PD-173955featured
WARNING: This product is for research use only, not for human or veterinary use.
MedKoo CAT#:406164
CAS#:260415-63-2
Description:PD-173955 is a src tyrosine kinase inhibitor. PD173955 inhibited Bcr-Abl-dependent cell growth. PD173955 showed cell cycle arrest in G(1). PD173955 has an IC(50) of 1-2 nM in kinase inhibition assays of Bcr-Abl, and in cellular growth assays it inhibits Bcr-Abl-dependent substrate tyrosine phosphorylation. PD173955 inhibited kit ligand-dependent c-kit autophosphorylation (IC(50) = approximately 25 nM) and kit ligand-dependent proliferation of M07e cells (IC(50) = 40 nM) but had a lesser effect on interleukin 3-dependent (IC(50) = 250 nM) or granulocyte macrophage colony-stimulating factor (IC(50) = 1 microM)-dependent cell growth.
Price and Availability
PD173955, purity > 98%, is in stock. Current shipping out time is about 2 weeks after order is received. CoA, QC data and MSDS documents are available in one week after order is received.
Chemical Structure
Theoretical Analysis
MedKoo Cat#: 406164Name: PD-173955CAS#: 260415-63-2Chemical Formula: C21H16Cl2N4OSExact Mass: 442.04219Molecular Weight: 443.34894Elemental Analysis: C, 56.89; H, 3.64; Cl, 15.99; N, 12.64; O, 3.61; S, 7.23
Synonym:PD173955; PD 173955; PD173955.
IUPAC/Chemical Name:6-(2,6-dichlorophenyl)-8-methyl-2-((3-(methylthio)phenyl)amino)pyrido[2,3-d]pyrimidin-7(8H)-one
InChi Key:VAARYSWULJUGST-UHFFFAOYSA-N
InChi Code:InChI=1S/C21H16Cl2N4OS/c1-27-19-12(9-15(20(27)28)18-16(22)7-4-8-17(18)23)11-24-21(26-19)25-13-5-3-6-14(10-13)29-2/h3-11H,1-2H3,(H,24,25,26)
SMILES Code:O=C1C(C2=C(Cl)C=CC=C2Cl)=CC3=CN=C(NC4=CC=CC(SC)=C4)N=C3N1C
Technical Data
Additional Information
References
1: Kraus GA, Gupta V, Mokhtarian M, Mehanovic S,Nilsen-Hamilton M. New effective inhibitors of the Abelson kinase.Bioorg Med Chem. 2010 Sep 1;18(17):6316-21. doi:10.1016/j.bmc.2010.07.021. Epub 2010 Jul 14. PubMed PMID: 20674368.
2: Sylvester JE, Kron SJ. A bead-based activity screen forsmall-molecule inhibitors of signal transduction in chronic myelogenousleukemia cells. Mol Cancer Ther. 2010 May;9(5):1469-81. doi:10.1158/1535-7163.MCT-10-0157. Epub 2010 Apr 27. PubMed PMID: 20423990;PubMed Central PMCID: PMC2868067.
3: Crespo A, Fernández A. Induced disorder in protein-ligand complexesas a drug-design strategy. Mol Pharm. 2008 May-Jun;5(3):430-7. doi:10.1021/mp700148h. Epub 2008 Feb 16. Erratum in: Mol Pharm. 2008Jul-Aug;5(4):680. Mol Pharm. 2010 Feb 1;7(1):306. Mol Pharm. 2010 Oct4;7(5):1877. PubMed PMID: 18278867.
4: Gunby RH, Ahmed S, Sottocornola R, Gasser M, Redaelli S, Mologni L,Tartari CJ, Belloni V, Gambacorti-Passerini C, Scapozza L. Structuralinsights into the ATP binding pocket of the anaplastic lymphoma kinaseby site-directed mutagenesis, inhibitor binding analysis, and homologymodeling. J Med Chem. 2006 Sep 21;49(19):5759-68. PubMed PMID: 16970400.
5: Caligiuri M, Molz L, Liu Q, Kaplan F, Xu JP, Majeti JZ, Ramos-KelseyR, Murthi K, Lievens S, Tavernier J, Kley N. MASPIT: three-hybrid trapfor quantitative proteome fingerprinting of small molecule-proteininteractions in mammalian cells. Chem Biol. 2006 Jul;13(7):711-22.PubMed PMID: 16873019.
6: Verkhivker GM. Imprint of evolutionary conservation and proteinstructure variation on the binding function of protein tyrosine kinases.Bioinformatics. 2006 Aug 1;22(15):1846-54. Epub 2006 May 23. PubMedPMID: 16720585.
