时,携带肿瘤的小鼠被分配到肿瘤体积匹配的群组中。 vismodegib抗性成神经管细胞瘤同种异体移植物sg274是通过Ptch +/-,p53 - / - 成神经管细胞瘤同种异体移植物的间歇性次优给药而发展的。 Vismodegib配制成0.5%甲基纤维素,0.2%吐温-80(MCT)的悬浮液,并口服给药。使用卡尺确定肿瘤体积。数据来源文献[1]. Scales SJ, et al. Mechanisms of Hedgehog pathway activation in cancer and implications for therapy. Trends Pharmacol Sci. 2009, 30(6), 303-312.[2]. Zhang Y, et al. Hedgehog pathway inhibitor HhAntag691 is a potent inhibitor of ABCG2/BCRP and ABCB1/Pgp. Neoplasia. 2009, 11(1), 96-101.[3]. Tian F, et al. The hedgehog pathway inhibitor GDC-0449 alters intracellular Ca2+ homeostasis and inhibits cell growth in cisplatin-resistant lung cancer cells. Anticancer Res. 2012, 32(1), 89-94.[4]. Wong H, et al. Pharmacokinetic-pharmacodynamic analysis of vismodegib in preclinical models of mutational and ligand-dependent Hedgehog pathway activation. Clin Cancer Res. 2011, 17(14), 4682-4692.[5]. Elhenawy AA, et al. Possible antifibrotic effect of GDC-0449 (Vismodegib), a hedgehog-pathway inhibitor, in mice model of Schistosoma-induced liver fibrosis. Parasitol Int. 2017 Oct;66(5):545-554.[6]. Ma W, et al. Reduced Smoothened level rescued Aβ-induced memory deficits and neuronal inflammation in animal models of Alzheimer's disease. J Genet Genomics. 2018 May 20;45(5):237-246.规格5mg 25mg 50mg单位瓶Vismodegib 是一种 hedgehog 抑制剂;同时可抑制 P-gp 和 ABCG2 的活性。
Ivacaftor;依伐卡托产品简介CAS873054-44-5中文名称依伐卡托英文名称Ivacaftor别名VX-770纯度≥98%分子式C24H28N2O3 分子量392.49外观(性状)White to off-white Solid储存条件Powder : 2-8℃, 2 years; In solvent(母液): -20℃, 1 month; -80℃, 6 months溶解性Soluble in DMSOMDLMFCD17171361SMILESCC(C)(C1=C(C=C(C(C(C)(C)C)=C1)O)NC(C2=CNC3=C(C2=O)C=CC=C3)=O)C描述Ivacaftor是一种有效的 CFTR 增效剂。(Ivacaftor is a potent CFTR synergist.)靶点CFTR通路Membrane Transporter&Ion Channel生物活性Ivacaftor是一种有效的 CFTR 增效剂,靶向G551D-CFTR和F508del-CFTR的EC50分别为100 nM 和 25 nM。[1-4]In VitroIvacaftor(10μM)使ABCB4-G535D的PC分泌活性增加3倍,ABCB4-G536R增加13.7倍,ABCB4-S1076C增加6.7倍,ABCB4-S1176L增加9.4倍,ABCB4增加5.7倍 - G1178S。 Ivacaftor纠正了ABCB4突变体的功能缺陷[1]。与R1162X CFTR细胞相比,Ivacaftor(10μM)显著增加表达W1282X的细胞中的CFTR活性[2]。 Ivacaftor显示对160个测试目标没有显著活性,包括GABAA苯二氮卓受体。 Ivacaftor增加氯离子分泌,EC50为0.236±0.200μM,与F508del HBE相比效力变化10倍[3]。在重组细胞中,VX-770增加F508del加工突变和G551D门控突变中的CFTR通道开放概率(Po)。 VX-770可将温度校正的F508del-FRT细胞中毛喉素刺激的IT增加6倍,EC50为25 nM [4]。In VivoIvacaftor(1-200 mg/kg,po)在大鼠中表现出良好的口服生物利用度[3]。数据来源文献[1]. Delaunay JL, et al. Functional defect of variants in the adenosine triphosphate-binding sites of ABCB4 and their rescue by the cystic fibrosis transmembrane conductance regulator potentiator, ivacaftor (VX-770). Hepatology. 2017 Feb;65(2):560-570[2]. Mutyam V, et al. Therapeutic benefit observed with the CFTR potentiator, ivacaftor, in a CF patient homozygous for the W1282X CFTR nonsense mutation. J Cyst Fibros. 2017 Jan;16(1):24-29[3]. Hadida S, et al. Discovery of N-(2,4-di-tert-butyl-5-hydroxyphenyl)-4-oxo-1,4-dihydroquinoline-3-carboxamide (VX-770, ivacaftor), a potent and orally bioavailable CFTR potentiator. J Med Chem. 2014 Dec 11;57(23):9776-9[4]. Van Goor F, et al. Rescue of CF airway epithelial cell function in vitro by a CFTR potentiator, VX-770. Proc Natl Acad Sci U S A. 2009 Nov 3;106(44):18825-30.规格10mg 50mg单位瓶是一种有效的 CFTR 增效剂。备注:以上数据均来自公开文献, Solarbio暂未进行独立验证, 仅供参考。These protocols are for reference only. Solarbio does not independently validate these methods.
Lapatinib 拉帕替尼产品简介CAS231277-92-2中文名称拉帕替尼英文名称Lapatinib别名拉帕替尼;WR-2721;UNII-M487QF2F4V;纯度HPLC≥98%分子式C29H26ClFN4O4S分子量581.06外观(性状)Light yellow to yellow Solid储存条件Powder : 2-8℃, 2 years; In solvent(母液): -20℃, 1 month; -80℃, 6 months溶解性Soluble in DMSOMDLMFCD09264194ECEINECS 1806241-263-5InChIKeyBCFGMOOMADDAQU-UHFFFAOYSA-NInChIInChI=1S/C29H26ClFN4O4S/c1-40(36,37)12-11-32-16-23-7-10-27(39-23)20-5-8-26-24(14-20)29(34-18-33-26)35-22-6-9-28(25(30)15-22)38-17-19-3-2-4-21(31)13-19/h2-10,13-15,18,32H,11-12,16-17H2,1H3,(H,33,34,35)PubChem CID208908SMILESO=S(CCNCC1=CC=C(C2=CC=C3C(C(NC4=CC(Cl)=C(C=C4)OCC5=CC(F)=CC=C5)=NC=N3)=C2)O1)(C)=O描述Lapatinib是有效的 EGFR 和 ErbB2 抑制剂。(Lapatinib is a potent EGFR and ErbB2 inhibitor.)