Lenalidomidefeatured
WARNING: This product is for research use only, not for human or veterinary use.
MedKoo CAT#:100500
CAS#:191732-72-6
Description:Lenalidomide, also known as CC-5013, is the thalidomide analog with potential antineoplastic activity. Lenalidomide inhibits TNF-alpha production, stimulates T cells, reduces serum levels of the cytokines vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF), and inhibits angiogenesis. This agent also promotes G1 cell cycle arrest and apoptosis of malignant cells. Lenalidomide is an approved drug.
Price and Availability
Lenalidomide, purity > 98%, is in stock. The same day shipping out after order is received.
Chemical Structure
Theoretical Analysis
MedKoo Cat#: 100500Name: LenalidomideCAS#: 191732-72-6Chemical Formula: C13H13N3O3Exact Mass: 259.09569Molecular Weight: 259.26Elemental Analysis:C, 60.22; H, 5.05; N, 16.21; O, 18.51
Synonym:CC5013; CC-5013; CC 5013; IMiD1; Lenalidomide; US brand name: Revlimid.
IUPAC/Chemical Name:3-(4-amino-1-oxoisoindolin-2-yl)piperidine-2,6-dione
InChi Key:GOTYRUGSSMKFNF-UHFFFAOYSA-N
InChi Code:InChI=1S/C13H13N3O3/c14-9-3-1-2-7-8(9)6-16(13(7)19)10-4-5-11(17)15-12(10)18/h1-3,10H,4-6,14H2,(H,15,17,18)
SMILES Code:O=C(C(N(CC1=C2C=CC=C1N)C2=O)CC3)NC3=O
Technical Data
Additional Information
Chemical structures:Chemical structures of Pomalidomide ; Thalidomide and Lenalidomide are very similar: Lenalidomide, initially known as CC-5013 and marketed as Revlimid by Celgene, is a derivative of thalidomide introduced in 2004. It was initially intended as a treatment for multiple myeloma, for which thalidomide is an accepted therapeutic modality, but has also shown efficacy in the class of hematological disorders known as myelodysplastic syndromes (MDS). Revlimid is also known as Revamid in the UK.The exact mechanism of the immunomodulatory drugs (i.e., thalidomide, CC-4047/Actimid and lenalidomide) is not known. Apart from interfering with the immune system, they are also thought to act on angiogenesis. Lenalidomide and bortezomib are considered therapeutic breakthroughs in myeloma, which generally carries a poor prognosis. Lenalidomide is an off-white to pale-yellow solid powder. It is soluble in organic solvent/water mixtures, and buffered aqueous solvents. Lenalidomide is more soluble in organic solvents and low pH solutions. Solubility was significantly lower in less acidic buffers, ranging from about 0.4 to 0.5 mg/ml. Lenalidomide has an asymmetric carbon atom and can exist as the optically active forms S(-) and R(+), and is produced as a racemic mixture with a net optical rotation of zero. REVLIMID® (lenalidomide) is available in 5 mg, 10 mg, 15 mg and 25 mg capsules for oral administration. Each capsule contains lenalidomide as the active ingredient and the following inactive ingredients: lactose anhydrous, microcrystalline cellulose, croscarmellose sodium, and magnesium stearate. The 5 mg and 25 mg capsule shell contains gelatin, titanium dioxide and black ink. The 10 mg capsule shell contains gelatin, FD&C blue #2, yellow iron oxide, titanium dioxide and black ink. The 15 mg capsule shell contains gelatin, FD&C blue #2, titanium dioxide and black ink. The mechanism of action of lenalidomide remains to be fully characterized. Lenalidomide possesses antineoplastic, immunomodulatory and antiangiogenic properties. Lenalidomide inhibited the secretion of pro-inflammatory cytokines and increased the secretion of antiinflammatory cytokines from peripheral blood mononuclear cells. Lenalidomide inhibited cell proliferation with varying effectiveness (IC50s) in some but not all cell lines. Of cell lines tested, lenalidomide was effective in inhibiting growth of Namalwa cells (a human B cell lymphoma cell line with a deletion of one chromosome 5) but was much less effective in inhibiting growth of KG-1 cells (human myeloblastic cell line, also with a deletion of one chromosome 5) and other cell lines without chromosome 5 deletions. Lenalidomide inhibited the growth of multiple myeloma cells from patients, as well as MM.1S cells (a human multiple myeloma cell line), by inducing cell cycle arrest and apoptosis. Lenalidomide inhibited the expression of cyclooxygenase-2 (COX-2) but not COX-1 in vitro.
