CL-387785newfeatured
WARNING: This product is for research use only, not for human or veterinary use.
MedKoo CAT#:406106
CAS#:194423-06-8
Description:CL-387785, also known as EKI-785 , is a n irreversible inhibitor of EGF-receptor (EGFR) kinase activity in vivo (IC50 = 250-490 pM). CL-387785 covalently bound to EGF-R. It also specifically inhibited kinase activity of the protein (IC50 = 370+/-120 pM), blocked EGF-stimulated autophosphorylation of the receptor in cells (ic50 approximately 5 nM), inhibited cell proliferation (IC50 = 31-125 nM) primarily in a cytostatic manner in cell lines that overexpress EGF-R or c-erbB-2, and profoundly blocked the growth of a tumor that overexpresses EGF-R in nude mice (when given orally at 80 mg/kg/day for 10 days, daily). CL-387,785 is useful for studying the interaction of small molecules with EGF-R and may have clinical utility.
Price and Availability
CL-387785, purity > 98%, is in stock. The same day shipping out after order is received.
Chemical Structure
Theoretical Analysis
MedKoo Cat#: 406106Name: CL-387785CAS#: 194423-06-8Chemical Formula: C18H13BrN4OExact Mass: 380.02727Molecular Weight: 381.23Elemental Analysis: C, 56.71; H, 3.44; Br, 20.96; N, 14.70; O, 4.20
Synonym:CL387785; CL 387785; CL-387785; EKI785; EK-I785; EK I785.
IUPAC/Chemical Name:N-[4-[(3-Bromophenyl)amino]-6-quinazolinyl]-2-butynamide
InChi Key:BTYYWOYVBXILOJ-UHFFFAOYSA-N
InChi Code:InChI=1S/C18H13BrN4O/c1-2-4-17(24)22-14-7-8-16-15(10-14)18(21-11-20-16)23-13-6-3-5-12(19)9-13/h3,5-11H,1H3,(H,22,24)(H,20,21,23)
SMILES Code:CC#CC(NC1=CC2=C(NC3=CC=CC(Br)=C3)N=CN=C2C=C1)=O
Technical Data
Additional Information
References
1: Tomioka H, Mukohara T, Kataoka Y, Ekyalongo RC,Funakoshi Y, Imai Y, Kiyota N, Fujiwara Y, Minami H. Inhibition of themTOR/S6K signal is necessary to enhance fluorouracil-induced apoptosisin gastric cancer cells with HER2 amplification. Int J Oncol. 2012Aug;41(2):551-8. doi: 10.3892/ijo.2012.1485. Epub 2012 May 17. PubMedPMID: 22614071.
2: Chiu HC, Chang TY, Huang CT, Chao YS, Hsu JT. EGFR and myosin IIinhibitors cooperate to suppress EGFR-T790M-mutant NSCLC cells. MolOncol. 2012 Jun;6(3):299-310. doi: 10.1016/j.molonc.2012.02.001. Epub2012 Feb 10. PubMed PMID: 22366308.
3: Zannetti A, Iommelli F, Speranza A, Salvatore M, Del Vecchio S.3"-deoxy-3"-18F-fluorothymidine PET/CT to guide therapy with epidermalgrowth factor receptor antagonists and Bcl-xL inhibitors in non-smallcell lung cancer. J Nucl Med. 2012 Mar;53(3):443-50. doi:10.2967/jnumed.111.096503. Epub 2012 Feb 13. PubMed PMID: 22331221.
4: Kancha RK, von Bubnoff N, Bartosch N, Peschel C, Engh RA, Duyster J.Differential sensitivity of ERBB2 kinase domain mutations towardslapatinib. PLoS One. 2011;6(10):e26760. doi:10.1371/journal.pone.0026760. Epub 2011 Oct 28. PubMed PMID: 22046346;PubMed Central PMCID: PMC3203921.
5: Hama T, Yuza Y, Suda T, Saito Y, Norizoe C, Kato T, Moriyama H,Urashima M. Functional mutation analysis of EGFR family genes andcorresponding lymph node metastases in head and neck squamous cellcarcinoma. Clin Exp Metastasis. 2012 Jan;29(1):19-25. doi:10.1007/s10585-011-9425-5. Epub 2011 Sep 28. PubMed PMID: 21953075.