靶点EGFR通路Angiogenesis;Protein Tyrosine Kinase/RTK; JAK/STAT Signaling生物活性Lapatinib (formerly GW572016, trade names Tykerb & Tyverb), usually used in the Ditosylate form, is a potent, orally bioavailable dual EGFR/ErbB2 inhibitor with potential anticancer activity. It inhibits epidermal growth factor receptor (EGFR)/ErbB2 with IC50 of 10.8 and 9.2 nM in cell-free assays, respectively. It is an FDA approved medication used for the treatment of breast cancer and other solid tumors. Lapatinib acts by reversibly blocking the phosphorylation of EGFR, ErbB2, and the Erk-1 and-2 and AKT kinases. [1]In VitroLapatinib (1 μM) induces apoptosis in NCI-N87 and OD19 cells [2]. Lapatinib inhibits the growth of EGFRoverexpressing A431 skin cancer (IC50: 0.14 μM) and ErbB2-overexpressing SK-BR-3 breast cancer cells (IC50:0.124 μM). It also inhibits the growth of ErbB2-amplified OD19 esophageal (IC50: 0.09 μM)and NCI-N87 gastric cancer cells (IC50: 0.01 μM) as well as several types of gastric cancer cells in which ErbB2 is not amplified (IC50s:0.35-8.58 μM) [3] .In VivoLapatinib (100 mg/kg/day, p.o.) induces severe oxidative damage in the cardiac tissue of rat [4].Lapatinib ( 30 and 100 mg/kg, p.o., b.i.d) dose-responsive inhibited the growth of BT474 and HN5 human tumor xenografts. Complete inhibition of tumor growth is seen at the 100 mg/kg dose. At this dose, there is <10% weight loss in treated animals over the course of the 21-day treatment. Lapatinib treatment inhibits tumor xenograft growth of the HN5 and BT474 cells in a dose-responsive manner at 30 and 100 mg/kg orally, twice daily, with complete inhibition of tumor growth at the higher dose [5].数据来源文献[1]. Mol Cancer Ther. 2001 Dec;1(2):85-94; Cancer Res. 2006 Feb 1;66(3):1630-9.[2]. Chefrour M et al. Positive interaction between lapatinib and capecitabine in human breast cancer models: study of molecular determinants. Fundam Clin Pharmacol. 2012 Aug;26(4):530-7.[3]. Wainberg ZA, et al. Lapatinib, a dual EGFR and HER2 kinase inhibitor, selectively inhibits HER2-amplified human gastric cancer cells and is synergistic with trastuzumab in vitro and in vivo. Clin Cancer Res. 2010 Mar 1;16(5):1509-19.[4]. Eryilmaz U, et al. S100A1 as a Potential Diagnostic Biomarker for Assessing Cardiotoxicity and Implications for the Chemotherapy of Certain Cancers. PLoS One. 2015 Dec 18;10(12):e0145418.[5]. Rusnak DW, et al. The effects of the novel, reversible epidermal growth factor receptor/ErbB-2 tyrosine kinase inhibitor, GW2016, on the growth of human normal and tumor-derived cell lines in vitro and in vivo. Mol Cancer Ther. 2001 Dec;1(2):85-94规格5mg 10mM*1mL (in DMSO) 10mg单位瓶是有效的 EGFR 和 ErbB2 抑制剂。备注:以上数据均来自公开文献, Solarbio暂未进行独立验证, 仅供参考。These protocols are for reference only. Solarbio does not independently validate these methods.
Scopoletin;东莨菪内酯产品简介CAS92-61-5中文名称东莨菪内酯英文名称Scopoletin别名Esculetin 6-methyl ether;Gelseminic acid;6-Methylesculetin;Chrysatropic acid纯度HPLC≥98%分子式C10H8O4 分子量192.17外观(性状)Light yellow to yellow Solid储存条件Powder : 2-8℃, 2 years; In solvent(母液): -20℃, 1 month; -80℃, 6 months溶解性Soluble in DMSOECEINECS 202-171-9MDLMFCD00006872SMILESO=C1C=CC2=CC(OC)=C(O)C=C2O1描述Scopoletin 是一种乙酰胆碱酯酶 (AChE) 抑制剂。(Scopoletin is an acetylcholinesterase (AChE) inhibitor.)靶点AChE通路Neuronal Signaling生物活性Scopoletin 是一种乙酰胆碱酯酶 (AChE) 抑制剂。[1-2]In VitroScopoletin(SCT)被鉴定为乙酰胆碱酯酶(AChE)的推定抑制剂。 Scopoletin增强了大鼠额叶皮质突触体中K +刺激的ACh释放,显示出钟形剂量效应曲线(Emax:4μM)[1]。东莨菪碱通过诱导PC3细胞凋亡来抑制PC3增殖。用于抑制PC3,PAA(人肺癌细胞)和Hela细胞增殖的Scopoletin的IC50分别为(157±25),(154±51)和(294±100)mg/L.东莨菪素诱导显著的时间和浓度依赖性抑制PC3细胞增殖。东莨菪素以浓度依赖性方式降低蛋白质含量并降低PC3细胞中的酸性磷酸酶活性(ACP)水平。用Scopoletin处理的细胞通过光学显微镜,荧光显微镜和透射电子显微镜显示细胞凋亡的典型形态变化。 Scopoletin 0,100,200和400 mg/L的细胞凋亡率分别为0.3%,2.1%,9.3%和35%,用Scopoletin处理后G2期细胞明显减少[2]。In Vivo东莨菪素(2μg,icv)增加T迷宫交替并改善东莨菪碱诱导的胆碱能缺乏对小鼠的新物体识别。它还减少了15-18个月大的小鼠(2mg/kg sc)的对象记忆中与年龄相关的缺陷。注射2μgScopoletin的小鼠显示交替率增加71.3±2.5%[1]。细胞实验将指数生长的1mL PC3细胞(5×107/L)接种到4个24孔板中。将板在37℃下在潮湿的5%CO 2气氛中温育。 24小时后,向孔中加入Scopoletin 33,66,133,266和533mg/L(每个板的每个浓度3个孔)。对于对照细胞(前板3个孔),仅加入DMEM。将板连续孵育。通过台盼蓝染料排除法[4],每天在第4天用血细胞计数器计数活细胞。动物实验小鼠[1] C56BL/6N雄性,4-6个月大和16-18个月大的小鼠用于行为研究。在恒定湿度(50-55%)和温度(22±1℃)下,在12:12小时光照/黑暗循环(7:00-19:00h)下将小鼠分成4只一组饲养。食物和水随意。较年轻的小鼠(4-6个月)植入icv套管,用于施用东莨菪碱(SCOP)和东莨菪素。通过sc途径向老年小鼠注射东莨菪素。实验在8:00至16:00之间进行。将具有icv套管的小鼠随机分成四个实验组:载体; SCOP20μg; Scopoletin2μg;和SCOP20μg加Scopoletin2μg。将药物施用于1μL载体溶液(SCOP:盐水,Scopoletin:3DMSO:7无菌水)中。在测试开始前15分钟进行Icv注射。在对象记忆测试前30分钟,老年小鼠获得Scopoletin sc(载体:1 DMSO:1 EtOH,根据需要用橄榄油稀释)[1]。数据来源文献[1]. Hornick A, et al. The coumarin Scopoletin potentiates acetylcholine release from synaptosomes, amplifies hippocampal long-term potentiation and ameliorates anticholinergic- and age-impaired memory. Neuroscience. 2011 Dec 1;197:280-92.[2]. Liu XL, et al. Effect of Scopoletin on PC3 cell proliferation and apoptosis. Acta Pharmacol Sin. 2001 Oct;22(10):929-33.规格10mg 10mM*1mL in DMSO 20mg单位瓶Scopoletin 是一种乙酰胆碱酯酶 (AChE) 抑制剂。备注:以上数据均来自公开文献, Solarbio暂未进行独立验证, 仅供参考。These protocols are for reference only. Solarbio does not independently validate these methods.
