For research use only. Not for therapeutic Use.
XL019（Cat No.:I005630）is a selective inhibitor of the protein kinase PAK4, which is involved in various cellular processes, including cell growth, migration, and survival. By targeting PAK4, XL019 disrupts oncogenic signaling pathways, making it a promising candidate for cancer research, particularly in tumors exhibiting elevated PAK4 activity. Preclinical studies have shown that XL019 can inhibit tumor growth and reduce metastasis in certain cancer models. Its unique mechanism of action provides valuable insights into the development of targeted therapies aimed at cancers that rely on PAK4 for progression and survival.
| Catalog Number | I005630 |
| CAS Number | 945755-56-6 |
| Synonyms | (2S)-N-[4-[2-(4-morpholin-4-ylanilino)pyrimidin-4-yl]phenyl]pyrrolidine-2-carboxamide |
| Molecular Formula | C₂₅H₂₈N₆O₂ |
| Purity | ≥95% |
| Target | JAK |
| Solubility | in DMSO > 10 mM |
| Storage | Store at -20°C |
| IC50 | 2.2 nM (JAK2); 214.2 nM (JAK3) [1] |
| IUPAC Name | (2S)-N-[4-[2-(4-morpholin-4-ylanilino)pyrimidin-4-yl]phenyl]pyrrolidine-2-carboxamide |
| InChI | InChI=1S/C25H28N6O2/c32-24(23-2-1-12-26-23)28-19-5-3-18(4-6-19)22-11-13-27-25(30-22)29-20-7-9-21(10-8-20)31-14-16-33-17-15-31/h3-11,13,23,26H,1-2,12,14-17H2,(H,28,32)(H,27,29,30)/t23-/m0/s1 |
| InChIKey | ISOCDPQFIXDIMS-QHCPKHFHSA-N |
| SMILES | C1C[C@H](NC1)C(=O)NC2=CC=C(C=C2)C3=NC(=NC=C3)NC4=CC=C(C=C4)N5CCOCC5 |
| Reference | 1:Leuk Res. 2014 Mar;38(3):316-22. doi: 10.1016/j.leukres.2013.12.006. Epub 2013 Dec 11. Phase I evaluation of XL019, an oral, potent, and selective JAK2 inhibitor.Verstovsek S,Tam CS,Wadleigh M,Sokol L,Smith CC,Bui LA,Song C,Clary DO,Olszynski P,Cortes J,Kantarjian H,Shah NP, PMID: 24374145 PMCID: PMC4414320 DOI: 10.1016/j.leukres.2013.12.006 </br><span>Abstract:</span> This phase I study evaluated selective JAK2 inhibitor XL019 in 30 patients with myelofibrosis. The initial dose cohorts were 100, 200, and 300 mg orally on days 1-21 of a 28-day cycle. Central and/or peripheral neurotoxicity developed in all patients. Subsequently, patients were treated on lower doses; neurotoxicity was again observed, leading to study termination. Peripheral neuropathy resolved in 50%, and central neurotoxicity in all patients within months after therapy cessation. Myelosuppression was minimal. The terminal half-life of XL019 was approximately 21 h, with steady state reached by Day 8. International Working Group defined responses were seen in three (10%) patients.Copyright © 2013 Elsevier Ltd. All rights reserved. |
