Buparlisib (BKM120)featured
WARNING: This product is for research use only, not for human or veterinary use.
MedKoo CAT#:204690
CAS#:944396-07-0 (free base)
Description:Buparlisib, also known as BKM120, is an orally bioavailable specific oral inhibitor of the pan-class I phosphatidylinositol 3-kinase (PI3K) family of lipid kinases with potential antineoplastic activity. PI3K inhibitor BKM120 specifically inhibits class I PIK3 in the PI3K/AKT kinase (or protein kinase B) signaling pathway in an ATP-competitive manner, thereby inhibiting the production of the secondary messenger phosphatidylinositol-3,4,5-trisphosphate and activation of the PI3K signaling pathway.
Price and Availability
Buparlisib, purity > 98%, is in stock. The same day shipping out after order is received.
Chemical Structure
Theoretical Analysis
MedKoo Cat#: 204690Name: Buparlisib (BKM120)CAS#: 944396-07-0 (free base)Chemical Formula: C18H21F3N6O2Exact Mass: 410.16781Molecular Weight: 410.39Elemental Analysis:C, 52.68; H, 5.16; F, 13.89; N, 20.48; O, 7.80
Related CAS #:944396-07-0 (free base)1312445-63-8 (HCl)
Synonym:NVPBKM120; NVP BKM120; NV- BKM120; BKM120; BKM-120; BKM 120; Buparlisib.
IUPAC/Chemical Name:5-[2,6-Di(4-morpholinyl)-4-pyrimidinyl]-4-(trifluoromethyl)-2-pyridinamine.
InChi Key:CWHUFRVAEUJCEF-UHFFFAOYSA-N
InChi Code:InChI=1S/C18H21F3N6O2/c19-18(20,21)13-9-15(22)23-11-12(13)14-10-16(26-1-5-28-6-2-26)25-17(24-14)27-3-7-29-8-4-27/h9-11H,1-8H2,(H2,22,23)
SMILES Code:NC1=NC=C(C2=NC(N3CCOCC3)=NC(N4CCOCC4)=C2)C(C(F)(F)F)=C1
Technical Data
Additional Information
Related:944396-07-0 (free base)1312445-63-8 (HCl).
NVP-BKM120 is a selective pan class 1 PI3 Kinase inhibitor. It was found that NVP-BKM120 inhibited the PI3 signaling pathways, leading to different forms of cell death based on P53 statuses. Further studies are warranted to determine if NVP-BKM120 has potential as a glioma treatment. (source: http://www.ncbi.nlm.nih.gov/pubmed/22065080 ).
References
1: Rodon J, Braña I, Siu LL, De Jonge MJ, Homji N,Mills D, Di Tomaso E, Sarr C, Trandafir L, Massacesi C, Eskens F,Bendell JC. Phase I dose-escalation and -expansion study of buparlisib(BKM120), an oral pan-Class I PI3K inhibitor, in patients with advancedsolid tumors. Invest New Drugs. 2014 Mar 21. [Epub ahead of print]PubMed PMID: 24652201.
2: Ando Y, Inada-Inoue M, Mitsuma A, Yoshino T, Ohtsu A, Suenaga N, SatoM, Kakizume T, Robson M, Quadt C, Doi T. Phase I dose-escalation studyof buparlisib (BKM120), an oral pan-class I PI3K inhibitor, in Japanesepatients with advanced solid tumors. Cancer Sci. 2014 Mar;105(3):347-53.doi: 10.1111/cas.12350. Epub 2014 Feb 13. PubMed PMID: 24405565.
3: Liang YC, Wu HG, Xue HJ, Liu Q, Shi LL, Liu T, Wu G. Effects of PI3Kinhibitor NVP-BKM120 on acquired resistance to gefitinib of human lungadenocarcinoma H1975 cells. J Huazhong Univ Sci Technolog Med Sci. 2013Dec;33(6):845-51. doi: 10.1007/s11596-013-1209-5. Epub 2013 Dec 13.PubMed PMID: 24337846.
4: Lonetti A, Antunes IL, Chiarini F, Orsini E, Buontempo F, Ricci F,Tazzari PL, Pagliaro P, Melchionda F, Pession A, Bertaina A, LocatelliF, McCubrey JA, Barata JT, Martelli AM. Activity of the pan-class Iphosphoinositide 3-kinase inhibitor NVP-BKM120 in T-cell acutelymphoblastic leukemia. Leukemia. 2013 Nov 6. doi: 10.1038/leu.2013.369.[Epub ahead of print] PubMed PMID: 24310736.
5: Geisthoff UW, Nguyen HL, Hess D. Improvement in hereditaryhemorrhagic telangiectasia after treatment with the phosphoinositide3-kinase inhibitor BKM120. Ann Hematol. 2014 Apr;93(4):703-4. doi:10.1007/s00277-013-1845-7. Epub 2013 Jul 27. PubMed PMID: 23892886.
6: Rosich L, Saborit-Villarroya I, López-Guerra M, Xargay-Torrent S,Montraveta A, Aymerich M, Villamor N, Campo E, Pérez-Galán P, Roué G,Colomer D. The phosphatidylinositol-3-kinase inhibitor NVP-BKM120overcomes resistance signals derived from microenvironment by regulatingthe Akt/FoxO3a/Bim axis in chronic lymphocytic leukemia cells.Haematologica. 2013 Nov;98(11):1739-47. doi:10.3324/haematol.2013.088849. Epub 2013 Jul 12. PubMed PMID: 23850807;PubMed Central PMCID: PMC3815175.
7: Zang C, Eucker J, Liu H, Coordes A, Lenarz M, Possinger K, Scholz CW.Inhibition of pan-class I phosphatidyl-inositol-3-kinase by NVP-BKM120effectively blocks proliferation and induces cell death in diffuse largeB-cell lymphoma. Leuk Lymphoma. 2014 Feb;55(2):425-34. doi:10.3109/10428194.2013.806800. Epub 2013 Jul 25. PubMed PMID: 23721513.
8: Ren H, Zhao L, Li Y, Yue P, Deng X, Owonikoko TK, Chen M, Khuri FR,Sun SY. The PI3 kinase inhibitor NVP-BKM120 induces GSK3/FBXW7-dependentMcl-1 degradation, contributing to induction of apoptosis andenhancement of TRAIL-induced apoptosis. Cancer Lett. 2013 Sep28;338(2):229-38. doi: 10.1016/j.canlet.2013.03.032. Epub 2013 Apr 2.PubMed PMID: 23562472; PubMed Central PMCID: PMC3750077.
9: Kirstein MM, Boukouris AE, Pothiraju D, Buitrago-Molina LE, MarhenkeS, Schütt J, Orlik J, Kühnel F, Hegermann J, Manns MP, Vogel A. Activityof the mTOR inhibitor RAD001, the dual mTOR and PI3-kinase inhibitorBEZ235 and the PI3-kinase inhibitor BKM120 in hepatocellular carcinoma.Liver Int. 2013 May;33(5):780-93. doi: 10.1111/liv.12126. Epub 2013 Mar15. PubMed PMID: 23489999.
10: Amrein L, Shawi M, Grenier J, Aloyz R, Panasci L. Thephosphatidylinositol-3 kinase I inhibitor BKM120 induces cell death inB-chronic lymphocytic leukemia cells in vitro. Int J Cancer. 2013Jul;133(1):247-52. doi: 10.1002/ijc.27989. Epub 2013 Jan 15. PubMedPMID: 23238639; PubMed Central PMCID: PMC3847963.
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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