维生素C产品简介CAS50-81-7中文名称维生素C英文名称L-Ascorbic Acid别名L(+)-Ascorbic acid;Vitamin C;L-抗坏血酸纯度HPLC≥98%分子式C6H8O6 分子量176.12外观(性状)White to off-white Solid储存条件Powder : 2-8℃, 2 years; In solvent(母液): -20℃, 1 month; -80℃, 6 months溶解性Soluble in Water ≥20mg/mLMDLMFCD00064328ECEINECS 200-066-2InChIKeyCIWBSHSKHKDKBQ-JLAZNSOCSA-NInChIInChI=1S/C6H8O6/c7-1-2(8)5-3(9)4(10)6(11)12-5/h2,5,7-10H,1H2/t2-,5+/m0/s1PubChem CID54670067SMILESOC([C@@]1([H])[C@H](CO)O)=C(O)C(O1)=O描述L-Ascorbic Acid是一种有效的还原剂和抗氧化剂。(L-Ascorbic Acid is a potent reducing agent and antioxidant.)生物活性L-Ascorbic acid exhibits anti-cancer effects through the generation of reactive oxygen species (ROS) and selective damage to cancer cells[1].In VitroThe anti-cancer effects of L-Ascorbic acid are determined by sodium-dependent vitamin C transporter 2 (SVCT-2), a transporter of L-ascorbic acid. L-Ascorbic acid (0.1 μM-2 mM) exhibits anti-cancer effects according to SVCT-2 expression and L-ascorbic acid uptake. Human colorectal cancer cell lines displays differential responses to L-ascorbic acid, primarily depending on the expression level of SVCT-2[1].In VivoL-Ascorbic acid/Tolbutamide produces hypoglycaemic activity in a dose dependant manner in normal (60 mg/kg) and diabetic (40 mg/kg) condition. In the presence of L-ascorbic acid, Tolbuatmide (20 mg/kg) produces early onset of action and maintained for longer period compared to Tolbutamide matching control[2].数据来源文献[1]. Sungrae Cho, et al. Hormetic dose response to L-ascorbic acid as an anti-cancer drug in colorectal cancer cell lines according to SVCT-2 expression. Sci Rep. 2018 Jul 27;8(1):11372.[2]. Satyanarayana Sreemantula, et al. Influence of antioxidant (L- ascorbic acid) on tolbutamide induced hypoglycaemia/antihyperglycaemia in normal and diabetic rats. BMC Endocr Disord. 2005 Mar 3;5(1):2.规格20mg 10mM*1mL (in Water) 100mg单位瓶一种重要的营养素和氧化还原剂,在骨盐代谢及骨形成中具有重要作用。在体外,它能增加钙盐的沉积,促进矿化结节的形成,并通过间充质细胞间接调节破骨细胞的分化。维生素C能直接抑制核因子κB受体活化子配体(RANKL)诱导的破骨细胞形成 。 使用本产品的应用案例(仅供参考) In VitroCell(Osteogenic/成骨诱导;50 mg/l ascorbic acid) The osteogenic medium was the complete culture medium supplemented with 10 nM dexamethasone(Solarbio), 10 mM β-glycerophosphate (Solarbio), and 50 mg/l ascorbic acid (Solarbio). 数据来源文献:Jia L, Zhang Y, Ji Y, Li X, Xing Y, Wen Y, Huang H, Xu X. Comparative analysis of lncRNA and mRNA expression profiles between periodontal ligament stem cells and gingival mesenchymal stem cells. Gene. 2019 May 30;699:155-164. doi: 10.1016/j.gene.2019.03.015. Epub 2019 Mar 12. PMID: 30876821. Cell(Osteogenic/成骨诱导;50 mg/l ascorbic acid) Osteogenic induced medium contained complete culture medium supplemented with 100 nM dexamethasone (Solarbio, Beijing, China), 10 mM β-glycerophosphate (Solarbio) and 50 mg/l ascorbic acid (Solarbio). The medium was replaced every other day. Alizarin Red–positive mineralized matrix was used to evaluate osteogenic capacity by Alizarin red (AR) staining. 数据来源文献:Zhao Y, Liu H, Xi X, Chen S, Liu D. TRIM16 protects human periodontal ligament stem cells from oxidative stress-induced damage via activation of PICOT. Exp Cell Res. 2020 Dec 1;397(1):112336. doi: 10.1016/j.yexcr.2020.112336. Epub 2020 Oct 19. PMID: 33091421. In Vivo Rat(雄性新生SD Rat;100 mg vitamin C/kg bw/d;灌胃;30d) Forty-five male neonatal SD rats were randomly divided into five groups (n=9 each): corn oil control group, 500 mg DEHP/kg of body weight per day (bw/d) group, 500 mg DEHP/kg bw/d+200 mg vitamin E/kg bw/d group, 500 mg DEHP/kg bw/d+100 mg vitamin C/kg bw/d group, and 500 mg DEHP/kg bw/d+200 mg vitamin E/kg bw/d+100 mg vitamin C/kg bw/d group. DEHP and vitamin E (Solarbio, China) were dissolved in corn oil, and vitamin C (Solarbio,China) was dissolved in distilled water. From postnatal day (PND) 1 to 30, the male rats were administered corn oil, DEHP, vitamin C, and/or vitamin E by gavage each day according to their group. On PND 36, six rats of each groups were sacrificed and their testes were immediately isolated. The rest of rats were fed with routine feed until PND 90. 来源文献:Tang X, Wu S, Shen L, Wei Y, Cao X, Wang Y, Long C, Zhou Y, Li D, Huang F, Liu B, Wei G. Di-(2-ethylhexyl) phthalate (DEHP)-induced testicular toxicity through Nrf2-mediated Notch1 signaling pathway in Sprague-Dawley rats. Environ Toxicol. 2018 Jul;33(7):720-728. doi: 10.1002/tox.22559. Epub 2018 Apr 16. PMID: 29663635. 备注:以上数据均来自公开文献, Solarbio暂未进行独立验证, 仅供参考。These protocols are for reference only. Solarbio does not independently validate these methods
Ivacaftor;依伐卡托产品简介CAS873054-44-5中文名称依伐卡托英文名称Ivacaftor别名VX770纯度≥98%分子式C24H28N2O3 分子量392.49外观(性状)White to off-white Solid储存条件Powder : 2-8℃, 2 years; In solvent(母液): -20℃, 1 month; -80℃, 6 months溶解性Soluble in DMSOSMILESCC(C)(C1=C(C=C(C(C(C)(C)C)=C1)O)NC(C2=CNC3=C(C2=O)C=CC=C3)=O)C描述Ivacaftor是一种有效的 CFTR 增效剂。(Ivacaftor is a potent CFTR synergist.)靶点CFTR通路Membrane Transporter&Ion Channel生物活性Ivacaftor是一种有效的 CFTR 增效剂,靶向G551D-CFTR和F508del-CFTR的EC50分别为100 nM 和 25 nM。[1-4]In VitroIvacaftor(10μM)使ABCB4-G535D的PC分泌活性增加3倍,ABCB4-G536R增加13.7倍,ABCB4-S1076C增加6.7倍,ABCB4-S1176L增加9.4倍,ABCB4增加5.7倍 - G1178S。 Ivacaftor纠正了ABCB4突变体的功能缺陷[1]。与R1162X CFTR细胞相比,Ivacaftor(10μM)显著增加表达W1282X的细胞中的CFTR活性[2]。 Ivacaftor显示对160个测试目标没有显著活性,包括GABAA苯二氮卓受体。 Ivacaftor增加氯离子分泌,EC50为0.236±0.200μM,与F508del HBE相比效力变化10倍[3]。在重组细胞中,VX-770增加F508del加工突变和G551D门控突变中的CFTR通道开放概率(Po)。 VX-770可将温度校正的F508del-FRT细胞中毛喉素刺激的IT增加6倍,EC50为25 nM [4]。In VivoIvacaftor(1-200 mg/kg,po)在大鼠中表现出良好的口服生物利用度[3]。数据来源文献[1]. Delaunay JL, et al. Functional defect of variants in the adenosine triphosphate-binding sites of ABCB4 and their rescue by the cystic fibrosis transmembrane conductance regulator potentiator, ivacaftor (VX-770). Hepatology. 2017 Feb;65(2):560-570[2]. Mutyam V, et al. Therapeutic benefit observed with the CFTR potentiator, ivacaftor, in a CF patient homozygous for the W1282X CFTR nonsense mutation. J Cyst Fibros. 2017 Jan;16(1):24-29[3]. Hadida S, et al. Discovery of N-(2,4-di-tert-butyl-5-hydroxyphenyl)-4-oxo-1,4-dihydroquinoline-3-carboxamide (VX-770, ivacaftor), a potent and orally bioavailable CFTR potentiator. J Med Chem. 2014 Dec 11;57(23):9776-9[4]. Van Goor F, et al. Rescue of CF airway epithelial cell function in vitro by a CFTR potentiator, VX-770. Proc Natl Acad Sci U S A. 2009 Nov 3;106(44):18825-30.规格10mg 50mg单位瓶是一种有效的 CFTR 增效剂。备注:以上数据均来自公开文献, Solarbio暂未进行独立验证, 仅供参考。These protocols are for reference only. Solarbio does not independently validate these methods.