References
1: Nojkov B, Signori C, Konda A, Fontana RJ.Lenalidomide-associated hepatotoxicity--a case report and literaturereview. Anticancer Res. 2012 Sep;32(9):4117-9. Review. PubMed PMID:22993370.
2: Kimby E. Biological therapy doublets: pairing rituximab withinterferon, lenalidomide, and other biological agents in patients withfollicular lymphoma. Curr Hematol Malig Rep. 2012 Sep;7(3):221-7. doi:10.1007/s11899-012-0133-2. Review. PubMed PMID: 22895878.
3: Bringhen S, Gay F, Pautasso C, Cerrato C, Boccadoro M, Palumbo A.Evaluation of the pharmacokinetics, preclinical, and clinical efficacyof lenalidomide for the treatment of multiple myeloma. Expert Opin DrugMetab Toxicol. 2012 Sep;8(9):1209-22. doi: 10.1517/17425255.2012.712685.Epub 2012 Aug 3. Review. PubMed PMID: 22862790.
4: Brower V. Lenalidomide maintenance for multiple myeloma. Lancet Oncol.2012 Jun;13(6):e238. Review. PubMed PMID: 22833889.
5: Dawar R, Hernandez-Ilizaliturri F. The emerging role of lenalidomidein the management of mantle cell lymphoma (MCL). Best Pract Res ClinHaematol. 2012 Jun;25(2):185-90. doi: 10.1016/j.beha.2012.04.005. Epub2012 May 18. Review. PubMed PMID: 22687454.
6: Dimopoulos MA, Terpos E, Goldschmidt H, Alegre A, Mark T, NiesvizkyR. Treatment with lenalidomide and dexamethasone in patients withmultiple myeloma and renal impairment. Cancer Treat Rev. 2012Dec;38(8):1012-9. doi: 10.1016/j.ctrv.2012.02.009. Epub 2012 May 18.Review. PubMed PMID: 22609463.
7: Segler A, Tsimberidou AM. Lenalidomide in solid tumors. CancerChemother Pharmacol. 2012 Jun;69(6):1393-406. doi:10.1007/s00280-012-1874-2. Epub 2012 May 15. Review. PubMed PMID:22584909.
8: Kunimasa K, Ueda T, Arita M, Maeda T, Hotta M, Ishida T. Drug-inducedinterstitial pneumonitis due to low-dose lenalidomide. Intern Med.2012;51(9):1081-5. Epub 2012 Apr 29. Review. PubMed PMID: 22576392.
9: Komrokji RS, List AF. Lenalidomide for treatment of myelodysplasticsyndromes. Curr Pharm Des. 2012;18(22):3198-203. Review. PubMed PMID:22571699.
10: Barosi G, Merlini G, Billio A, Boccadoro M, Corradini P, MarchettiM, Massaia M, Tosi P, Palumbo A, Cavo M, Tura S. SIE, SIES, GITMOevidence-based guidelines on novel agents (thalidomide, bortezomib, andlenalidomide) in the treatment of multiple myeloma. Ann Hematol. 2012Jun;91(6):875-88. doi: 10.1007/s00277-012-1445-y. Epub 2012 Apr 4.Review. PubMed PMID: 22476884.
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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