7: Liu L, D"Mello SR. Phosphorylation of IkappaB-beta is necessary forneuronal survival. J Biol Chem. 2006 Jan 20;281(3):1506-15. Epub 2005Nov 11. PubMed PMID: 16286457.
8: O"Hare T, Pollock R, Stoffregen EP, Keats JA, Abdullah OM, MosesonEM, Rivera VM, Tang H, Metcalf CA 3rd, Bohacek RS, Wang Y,Sundaramoorthi R, Shakespeare WC, Dalgarno D, Clackson T, Sawyer TK,Deininger MW, Druker BJ. Inhibition of wild-type and mutant Bcr-Abl byAP23464, a potent ATP-based oncogenic protein kinase inhibitor:implications for CML. Blood. 2004 Oct 15;104(8):2532-9. Epub 2004 Jul15. PubMed PMID: 15256422.
9: Cowan-Jacob SW, Guez V, Fendrich G, Griffin JD, Fabbro D, Furet P,Liebetanz J, Mestan J, Manley PW. Imatinib (STI571) resistance inchronic myelogenous leukemia: molecular basis of the underlyingmechanisms and potential strategies for treatment. Mini Rev Med Chem.2004 Mar;4(3):285-99. Review. PubMed PMID: 15032675.
10: Strife A, Wisniewski D, Liu C, Lambek CL, Darzynkiewicz Z, SilverRT, Clarkson B. Direct evidence that Bcr-Abl tyrosine kinase activitydisrupts normal synergistic interactions between Kit ligand andcytokines in primary primitive progenitor cells. Mol Cancer Res. 2003Jan;1(3):176-85. PubMed PMID: 12556557.
MedKoo,由化学家和药学家陈清奇博士。北卡罗莱纳州的研究三角区(ResearchTrianglePark,简称RTP),是一家以研发、生产和销售小分子抗癌化合物为主的医药科技公司,该公司的业务范围主要是为全球所有从事抗癌药物研究和开发的制药公司,高校,研究院所,政府相关机构提供与抗癌药物分子相关的产品、试剂和技术服务。
中文名MedKoo中 文美帝药库医药科技公司创立于2008年总部位于美国东海岸
MedKoo是世界领先的供应商之一的抗癌化学试剂和激酶抑制剂。我们制造、销售和分发高质量的抗癌小分子肿瘤学研究试剂。我们的使命是建立世界上最全面的抗癌小分子的集合。我们也为医药行业提供高质量的研究服务、医学研究机构和学术机构。我们致力于提供优质的服务。 MedKoo是世界领先的供应商之一的抗癌化学试剂和激酶抑制剂。我们制造、销售和分发高质量的抗癌小分子肿瘤学研究试剂。我们的使命是建立世界上最全面的抗癌小分子的集合。我们也为医药行业提供高质量的研究服务、医学研究机构和学术机构。我们致力于提供优质的服务和分子有竞争力的价格。MedKoo是您可靠的合作伙伴采购药物发现和药物分子。 MedKoo是世界的抗癌化学试剂和激酶抑制剂供应商之一。我们制造,销售和分销用于肿瘤学研究的高质量抗癌小分子试剂。我们的使命是建立世界上全面的抗癌小分子集合。我们还为制药行业,医学研究组织和学术机构提供高质量的研究服务。我们致力于以具有竞争力的价格提供服务和分子。MedKoo是您可靠的药物发现和药物分子采购合作伙伴。 CRISPR-Cas9是近年兴起的用于靶向基因组特定位置,进行DNA修饰的重要工具。研究发现CRISPR是细菌为了应对病毒的攻击而演化而来的获得性免疫防御机制。具体来说,在CRISPR和Cas9的作用下,经由小RNA分子的引导,靶向并沉默入侵者遗传物质核酸的关键部分。在该系统中,crRNA(CRISPR-derivedRNA)与tracrRNA(trans-activatingRNA)结合形成的复合物能特异性识别靶基因序列,并引导Cas9核酸内切酶在靶定位点剪切双链DNA,随后,细胞的非同源末端连接修复机制(NHEJ)重新连接断裂处的基因组DNA,并引入插入或缺失突变。另外也可以提供一个外源双链供体DNA(Donor)通过同源重组(HR)整合进断裂处的基因组,从而达到对基因组DNA进行修饰的目的。
目前,CRISPR-Cas9系统的高效基因组编辑功能已被应用于多种生物,包括小鼠、大鼠、斑马鱼、秀丽隐杆线虫,也包含多种细菌和植物,甚至在人体上也有应用。
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