阿尼西坦产品简介CAS72432-10-1中文名称阿尼西坦英文名称Aniracetam别名Ro 13-5057纯度≥99%分子式C12H13NO3 分子量219.24外观(性状)White to off-white Solid储存条件Powder : 2-8℃, 2 years; In solvent(母液): -20℃, 1 month; -80℃, 6 months溶解性Soluble in DMSOMDLMFCD00153767ECEINECS 615-758-3InChIKeyZXNRTKGTQJPIJK-UHFFFAOYSA-NInChIInChI=1S/C12H13NO3/c1-16-10-6-4-9(5-7-10)12(15)13-8-2-3-11(13)14/h4-7H,2-3,8H2,1H3PubChem CID2196SMILESO=C(N1CCCC1=O)C2=CC=C(OC)C=C2描述可调节AMPA受体和nAChR,具有神经保护和益智活性。(Modulates AMPA receptors and nAChRs with neuroprotective and nootropic activities.)靶点nAChR;AMPAR通路Neuronal Signaling;Membrane Transporter&Ion Channel规格200mg 1g 2g单位瓶备注:以上数据均来自公开文献, Solarbio暂未进行独立验证, 仅供参考。These protocols are for reference only. Solarbio does not independently validate these methods.
SB-203580产品简介CAS152121-47-6英文名称SB-203580别名4-(4-氟苯基)-2-(4-甲基亚磺酰基苯基)-5-(4-吡啶基)-1H-咪唑;PB203580;RWJ64809;SB203580纯度≥98%分子式C21H16FN3OS分子量377.43外观(性状)White to light yellow Solid储存条件Powder :2-8℃, 2 years;In solvent(母液): -20℃, 1 month; -80℃, 6 months溶解性Soluble in DMSOMDLMFCD00922198SMILESO=S(C1=CC=C(C2=NC(C3=CC=C(F)C=C3)=C(C4=CC=NC=C4)N2)C=C1)C描述SB-203580是一种选择性的,ATP 竞争性的 p38 MAPK 抑制剂,也抑制 LCK,GSK3β 和 PKBα。SB-203580是一种自噬和线粒体自噬 (mitophagy) 激活剂。(SB-203580 is a selective, ATP-competitive inhibitor of p38 MAPK that also inhibits LCK, GSK3β and PKα. SB-203580 is an activator of autophagy and mitophagy.)靶点p38 MAPK,LCK,GSK3β,PKBα,Autophagy, Mitophagy通路MAPK;PI3K/Akt/mTOR;Stem Cells;Protein Tyrosine Kinase/RTK;Autophagy生物活性SB 203580是一种广泛使用的 p38 MAPK 抑制剂, IC50 介于 0.3-0.5μM 之间。 对 p38 MAPK 的选择性比 PKB, LCK, 和 GSK-3β 高100倍。SB 203580能够以剂量依赖性方式抑制PDK1的活性,IC50在3-10μM范围内。[1-5]In VitroSB 203580抑制IL-2驱动的T细胞增殖,IC50为3-5μM,SB 203580能够以剂量依赖性方式抑制PDK1的活性,IC50在3-10μM范围内[1]。浓度为1μM的SB 203580足以抑制TF-1细胞中的p38激酶活性。 5和10μM的SB 203580增强NF-κB介导的基因转录,而与p65亚基的反式激活结构域上的磷酸化无关。 10μM的SB 203580增强了ERK1/2和JNK的磷酸化[1]。In Vivo所有动物用NS(未感染的对照)攻击并用SB203580或安慰剂治疗存活。与安慰剂相比,在大肠杆菌前1小时用最高剂量的SB203580(100mg/kg)预处理增加了死亡的危害比。对于大肠杆菌,与安慰剂相比,在48小时但不是24小时,低剂量和高剂量SB203580降低磷酸化的p38MAPK和磷酸化与总p38的比率。高剂量SB203580在24小时时在组织学上降低肺中性粒细胞的趋势接近显著性(p = 0.09)并且在48小时时显著增加(p = 0.01),其模式随时间不同[3]。在几种细胞因子抑制和炎性疾病模型中评估SB 203580。显然,它是小鼠和大鼠中炎性细胞因子产生的有效抑制剂,IC50值为15至25mg/kg [4]。细胞实验通过蛋白质印迹分析p38,JNK1/2和ERK1/2的磷酸化。简而言之,将TF-1细胞在含有0.1%FBS的RPMI 1640中培养16小时,随后用培养基或OA(30ng/mL)或SB 203580(1μM,5μM,10μM)加刺激不同时间段。 OA。收获后,通过将细胞重悬于500μL1×样品缓冲液(含有2%SDS,10%甘油,2%β-巯基乙醇,60mM Tris-HCl(pH6.8)和溴酚蓝)中并裂解来制备总细胞提取物。将细胞通过23G1针头(三次)。将细胞提取物直接煮沸10分钟并储存在-20℃。在上样之前,将样品再次煮沸5分钟,并通过在SDS/12.5%PAGE凝胶(丙烯酰胺:双丙烯酰胺为173:1)上运行1/10体积来分离细胞提取物并转移至纤维素硝酸盐膜。用抗体进行免疫印迹通过标准程序进行并进行检测[2]。动物实验小鼠[3]在存活研究中,将体重为20g至30g的C57BL/6J小鼠用异氟烷短暂麻醉并用0.05mL IT生理盐水(NS,未感染对照)或大肠杆菌(15×109CFU/kg)攻击。 。在NS攻击前1小时,小鼠(n = 24)接受腹膜内SB203580(100mg/kg,0.25mL)或仅稀释剂(安慰剂)。受感染的动物在IT大肠杆菌(n = 241)之前1小时接受剂量为100,10,1或0.1mg/kg的SB203580或安慰剂; SB203580 100或0.1 mg/kg或安慰剂在大肠杆菌后1小时(n = 121);在大肠杆菌(n = 72)后12小时或SB203580 100mg/kg或安慰剂。所有动物在攻击后4小时开始接受头孢曲松(100mg/kg,0.1mL,皮下)4天和NS(0.5mL,皮下)1天。最初48小时每2小时观察动物,48小时至72小时每4小时观察一次动物,72小时至96小时每8小时观察动物,然后每天观察两次直至研究完成(168小时)[3]。数据来源文献[1]. Lali FV, et al. The pyridinyl imidazole inhibitor SB203580 blocks phosphoinositide-dependent protein kinase activity, protein kinase B phosphorylation, and retinoblastoma hyperphosphorylation in interleukin-2-stimulated T cells independently of p38 mitogen-activated protein kinase. J Biol Chem. 2000 Mar 10;275(10):7395-402.[2]. Birkenkamp KU, et al. The p38 MAP kinase inhibitor SB203580 enhances nuclear factor-kappa B transcriptional activity by a non-specific effect upon the ERK pathway. Br J Pharmacol. 2000 Sep;131(1):99-107.[3]. Su J, et al. SB203580, a p38 inhibitor, improved cardiac function but worsened lung injury and survival during Escherichia coli pneumonia in mice. J Trauma. 2010 Jun;68(6):1317-27.[4]. Badger AM, et al. Pharmacological profile of SB 203580, a selective inhibitor of cytokine suppressive binding protein/p38 kinase, in animal models of arthritis, bone resorption, endotoxin shock and immune function. J Pharmacol Exp Ther. 1996 Dec;279(3):1453-61.[5]. Lin Y, et al. Critical role of astrocytic interleukin-17?A in post-stroke survival and neuronal differentiation of neural precursor cells in adult mice. Cell Death Dis. 2016 Jun 23;7(6):e2273规格10mg 20mg 50mg单位支备注:以上数据均来自公开文献, Solarbio暂未进行独立验证, 仅供参考。These protocols are for reference only. Solarbio does not independently validate these methods.