6: Chung JH, Rho JK, Xu X, Lee JS, Yoon HI, Lee CT, Choi YJ, Kim HR, KimCH, Lee JC. Clinical and molecular evidences of epithelial tomesenchymal transition in acquired resistance to EGFR-TKIs. Lung Cancer.2011 Aug;73(2):176-82. doi: 10.1016/j.lungcan.2010.11.011. Epub 2010 Dec17. PubMed PMID: 21168239.
7: Eisinger DA, Ammer H. Epidermal growth factor treatment switches δ-opioidreceptor-stimulated extracellular signal-regulated kinases 1 and 2signaling from an epidermal growth factor to an insulin-like growthfactor-1 receptor-dependent mechanism. Mol Pharmacol. 2011Feb;79(2):326-35. doi: 10.1124/mol.110.064956. Epub 2010 Nov 15. PubMedPMID: 21078885.
8: Yu Z, Boggon TJ, Kobayashi S, Jin C, Ma PC, Dowlati A, Kern JA, TenenDG, Halmos B. Resistance to an irreversible epidermal growth factorreceptor (EGFR) inhibitor in EGFR-mutant lung cancer reveals noveltreatment strategies. Cancer Res. 2007 Nov 1;67(21):10417-27. PubMedPMID: 17974985.
9: Kobayashi S, Shimamura T, Monti S, Steidl U, Hetherington CJ, LowellAM, Golub T, Meyerson M, Tenen DG, Shapiro GI, Halmos B. Transcriptionalprofiling identifies cyclin D1 as a critical downstream effector ofmutant epidermal growth factor receptor signaling. Cancer Res. 2006 Dec1;66(23):11389-98. PubMed PMID: 17145885.
10: Engelman JA, Mukohara T, Zejnullahu K, Lifshits E, Borrás AM, GaleCM, Naumov GN, Yeap BY, Jarrell E, Sun J, Tracy S, Zhao X, Heymach JV,Johnson BE, Cantley LC, Jänne PA. Allelic dilution obscures detection ofa biologically significant resistance mutation in EGFR-amplified lungcancer. J Clin Invest. 2006 Oct;116(10):2695-706. Epub 2006 Aug 10.PubMed PMID: 16906227; PubMed Central PMCID: PMC1570180.
11: Greulich H, Chen TH, Feng W, Jänne PA, Alvarez JV, Zappaterra M,Bulmer SE, Frank DA, Hahn WC, Sellers WR, Meyerson M. Oncogenictransformation by inhibitor-sensitive and -resistant EGFR mutants. PLoSMed. 2005 Nov;2(11):e313. Epub 2005 Oct 4. PubMed PMID: 16187797; PubMedCentral PMCID: PMC1240052.
12: Kobayashi S, Ji H, Yuza Y, Meyerson M, Wong KK, Tenen DG, Halmos B.An alternative inhibitor overcomes resistance caused by a mutation ofthe epidermal growth factor receptor. Cancer Res. 2005 Aug15;65(16):7096-101. PubMed PMID: 16103058.
13: Desai AA, Ratain MJ. EGFR pharmacogenomics: the story continues tomutate and evolve. Am J Pharmacogenomics. 2005;5(2):137-9. PubMed PMID:15813677.
14: Sweeney WE, Chen Y, Nakanishi K, Frost P, Avner ED. Treatment ofpolycystic kidney disease with a novel tyrosine kinase inhibitor. KidneyInt. 2000 Jan;57(1):33-40. PubMed PMID: 10620185.
15: Sweeney WE, Futey L, Frost P, Avner ED. In vitro modulation of cystformation by a novel tyrosine kinase inhibitor. Kidney Int. 1999Aug;56(2):406-13. PubMed PMID: 10432378.
16: Discafani CM, Carroll ML, Floyd MB Jr, Hollander IJ, Husain Z,Johnson BD, Kitchen D, May MK, Malo MS, Minnick AA Jr, Nilakantan R,Shen R, Wang YF, Wissner A, Greenberger LM. Irreversible inhibition ofepidermal growth factor receptor tyrosine kinase with in vivo activityby N-[4-[(3-bromophenyl)amino]-6-quinazolinyl]-2-butynamide(CL-387,785). Biochem Pharmacol. 1999 Apr 15;57(8):917-25. PubMed PMID:10086326.
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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