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Submit ReviewI-CBP 112 is a CBP/p300 bromodomain inhibitor (IC50 values are 0.142-0.17 and 0.625 μM for CBP and p300 respectively). Selective for CBP and p300 over ATAD2, BAZ2B, BRD2(2), BRD4(1), PB1(5), PCAF, PHIP(2) and TIF1α bromodomains in a BLI assay. Accelerates FRAP recovery in cells at a concentration of 1 μM.
This probe is supplied in conjunction with the Structural Genomics Consortium. For further characterization details, please visit the I-CBP 112 probe summary on the SGC website.
Chemicalprobes.org is a portal that offers independent guidance on the selection and/or application of small molecules for research. The use of I-CBP 112 is reviewed on the chemical probes website.
分子量 | 468.59 |
公式 | C27H36N2O5 |
储存 | Desiccate at RT |
纯度 | ≥98% (HPLC) |
CAS Number | 1640282-31-0 |
PubChem ID | 90488984 |
InChI Key | YKNAKDFZAWQEEO-IBGZPJMESA-N |
Smiles | COC(C(OC)=C1)=CC=C1C2=CC(OC[C@H]3CCCN(C)C3)=C(OCCN(C(CC)=O)C4)C4=C2 |
上方提供的技术数据仅供参考。批次相关数据请参见分析证书。
Tocris products are intended for laboratory research use only, unless stated otherwise.
参考文献是支持产品生物活性的出版物。
Gallenkamp et al (2014) Bromodomains and their pharmacological inhibitors. ChemMedChem 9 438 PMID: 24497428
关键词: I-CBP 112, I-CBP 112 supplier, I-CBP112, CREBBP, EP300, bromodomains, selective, inhibitors, inhibits, chemical, probes, SGC, epigenetics, structural, genomics, consortium, Bromodomains, Histone, Acetyltransferases, 4891, Tocris Bioscience
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Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
*请注意,Tocris 仅会向正规科研企业/机构地址发送文献。
Written by Susanne Müller-Knapp and Peter J. Brown, this review gives an overview of the development of chemical probes for epigenetic targets, as well as the impact of these tool compounds being made available to the scientific community. In addition, their biological effects are also discussed. Epigenetic compounds available from Tocris are listed.
This poster summarizes the main epigenetic targets in cancer. The dysregulation of epigenetic modifications has been shown to result in oncogenesis and cancer progression. Unlike genetic mutations, epigenetic alterations are considered to be reversible and thus make promising therapeutic targets.
Rheumatoid arthritis (RA) is a chronic destructive inflammatory autoimmune disease that results from a breakdown in immune tolerance, for reasons that are as yet unknown. This poster summarizes the pathology of RA and the inflammatory processes involved, as well as describing some of the epigenetic modifications associated with the disease and the potential for targeting these changes in the discovery of new treatments.