WST-1产品简介CAS150849-52-8英文名称WST-1纯度≥98%分子式C19H13IN5NaO8S2 分子量653.36外观(性状)Light yellow to brown Solid储存条件Powder : 2-8℃, 2 years; In solvent(母液): -20℃, 1 month; -80℃, 6 months溶解性Soluble in Water ≥10mg/mLMDLMFCD01075079InChIKeyJUJBNYBVVQSIOU-UHFFFAOYSA-MInChIInChI=1S/C19H12IN5O8S2.Na/c20-12-1-3-13(4-2-12)23-21-19(22-24(23)14-5-7-15(8-6-14)25(26)27)17-10-9-16(34(28,29)30)11-18(17)35(31,32)33;/h1-11H,(H-,28,29,30,31,32,33);/q;+1/p-1PubChem CID6099081SMILESC1=CC(=CC=C1N2N=C(N=[N+]2C3=CC=C(C=C3)[N+](=O)[O-])C4=C(C=C(C=C4)S(=O)(=O)[O-])S(=O)(=O)[O-])I.[Na+]描述是一种 Tetrazolium 染料,广泛用于细胞活力测定。(It is a Tetrazolium dye widely used in cell viability assays.)规格10mg 20mg单位瓶备注:以上数据均来自公开文献, Solarbio暂未进行独立验证, 仅供参考。These protocols are for reference only. Solarbio does not independently validate these methods.
Liproxstatin-1产品简介CAS950455-15-9含量Purity≥98%英文名称Liproxstatin-1纯度≥98%分子式C19H21ClN4 分子量340.85外观(性状)White to off-white Solid储存条件Powder : 2-8℃, 2 years;In solvent(母液): -20℃, 1 month; -80℃, 6 months溶解性Soluble in DMSOMDLMFCD00023421InChIKeyYAFQFNOUYXZVPZ-UHFFFAOYSA-NInChIInChI=1S/C19H21ClN4/c20-15-5-3-4-14(12-15)13-22-18-19(8-10-21-11-9-19)24-17-7-2-1-6-16(17)23-18/h1-7,12,21,24H,8-11,13H2,(H,22,23)PubChem CID135735917SMILESClC1=CC(CNC2=NC3=CC=CC=C3NC24CCNCC4)=CC=C1描述Liproxstatin-1 是一种有效的 ferroptosis 抑制剂。(Liproxstatin-1 is a potent ferroptosis inhibitor.)靶点Ferroptosis通路Apoptosis生物活性Liproxstatin-1 是一种有效的 ferroptosis 抑制剂,IC50 值约为 38 nM。[1-2]In VitroLiproxstatin-1可防止Gpx4 - / - 细胞中BODIPY 581/591 C11氧化。此外,Liproxstatin-1不会干扰其他经典类型的细胞死亡,如TNFα诱导的细胞凋亡和H2O2诱导的坏死,以及TNFα/ zvad诱导的坏死样凋亡的真正L929模型[1]。 Liproxstatin-1具有很强的抗脂肪转移活性,EC50为约38 nM。 Fer-1和Liproxstatin-1本质上是良好的,但不是很好的自由基捕获抗氧化剂,但它们在磷脂双层中是优异的。 Fer-1(10μM)和Liproxstatin-1(10μM)在15-LOX-1过表达细胞中没有表现出显著的抑制活性,并且其浓度几乎是其EC50s的1000倍,以破坏RSL3诱导的细胞凋亡。这些细胞(分别为15和27 nM)[2]。In VivoLiproxstatin-1(10 mg/kg,ip)可抑制人体细胞,Gpx4 - / - 肾脏和缺血/再灌注诱导的组织损伤模型中的肺上垂[1]。细胞实验为了诱导敲除Gpx4,将细胞接种到96孔板(每孔1,000个细胞)上,并在接种后用1μM4-OH-他莫昔芬(TAM)处理。除非另有说明,否则使用AquaBluer在处理后(通常72小时)的不同时间点评估细胞活力,作为活细胞的指示物。或者,还通过使用细胞毒性检测试剂盒测量释放的乳酸脱氢酶(LDH)活性来定量细胞死亡。动物实验动物包括在诱导型Gpx4 - / - 小鼠的治疗研究中,在性别和体重之间平均分配,通常为8-10周龄。组内的平均重量在22至24克之间。形成群组以具有相同数量的相同年龄的女性/男性。动物体重被设置为在雌性和雄性之间具有相似的分布。对于药理学抑制剂实验,在第1天和第3天注射CreERT2; Gpx4fl/fl小鼠,其中0.5mg TAM溶解在Miglyol中。在第4天,开始化合物处理(Liproxstatin-1:10mg/kg)以及载体对照(PBS中的1%二甲基亚砜(DMSO))。通过ip注射每日一次施用Liproxstatin-1和载体对照。使用GraphPad Prism软件进行存活分析,并根据对数秩检验进行统计分析。数据来源文献[1]. Friedmann Angeli JP, et al. Inactivation of the ferroptosis regulator Gpx4 triggers acute renal failure in mice. Nat Cell Biol. 2014 Dec;16(12):1180-91.[2]. Zilka O, et al. On the Mechanism of Cytoprotection by Ferrostatin-1 and Liproxstatin-1 and the Role of Lipid Peroxidation in Ferroptotic Cell Death. ACS Cent Sci. 2017 Mar 22;3(3):232-243规格5mg 10mg单位支Liproxstatin-1 是一种有效的 ferroptosis 抑制剂。备注:以上数据均来自公开文献, Solarbio暂未进行独立验证, 仅供参考。These protocols are for reference only. Solarbio does not independently validate these methods.
