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In vitro transcription of capped mRNA with modified nucleotides and Poly(A) tail
TSA (Tyramide Signal Amplification), used for signal amplification of ISH, IHC and IC etc.
Separation of phosphorylated and non-phosphorylated proteins without phospho-specific antibody
A convenient and sensitive way for cell proliferation assay and cytotoxicity assay
Protect the integrity of proteins from multiple proteases and phosphatases for different applications.
Refametinib is a selective and orally available allosteric inhibitor of MEK 1 and MEK 2 with IC50 values of 19nM and 47nM, respectively [1].
Refametinib is a non–ATP-competitive inhibitor of MEK1/2. It inhibits MEK activity in an in vitro assay with IC50 values of 19nM and 47nM for MEK1 and MEK2, respectively. X-ray shows refametinib binds to an allosteric site of MEK. It does not affect ATP binding but precludes binding to the substrate ERK, thus preventing ERK phosphorylation. Refametinib inhibits MEK with EC50 values ranging from 2.5nM to 15.8nM in a variety of human cancer cells including A375, Colo205, HT-29 and MDA-MB-231. In addition, in the cancer cell lines harboring V600E BRAF mutant, refametinib suppresses cell growth with GI50 values ranging from 67nM to 89nM. Furthermore, in the human melanoma A375 tumor xenograft model, treatment of refametinib causes obvious tumor growth delay and regression. Refametinib also shows tumor growth inhibition in the xenograft model of human Colo205 tumor [1].
References:[1] Iverson C, Larson G, Lai C, et al. RDEA119/BAY 869766: a potent, selective, allosteric inhibitor of MEK1/2 for the treatment of cancer. Cancer research, 2009, 69(17): 6839-6847.