HXR9 hydrochloride |
| Catalog No.GC64485 |
HXR9 hydrochloride is a cell-permeable peptide and a competitive antagonist of HOX/PBX interaction. HXR9 hydrochloride antagonizes the interaction between HOX and a second transcrip-tion factor (PBX), which binds to HOX proteins in paralogue groups1 to 8. HXR9 hydrochloride selectively decreases cell proliferation and promotes apoptosis in cells with a high level of expression of the HOXA/PBX3 genes, such as MLL-rearranged leukemic cells.
Products are for research use only. Not for human use. We do not sell to patients.
Sample solution is provided at 25 µL, 10mM.
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HXR9 hydrochloride is a cell-permeable peptide and a competitive antagonist of HOX/PBX interaction. HXR9 hydrochloride antagonizes the interaction between HOX and a second transcrip-tion factor (PBX), which binds to HOX proteins in paralogue groups1 to 8. HXR9 hydrochloride selectively decreases cell proliferation and promotes apoptosis in cells with a high level of expression of the HOXA/PBX3 genes, such as MLL-rearranged leukemic cells[1][2][3].
HXR9 hydrochloride (60μM; 4 hours) blocks the interaction between PBX and HOX[1].HXR9 hydrochloride (60μM; 2 hours) triggers apoptosis in B16 and primary melanoma cells[1].HXR9 hydrochloride (60μM; 2 hours) causes specific transcriptional changes[1].HXR9 hydrochloride (B16 cells) shows antiproliferative activity with an IC50 of 20μM[1].
HXR9 hydrochloride (10 mg/kg; i.v. via the tail vein; twice weekly) blocks tumor growth[1].HXR9 hydrochloride (Initial dose of 100 mg/kg (subsequent dosing of 10 mg/kg twice weekly);Intraperitoneal; twice weekly for 18 days) blocks A549 tumour growth in vivo[3].
[1]. Morgan R, et al. Antagonism of HOX/PBX dimer formation blocks the in vivo proliferation of melanoma. Cancer Res. 2007;67(12):5806-5813.
[2]. Li Z, et al. PBX3 is an important cofactor of HOXA9 in leukemogenesis. Blood. 2013;121(8):1422-1431.
[3]. Plowright L, et al. HOX transcription factors are potential therapeutic targets in non-small-cell lung cancer (targeting HOX genes in lung cancer). Br J Cancer. 2009;100(3):470-475.
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