Parthenolide 小白菊内酯产品简介CAS20554-84-1中文名称小白菊内酯英文名称Parthenolide别名欧苷菊; PartheNAlide纯度HPLC≥98%分子式C15H20O3 分子量248.32外观(性状)White to off-white Solid储存条件Powder : 2-8℃, 2 years; In solvent(母液): -20℃, 1 month; -80℃, 6 months溶解性Soluble in DMSOMDLMFCD00134592ECEINECS 692-532-0InChIKeyKTEXNACQROZXEV-PVLRGYAZSA-NInChIInChI=1S/C15H20O3/c1-9-5-4-8-15(3)13(18-15)12-11(7-6-9)10(2)14(16)17-12/h5,11-13H,2,4,6-8H2,1,3H3/b9-5+/t11-,12-,13+,15+/m0/s1PubChem CID7251185SMILESC/C1=C\CC[C@@](C)(O2)[C@H]2[C@@H](OC(C3=C)=O)[C@H]3CC1描述Parthenolide 是一种 NF-κB 抑制剂,可降低组蛋白脱乙酰酶 1 (HDAC-1) 和 DNA 甲基转移酶 1。(Parthenolide is an NF-κB inhibitor that reduces histone deacetylase 1 (HDAC-1) and DNA methyltransferase 1.)靶点NF-KB通路NF-κB生物活性Parthenolide 是一种 NF-κB 抑制剂,可降低组蛋白脱乙酰酶 1 (HDAC-1) 和 DNA 甲基转移酶 1。[1-3]In Vitro小白菊内酯(PTL)对NSCLC细胞Calu-1,H1792,A549,H1299,H157和H460具有剂量依赖性生长抑制作用。在测试的肺癌细胞中,小白菊内酯可以浓度和时间依赖性方式诱导凋亡蛋白如CASP8,CASP9,CASP3和PARP1的切割,表明在小白菊内酯暴露后触发细胞凋亡。除诱导细胞凋亡外,小白菊内酯还在A549细胞中以浓度依赖性方式诱导G0/G1细胞周期停滞,在H1792细胞中诱导G2/M细胞周期停滞[2]。In Vivo只有具有抗炎特征的HDAC抑制剂小白菊内酯在Phb1 KO肝细胞中显示出有效的抗细胞凋亡作用。实际上,TSA和小白菊内酯处理的肝细胞显示FXR水平增加,CYP7A1,HDAC4,TNFα,TRAIL和Bax水平降低,表明胆汁酸作为特异性HDAC抑制作用的毒性作用较小,导致Phb1的衰减。 KO肝细胞凋亡反应。重要的是,在Phb1 KO小鼠中,小白菊内酯对BDL后的肝损伤具有保护作用。实际上,小白蛋白治疗导致BDL后死亡率降低,并伴有较低的细胞凋亡反应,如坏死区域减少,Tunel染色以及ALT降低所示(8431±957 vs.4225±210)与对照Phb1 KO小鼠相比,U/L)和AST(4805±300 vs.2242±438 U/L)活性[3]。细胞实验将人肺癌细胞系接种在96孔板中,并在第二天用给定浓度的小白菊内酯(0,5,10,20μM)处理另外48小时,然后进行SRB或MTT测定。对于SRB测定,如前所述估计活细胞数。处理后,首先丢弃培养基。为了固定贴壁细胞,向每个孔中加入100μL冷的三氯乙酸(10%(w/v))并在4℃下孵育至少1小时。然后将板用去离子水洗涤五次并在空气中干燥。然后向每个孔中加入50μLSRB溶液(0.4%w/v在1%乙酸中)并在室温下温育5分钟。将板用1%乙酸洗涤五次以除去未结合的SRB,然后空气干燥。将残留的结合的SRB用100μL的10mM Tris碱缓冲液(pH 10.5)溶解,然后使用微量滴定板读数器在495nm处读数。执行MTT测定。向每个样品中加入20μLMTT(5mg/mL)并在37℃下孵育4小时,然后加入100μL溶解溶液。细胞活力在595nm处确定[2]。动物实验使用小鼠[3] Phb1 KO小鼠。治疗8-12周龄的男性。在胆管结扎(BDL)前24小时和1小时腹膜内注射小白菊内酯,或在两周内每周两次腹膜内注射小白菊内酯。将肝脏标本快速冷冻用于后续分析[3]。数据来源文献[1]. Nakshatri H, et al. NF-κB-dependent and -independent epigenetic modulation using the novel anti-cancer agent DMAPT. Cell Death Dis. 2015 Jan 22;6:e1608.[2]. Zhao X, et al. Parthenolide induces apoptosis via TNFRSF10B and PMAIP1 pathways in human lung cancer cells. J Exp Clin Cancer Res. 2014 Jan 6;33:3.[3]. Barbier-Torres L, et al. Histone deacetylase 4 promotes cholestatic liver injury in the absence of prohibitin-1. Hepatology. 2015 Oct;62(4):1237-48规格5mg 10mg 10mM*1mL (in DMSO)单位瓶Parthenolide 是一种 NF-κB 抑制剂,可降低组蛋白脱乙酰酶 1 (HDAC-1) 和 DNA 甲基转移酶 1。备注:以上数据均来自公开文献, Solarbio暂未进行独立验证, 仅供参考。These protocols are for reference only. Solarbio does not independently validate these methods.
Norepinephrine;去甲肾上腺素产品简介CAS51-41-2中文名称去甲肾上腺素英文名称Norepinephrine别名(R)-4-(2-氨基-1-羟基乙基)-1,2-苯二酚纯度HPLC≥98%分子式C8H11NO3 分子量169.18外观(性状)Light yellow to brown Solid储存条件Powder : 2-8℃, 2 years; In solvent(母液): -20℃, 1 month; -80℃, 6 months溶解性Soluble in Water ≥5mg/mL(Add HCl to help dissolve);Soluble in DMSO ≥1mg/mL(Need ultrasonic or Water bath)MDLMFCD00025592ECEINECS 205-750-4SMILESOC1=CC=C([C@@H](O)CN)C=C1O描述Norepinephrine是一种神经递质,也是一种激素。Norepinephrine是有效的α受体激动剂。(Norepinephrine is a neurotransmitter as well as a hormone. Norepinephrine is a potent alpha receptor agonist.)靶点Adrenergic Receptor通路Endocrinology & Hormones;GPCR & G Protein;Neuronal Signaling规格20mg 10mM*1mL in DMSO 50mg 100mg单位瓶Norepinephrine是一种神经递质,也是一种激素。Norepinephrine是有效的α受体激动剂。备注:以上数据均来自公开文献, Solarbio暂未进行独立验证, 仅供参考。These protocols are for reference only. Solarbio does not independently validate these methods.
