| Identification | Back Directory | [Name]
L-Arginine, L-tryptophyl-L-tyrosyl-L-prolyl-L-tryptophyl-L-methionyl-L-lysyl-L-lysyl-L-histidyl-L-histidyl-L-arginyl-L-arginyl-L-arginyl-L-arginyl-L-arginyl-L-arginyl-L-arginyl-L-arginyl- | [CAS]
917953-08-3 | [Synonyms]
HXR9
L-Arginine, L-tryptophyl-L-tyrosyl-L-prolyl-L-tryptophyl-L-methionyl-L-lysyl-L-lysyl-L-histidyl-L-histidyl-L-arginyl-L-arginyl-L-arginyl-L-arginyl-L-arginyl-L-arginyl-L-arginyl-L-arginyl- | [Molecular Formula]
C119H193N53O20S | [MOL File]
917953-08-3.mol | [Molecular Weight]
2718.21 |
| Hazard Information | Back Directory | [Uses]
HXR9 is a cell-permeable peptide and a competitive antagonist of HOX/PBX interaction. HXR9 antagonizes the interaction between HOX and a second transcrip-tion factor (PBX), which binds to HOX proteins in paralogue groups1 to 8. HXR9 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]. | [in vivo]
HXR9 (10 mg/kg; i.v. via the tail vein; twice weekly) blocks tumor growth[1].
HXR9 (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]. | Animal Model: | C57black/6 mice (bearing B16 cells) | | Dosage: | 10 mg/kg | | Administration: | I.v. via the tail vein; twice weekly (~30 days) | | Result: | Tumors showed a significant degree of growth retardation. |
| Animal Model: | Athymic nude mice (bearing A549 cells) | | Dosage: | Initial dose of 100?mg/kg (subsequent dosing of 10?mg/kg twice weekly)
| | Administration: | Intraperitoneal; twice weekly for 18 days | | Result: | The tumours of HXR9-treated mice were considerably smaller than those of the control groups. |
| [References]
[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. DOI:10.1158/0008-5472.CAN-06-4231
[2] Li Z, et al. PBX3 is an important cofactor of HOXA9 in leukemogenesis. Blood. 2013;121(8):1422-1431. DOI:10.1182/blood-2012-07-442004
[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. DOI:10.1038/sj.bjc.6604857 |
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