Apremilastfeatured
WARNING: This product is for research use only, not for human or veterinary use.
MedKoo CAT#:205894
CAS#:608141-41-9
Description:Apremilast, also known as CC-10004, is a thalidomide analog and is an orally available small molecule inhibitor of phosphodiesterase 4 (PDE4). Apremilast specifically inhibits PDE4 and inhibits spontaneous production of TNF-alpha from human rheumatoid synovial cells. It has anti-inflammatory activity. Apremilast was approved by the USFDA in March 2014 for treatment of adults with active psoriatic arthritis. It is also being tested for its efficacy in treating other chronic inflammatory diseases such as ankylosing spondylitis, Behcet's disease, and rheumatoid arthritis.
Price and Availability
Apremilast, purity > 98%, is in stock. The same day shipping out after order is received.
Chemical Structure
Theoretical Analysis
MedKoo Cat#: 205894Name: ApremilastCAS#: 608141-41-9Chemical Formula: C22H24N2O7SExact Mass: 460.13042Molecular Weight: 460.5Elemental Analysis: C, 57.38; H, 5.25; N, 6.08; O, 24.32; S, 6.96
Synonym:CC10004; CC-10004; CC 10004; Apremilast; brand name: Otezla.
IUPAC/Chemical Name:(S)-N-(2-(1-(3-ethoxy-4-methoxyphenyl)-2-(methylsulfonyl)ethyl)-1,3-dioxoisoindolin-4-yl)acetamide
InChi Key:IMOZEMNVLZVGJZ-QGZVFWFLSA-N
InChi Code:InChI=1S/C22H24N2O7S/c1-5-31-19-11-14(9-10-18(19)30-3)17(12-32(4,28)29)24-21(26)15-7-6-8-16(23-13(2)25)20(15)22(24)27/h6-11,17H,5,12H2,1-4H3,(H,23,25)/t17-/m1/s1
SMILES Code:CC(NC1=CC=CC(C(N2[C@@H](C3=CC=C(OC)C(OCC)=C3)CS(=O)(C)=O)=O)=C1C2=O)=O
Technical Data
References
1: Thompson BJ, Furniss M, Zhao W, Chakraborty B,Mackay-Wiggan J. An Oral Phosphodiesterase Inhibitor (Apremilast) forInflammatory Rosacea in Adults: A Pilot Study. JAMA Dermatol. 2014 Jul23. doi: 10.1001/jamadermatol.2013.10526. [Epub ahead of print] PubMedPMID: 25054629.
2: Liu Y, Zhou S, Wan Y, Wu A, Palmisano M. The impact ofco-administration of ketoconazole and rifampin on the pharmacokineticsof apremilast in healthy volunteers. Br J Clin Pharmacol. 2014 Jun 24.doi: 10.1111/bcp.12448. [Epub ahead of print] PubMed PMID: 24962564.
3: Schafer PH, Parton A, Capone L, Cedzik D, Brady H, Evans JF, Man HW,Muller GW, Stirling DI, Chopra R. Apremilast is a selective PDE4inhibitor with regulatory effects on innate immunity. Cell Signal. 2014Sep;26(9):2016-29. doi: 10.1016/j.cellsig.2014.05.014. Epub 2014 May 29.PubMed PMID: 24882690.
4: Apremilast (Otezla) for psoriatic arthritis. Med Lett Drugs Ther.2014 May 26;56(1443):41-2. PubMed PMID: 24869713.
5: FitzGerald O. Spondyloarthropathies: Apremilast: welcome advance intreatment of psoriatic arthritis. Nat Rev Rheumatol. 2014Jul;10(7):385-6. doi: 10.1038/nrrheum.2014.77. Epub 2014 May 20. PubMedPMID: 24846499.
6: Poole RM, Ballantyne AD. Apremilast: first global approval. Drugs.2014 May;74(7):825-37. doi: 10.1007/s40265-014-0218-4. PubMed PMID:24797159.
7: Varada S, Tintle SJ, Gottlieb AB. Apremilast for the treatment ofpsoriatic arthritis. Expert Rev Clin Pharmacol. 2014 May;7(3):239-50.doi: 10.1586/17512433.2014.904200. Epub 2014 Apr 4. PubMed PMID:24702658.
8: Kavanaugh A, Mease PJ, Gomez-Reino JJ, Adebajo AO, Wollenhaupt J,Gladman DD, Lespessailles E, Hall S, Hochfeld M, Hu C, Hough D, StevensRM, Schett G. Treatment of psoriatic arthritis in a phase 3 randomised,placebo-controlled trial with apremilast, an oral phosphodiesterase 4inhibitor. Ann Rheum Dis. 2014 Jun;73(6):1020-6. doi:10.1136/annrheumdis-2013-205056. Epub 2014 Mar 4. PubMed PMID: 24595547;PubMed Central PMCID: PMC4033106.
9: Gottlieb AB, Matheson RT, Menter A, Leonardi CL, Day RM, Hu C,Schafer PH, Krueger JG. Efficacy, tolerability, and pharmacodynamics ofapremilast in recalcitrant plaque psoriasis: a phase II open-labelstudy. J Drugs Dermatol. 2013 Aug;12(8):888-97. PubMed PMID: 23986162.
10: Schafer PH, Day RM. Novel systemic drugs for psoriasis: mechanism ofaction for apremilast, a specific inhibitor of PDE4. J Am Acad Dermatol.2013 Jun;68(6):1041-2. doi: 10.1016/j.jaad.2012.10.064. PubMed PMID:23680197.
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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