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产品名称 AVL 292 - CC 292
产品货号 Axon 2226 CAS [1202757-89-8] MF C22H22FN5O3MW 423.44 Purity: 98% Soluble in DMSO Description A potent, selective, orally bioavailable, covalent Bruton's tyrosine kinase (Btk) inhibitor with potential antineoplastic activity (IC50 value 1400 selective over a number of Src family kinases and B cell signaling components in full length recombinant Btk protein assay). More specific for BTK than PCI 32765 (Ibrutinib, Axon 1858) is, and with a shorter half-life.AVL 292 reduces migration of CLL cells towards CXCL12 and CXCL13, and reduces viability as well as markers of BCR activation, such as CCL3 and CCL4 chemokine production, in primary CLL cells cultured with Nurse-like Cells (NLC). References Certificates Categories Extra info E.K. Evans et al. Inhibition of Btk with CC-292 provides early pharmacodynamic assessment of activity in mice and humans. J. Pharmacol. Exp. Ther. 2013, 346, 219-228.    H. Eda et al. A novel Bruton′s tyrosine kinase inhibitor CC-292 in combination with the proteasome inhibitor carfilzomib impacts multiple myeloma  bone microenviroment with resultant anti-myeloma activity. Blood 2013, 122, 682. Certificate of Analysis Material Safety Data Sheet Cell Signaling & Oncology Immunology BTK EC 2.7.10.2 Potent, selective, covalent BTK inhibitor Chemical name N-(3-(5-Fluoro-2-(4-(2-methoxyethoxy)phenylamino)pyrimidin-4-ylamino)phenyl)acrylamide Parent CAS No. [1202757-89-8] Order Size Unit Price Stock 5 mg €120.00 In Stock
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AVL 292 - CC 292

Based on 12 reference(s) in Google Scholar 9 10 12

Axon 2226

CAS [1202757-89-8]

MF C22H22FN5O3
MW 423.44

  • Purity: 98%
  • Soluble in DMSO

AVL 292

Description

A potent, selective, orally bioavailable, covalent Bruton's tyrosine kinase (Btk) inhibitor with potential antineoplastic activity (IC50 value 1400 selective over a number of Src family kinases and B cell signaling components in full length recombinant Btk protein assay). More specific for BTK than PCI 32765 (Ibrutinib, Axon 1858) is, and with a shorter half-life.
AVL 292 reduces migration of CLL cells towards CXCL12 and CXCL13, and reduces viability as well as markers of BCR activation, such as CCL3 and CCL4 chemokine production, in primary CLL cells cultured with Nurse-like Cells (NLC).
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