Naringenin;柚皮素产品简介CAS480-41-1中文名称柚皮素英文名称Naringenin别名柚皮苷元;柑橘素纯度HPLC≥98%分子式C15H12O5 分子量272.25外观(性状)White to yellow Solid储存条件Powder : 2-8℃, 2 years; In solvent(母液): -20℃, 1 month; -80℃, 6 months溶解性Soluble in DMSO ≥5mg/mLECEINECS 266-769-1MDLMFCD00006844InChIKeyFTVWIRXFELQLPI-ZDUSSCGKSA-NInChIInChI=1S/C15H12O5/c16-9-3-1-8(2-4-9)13-7-12(19)15-11(18)5-10(17)6-14(15)20-13/h1-6,13,16-18H,7H2/t13-/m0/s1PubChem CID439246SMILESO=C1C[C@@H](C2=CC=C(O)C=C2)OC3=CC(O)=CC(O)=C13描述Naringenin是葡萄柚中主要的黄烷酮。(Naringenin is the main flavanone in grapefruit.)靶点Others通路Others生物活性Naringenin是葡萄柚中主要的黄烷酮; 显示出强烈的抗炎和抗氧化活性。[1-5]In Vitro柚皮素显示抑制HepG2细胞的增殖, 部分原因是细胞周期的G0 / G1期和G2 / M期细胞积聚。已经证明柚皮素可以诱导细胞凋亡, 这可以通过细胞核损伤和凋亡细胞比例增加来证明。 Naringenin触发线粒体介导的细胞凋亡途径, 如Bax / Bcl-2比例增加, 随后细胞色素C释放和caspase-3顺序激活所示[1]。柚皮素暴露显着降低A431细胞的细胞活力, 同时以剂量依赖性方式伴随核浓缩和DNA片段化的增加。细胞周期研究表明, 柚皮素诱导细胞周期G0 / G1期细胞周期停滞, caspase-3分析显示caspase-3活性呈剂量依赖性增加, 导致细胞凋亡[2]。In Vivo柚皮素补充剂导致血浆和肝脏中总甘油三酯和胆固醇的量显着减少。此外, 柚皮素补充剂可降低宫旁脂肪组织中的肥胖和甘油三酯含量。柚皮素喂养的动物显示肝脏中PPARα蛋白表达显着增加。已知受PPARα调节的CPT-1和UCP2的表达通过柚皮素治疗显着增强[3]。柚皮素通过PPARγ辅激活因子1α/PPARα介导的转录程序增加肝脏脂肪酸氧化。它通过减少空腹高胰岛素血症来预防甾醇调节元件结合蛋白1c介导的肝脏和肌肉脂肪生成。柚皮素可降低肝脏胆固醇和胆固醇酯的合成[4]。柚皮素以剂量依赖性方式抑制TNF-α诱导的VSMC增殖和迁移。机理研究表明, 柚皮素可阻止ERK / MAPK和Akt磷酸化, 同时保持p38 MAPK和JNK不变。柚皮素还可以阻断TNF-α诱导的ROS生成[5]。细胞实验将柚皮素溶解在DMSO中并在细胞培养基中稀释。用PBS冲洗细胞并在含有各种浓度的柚皮素 (50, 100, 150, 200, 250, 300μM) 的培养基中生长。溶剂DMSO处理的细胞用作对照。处理24小时后, 除去培养基并用含有MTT的另一种培养基替换。使用MTT测定法测量细胞活力[1]。动物实验大鼠:制备半纯化的粉末饮食, 用于浓度为柚皮素:0, 0.003, 0.006和0.012%的饮食。适应7天后, 将大鼠分成四组中的一组, 每组六只动物, 并喂食半纯化的实验饮食6周。实验饮食含有16%脂肪, 45.5%蔗糖和不同的柚皮素浓度 (0, 0.003, 0.006或0.012%) (表1) 。在研究期间, 大鼠可随意获取食物和水。在整个实验过程中测量食物摄入量和体重[3]。小鼠:8至12周龄的小鼠随意喂食啮齿动物标准饮食或含有42%来自脂肪加胆固醇 (0.05%wt / wt) 的卡路里的高脂肪饮食。柚皮素以1%或3% (wt / wt) 加入西方饮食中。 Ldlr - / - 小鼠喂养4周, C57BL / 6J小鼠喂养30周。每天测量食物摄入量, 每两周测量一次体重。在干预前将小鼠禁食6小时[4]。数据来源文献[1]. Arul D, et al. Naringenin (citrus flavonone) induces growth inhibition, cell cycle arrest and apoptosis in human hepatocellular carcinoma cells. Pathol Oncol Res. 2013 Oct; 19 (4) :763-70.[2]. Ahamad MS, et al. Induction of apoptosis and antiproliferative activity of naringenin in human epidermoid carcinomacell through ROS generation and cell cycle arrest. PLoS One. 2014 Oct 16; 9 (10) :e110003.[3]. Cho KW, et al. Dietary naringenin increases hepatic peroxisome proliferators-activated receptor α proteinexpression and decreases plasma triglyceride and adiposity in rats. Eur J Nutr. 2011 Mar; 50 (2) :81-8.[4]. Mulvihill EE, et al. Naringenin prevents dyslipidemia, apolipoprotein B overproduction, and hyperinsulinemia in LDLreceptor-null mice with diet-induced insulin resistance. Diabetes. 2009 Oct; 58 (10) :2198-210.[5]. Chen S, et al. Naringenin inhibits TNF-α induced VSMC proliferation and migration via induction of HO-1. Food Chem Toxicol. 2012 Sep; 50 (9) :3025-31Note以上数据均来自公开文献, Solarbio暂未进行独立验证, 仅供参考。These protocols are for reference only. Solarbio does not independently validate these methods.规格20mg 10mM*1mL in DMSO 50mg 100mg单位瓶备注:以上数据均来自公开文献, Solarbio暂未进行独立验证, 仅供参考。These protocols are for reference only. Solarbio does not independently validate these methods.
Cabazitaxel 卡巴他赛CAS183133-96-2中文名称卡巴他赛英文名称Cabazitaxel别名TXD258; XRP-6258纯度HPLC≥98%分子式C45H57NO14 分子量835.93外观(性状)White to off-white Solid储存条件Powder : 2-8℃, 2 years; In solvent(母液): -20℃, 1 month; -80℃, 6 months溶解性Soluble in DMSOECEINECS 680-632-7MDLMFCD18827611InChIKeyBMQGVNUXMIRLCK-OAGWZNDDSA-NInChIInChI=1S/C45H57NO14/c1-24-28(57-39(51)33(48)32(26-17-13-11-14-18-26)46-40(52)60-41(3,4)5)22-45(53)37(58-38(50)27-19-15-12-16-20-27)35-43(8,36(49)34(55-10)31(24)42(45,6)7)29(54-9)21-30-44(35,23-56-30)59-25(2)47/h11-20,28-30,32-35,37,48,53H,21-23H2,1-10H3,(H,46,52)/t28-,29-,30+,32-,33+,34+,35-,37-,43+,44-,45+/m0/s1PubChem CID9854073SMILESCC1=C([C@@H](OC)C([C@@]2(C)[C@@]3([H])[C@](OC(C)=O)(CO4)[C@H]4C[C@@H]2OC)=O)C(C)(C)[C@@]([C@H]3OC(C5=CC=CC=C5)=O)(O)C[C@@H]1OC([C@H](O)[C@H](C6=CC=CC=C6)NC(OC(C)(C)C)=O)=O描述Cabazitaxel 具有显著的抗肿瘤活性。(Cabazitaxel has significant antitumor activity.)靶点Microtubule/Tubulin通路Cytoskeleton生物活性Cabazitaxel 是天然紫杉烷脱乙酰基巴卡丁III的半合成衍生物,具有显著的抗肿瘤功效。[1-2]In Vitro卡巴他赛(100μg/ mL)对未照射的4T1细胞的细胞毒性为70.8%。卡巴他赛(100μg/ mL)具有浓度依赖性抗增殖作用,抗增殖活性为56.2%[1]。In Vivo卡巴他赛(10 mg/kg,iv)对肝脏和肾脏有一定的毒性,但可以通过整合到Ans中来避免。用AN-ICG-CBX和AN-CBX处理的小鼠的体重略有下降,而游离CBX组的体重与对照组相比显著降低[1]。细胞实验用MTT测定法评估负载CBX的AN和游离卡巴他赛(CBX)的细胞毒性。将细胞以每孔3000个细胞的密度接种到96孔板上并培养24小时。将装有CBX的AN和游离CBX用PBS稀释至预定浓度并加入每个孔中。还加入空白AN,AN-ICG和游离CBX溶剂(吐温-80和无水醇的混合物)至不同的最终浓度。孵化持续另外48小时。将20μLMTT溶液(在PBS中5mg/mL)加入每个孔中,并将细胞在37℃下再孵育4小时。随后除去培养基并加入150μL二甲基亚砜(DMSO)以溶解紫色甲salt盐晶体。然后通过酶标仪在490nm处测量吸光度。用培养基处理的细胞作为对照进行评估。动物实验为了评估联合化学疗法和PTT在体内的抗肿瘤效率,将携带4T1肿瘤的小鼠随机分成6个治疗组(n = 5)。当肿瘤达到50mm3-100mm3时开始治疗。给小鼠静脉注射生理盐水,AN-ICG,游离卡巴他赛(CBX),AN-CBX和AN-ICG-CBX(ICG 2mg/kg,CBX 10mg/kg)。 8小时后,注射AN-ICG和AN-ICG-CBX的组用808nm激光照射(0.8W/cm 2,5分钟)。每隔一天用卡尺测量每个肿瘤的长度和宽度。公式(体积(mm3)= 1/2×长度×宽度2)用于计算肿瘤体积。使用电子天平每两天记录这些小鼠的体重。在抗肿瘤研究结束时,处死携带4T1肿瘤的小鼠以收集肿瘤和主要器官。数据来源文献[1]. Tai X, et al. Cabazitaxel and indocyanine green co-delivery tumor-targeting nanoparticle for improved antitumor efficacy and minimized drug toxicity. J Drug Target. 2016 Sep 9:1-29.[2]. Gdowski AS, et al. Bone-targeted cabazitaxel nanoparticles for metastatic prostate cancer skeletal lesions and pain. Nanomedicine (Lond). 2017 Sep;12(17):2083-2095.规格10mg 10mM*1mL (in DMSO) 50mg单位瓶是一种紫杉烷的衍生物,能够抑制抑制微管生长和聚合。备注:以上数据均来自公开文献, Solarbio暂未进行独立验证, 仅供参考。These protocols are for reference only. Solarbio does not independently validate these methods.
