1. Apoptosis
  2. Apoptosis
  3. HXR9

HXR9 

Cat. No.: HY-P3245
Handling Instructions

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.

For research use only. We do not sell to patients.

Custom Peptide Synthesis

HXR9 Chemical Structure

HXR9 Chemical Structure

CAS No. : 917953-08-3

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Description

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 Vitro

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 IC50 of 20μM[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

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.
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].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

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.
Molecular Weight

2718.21

Formula

C₁₁₉H₁₉₃N₅₃O₂₀S

CAS No.
Sequence Shortening

WYPWMKKHHRRRRRRRRR

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

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Keywords:

HXR9HXR 9HXR-9ApoptosisbreastcancerB16 cellscompetitiveantagonistMLLInhibitorinhibitorinhibit

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