HXR9 is a cell-permeable peptide that acts as a competitive antagonist of the HOX/PBX interaction. It effectively inhibits the binding between HOX proteins and the transcription factor PBX, specifically in paralogue groups 1 to 8. HXR9 selectively impairs cell proliferation and induces apoptosis in cells with a high expression of the HOXA/PBX3 genes, for instance, MLL-rearranged leukemic cells.

HXR9 (60μM; 4 hours) blocks the interaction between PBX and HOX[1]. HXR9 (60μM; 2 hours) triggers apoptosis in B16 and primary melanoma cells[1]. HXR9 (60μM; 2 hours) causes specific transcriptional changes[1]. HXR9 (B16 cells) shows antiproliferative activity with an IC 50 of 20μM[1]. Western Blot Analysis Cell Line: murine B16melanoma cells Concentration: 60 μM Incubation Time: 4 hours Result: Blocked the binding of HOXD9 to PBX. Apoptosis Analysis Cell Line: B16 cells Concentration: 60 μM Incubation Time: 2 hours Result: A significant proportion of cells were in late phases of apoptosis. RT-PCR Cell Line: B16F10cells Concentration: 60 μM Incubation Time: 2 hours Result: Fos , Jun , Dusp1 , and Atf1 ，were allsignificantly up-regulate.

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.