Tofacitinib;托法替尼产品简介 CAS477600-75-2中文名称托法替尼英文名称Tofacitinib别名CP-690550纯度≥98%分子式C16H20N6O分子量312.37外观(性状)Solid储存条件Powder : -20℃, 2 years;In solvent(母液): -20℃, 1 month; -80℃, 6 months溶解性Soluble in DMSO ≥5mg/mL(Need ultrasonic)MDLMFCD11035919ECEINECS 689-145-4SMILESO=C(CC#N)N1C[C@H](N(C2=C3C(NC=C3)=NC=N2)C)[C@H](C)CC1描述Tofacitinib是 JAK1/2/3 抑制剂。(Tofacitinib is a JAK1/2/3 inhibitor.)靶点JAK通路JAK/STAT Signaling生物活性Tofacitinib是 JAK1/2/3 抑制剂,IC50 分别为1,20 和 112 nM。[1-4]IC50JAK3:1 nM ; JAK2:20 nM ; JAK1:112 nM ; Rock-II:3400 nM ; Lck:3870 nM [1-4]In VitroTofacitinib(CP-690550)柠檬酸盐可能在JAK3和JAK2处结合为2.2nM和5nM(Kd)。该报告包括在Camk1(Kd为5,000 nM),DCamkL3(Kd为4.5 nM),Mst2(Kd为4,300 nM),Pkn1(Kd为200 nM),Rps6ka2(Kin.Dom.2-C-)的Tofacitinib的额外结合。末端)(Kd为1,400 nM),Rps6ka6(Kin.Dom.2-C-末端)(Kd为1,200 nM),Snark(Kd为420 nM),Tnk1(Kd为640 nM)和Tyk2(Kd为620 nM) )[1]。In Vivo与PEG处理的对照小鼠相比,用Tofacitinib处理的动物显示出显着更低的抗药物抗体(ADA)产生(初次免疫后5周,p 4小时的血浆暴露[3]。激酶实验通过与专有标签融合的所选激酶的竞争结合测定记录激酶活性。在存在和不存在测试化合物(例如,托法替尼)的情况下,激酶量与固定的活性位点定向配体结合的测量提供了对配体结合的DMSO对照的%。选择0到10之间的活动用于Kd测定。树形图表示由名为PhyloChem [1]的内部可视化工具生成。细胞实验通过磁性分离(CD4 + MACS珠)从健康供体获得的外周血单核细胞富集人CD4 +阳性细胞。用平板结合的抗CD3和抗CD28抗体(各5μg/ mL)激活CD4 +细胞3天,然后在IL-2(50U / mL)存在下再膨胀4天。将细胞在1%RPMI中静置过夜,并以指定浓度(5nM,50nM,500nM;在所有制剂中DMSO浓度相等)与托法替尼或DMSO对照预孵育1小时,然后用IL-2活化( 1000 u / mL)或IL-12(100 ng / mL)15分钟。将细胞(10×10 6 /条件)在1%Triton-x裂解缓冲液中裂解,并在NuPage Bis-Tris凝胶(4-12%梯度)中运行等量的细胞裂解物。将蛋白质转移到硝酸纤维素膜上。使用Odyssey western印迹系统[1]用指定的抗体进行检测。动物实验小鼠[2]使用雌性BALB / c小鼠(6-8周龄)。小鼠通过渗透泵输注(Alzet Model2004,0.25μL/小时,28天)接受PEG300(100mg / mL)或单独载体(PEG300)中的Tofacitinib。免疫前4天,将小鼠麻醉并将其背部表面剃毛。在背部做一厘米的切口以形成皮下袋并插入泵。切口部位用伤口夹闭合。从第0天开始每周(ip)注射小鼠SS1P重组免疫毒素(RIT;5μg/小鼠);对照小鼠仅接受盐水注射。在SS1P或载体免疫前每周,抽取50μL血液以获得血清样品。将血清储存在-80℃直至分析。大鼠[3]在雌性Lewis大鼠中诱导佐剂诱导的关节炎(AIA)。根据后爪体积随机分配大鼠并将其分配给Tofacitinib或载体治疗方案。每个治疗组7-8只大鼠组和正常幼稚大鼠(每组n = 4)在开始治疗后4小时,4天或7天安乐死(分别在免疫后第16,20和23天) 。将Tofacitinib悬浮于0.5%甲基纤维素/0.025%吐温20中用于体内研究。每天一次口服给予载体或托法替尼(6.2mg / kg),在免疫后第16天开始并持续至第23天。在治疗开始后第4天和第7天(分别在免疫后第20天和第23天)重新评估爪体积。 )。对于微型计算机断层扫描(微CT)成像,以及爪组织中的抗酒石酸酸性磷酸酶(TRAP)染色,在单独的Lewis大鼠队列中诱导AIA。数据来源文献[1]. Jiang JK, et al. Examining the chirality, conformation and selective kinase inhibition of 3-((3R,4R)-4-methyl-3-(methyl(7H-pyrrolo[2,3-d]pyrimidin-4-yl)amino)piperidin-1-yl)-3-oxopropanenitrile (CP-690,550). J Med Chem. 2008 Dec 25;51(24):8012-8.[2]. Onda M, et al. Tofacitinib suppresses antibody responses to protein therapeutics in murine hosts. J Immunol. 2014 Jul 1;193(1):48-55.[3]. LaBranche TP, et al. JAK inhibition with tofacitinib suppresses arthritic joint structural damage through decreased RANKL production. Arthritis Rheum. 2012 Nov;64(11):3531-42.[4]. Calama E, et al. Tofacitinib ameliorates inflammation in a rat model of airway neutrophilia induced by inhaled LPS. Pulm Pharmacol Ther. 2017 Apr;43:60-67规格10mg 20mg 50mg单位瓶Tofacitinib是 JAK1/2/3 抑制剂。 备注: 以上数据均来自公开文献, Solarbio暂未进行独立验证, 仅供参考。 These protocols are for reference only. Solarbio does not independently validate these methods.