1. Metabolic Enzyme/Protease Apoptosis
  2. Proteasome Apoptosis
  3. DQ-9

DQ-9 is a selective immunoproteasome β5i inhibitor (IC50=0.0019 μM). DQ-9 generates additional inhibitory substances via iron-mediated intracellular activation, and induces oxidative stress, carbon-centered free radicals and macromolecular damage through its artemisinin domain. DQ-9 induces apoptosis in leukemia and multiple myeloma cells. DQ-9 exhibits selective cytotoxicity against leukemia and multiple myeloma cells by elevating the labile iron pool. DQ-9 can be used in the research of hematological malignancies (leukemia, multiple myeloma, mantle cell lymphoma, acute myeloid leukemia).

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DQ-9

DQ-9 Chemical Structure

CAS No. : 2803611-81-4

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Description

DQ-9 is a selective immunoproteasome β5i inhibitor (IC50=0.0019 μM). DQ-9 generates additional inhibitory substances via iron-mediated intracellular activation, and induces oxidative stress, carbon-centered free radicals and macromolecular damage through its artemisinin domain. DQ-9 induces apoptosis in leukemia and multiple myeloma cells. DQ-9 exhibits selective cytotoxicity against leukemia and multiple myeloma cells by elevating the labile iron pool. DQ-9 can be used in the research of hematological malignancies (leukemia, multiple myeloma, mantle cell lymphoma, acute myeloid leukemia)[1].

In Vitro

DQ-9 (0.2-1.0 μM; 6 h) induces the accumulation of polyubiquitinated proteins in MM.1S multiple myeloma cells[1].
DQ-9 (0.1-0.5 μM; 16 h) induces G2/M phase arrest in MM.1S multiple myeloma cells, significantly upregulates p21, and exerts a stronger effect than DQ-10 (HY-18078)[1].
DQ-9 (72 h) selectively inhibits the growth of human leukemia cell lines in the NCI-60 cell panel, and exhibits stronger potency than DQ-10 in most leukemia cell lines[1].
DQ-9 (0.1-1.0 μM; 6-16 h) potently induces apoptosis in MM.1S multiple myeloma cells and HL-60 acute myeloid leukemia cells, and its pro-apoptotic activity is stronger than that of DQ-10[1].

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

Western Blot Analysis[1]

Cell Line: MM.1S multiple myeloma cells, HL-60 acute myeloid leukemia cells
Concentration: 0.1-1.0 μM (16 h for apoptotic markers); 0.2-1.0 μM (6 h for polyubiquitination)
Incubation Time: 6 h (polyubiquitination); 16 h (apoptotic markers)
Result: Robust cleavage of PARP and Caspase-3 was detected in MM.1S cells treated with 0.5 μM DQ-9 for 6 h, and with 0.2 μM DQ-9 for 16 h.
In HL-60 cells, cleaved PARP and Caspase-3 were detected at 0.2 μM DQ-9 following 16 h of treatment.
DQ-10 required ≥2.5 μM to induce comparable apoptotic signaling.

Cell Cycle Analysis[1]

Cell Line: MM.1S multiple myeloma cells
Concentration: 0.1-0.5 μM
Incubation Time: 16 h
Result: DQ-9 induced significant G2/M phase arrest in MM.1S cells, with more pronounced arrest than DQ-10 at matched concentrations (e.g., 27.1% G2/M at 0.2 μM DQ-9 vs 19.8% at 0.2 μM DQ-10).
Treatment also induced robust accumulation of the CDK inhibitor p21, with strong upregulation observed at 0.1 μM DQ-9.
Molecular Weight

595.53

Formula

C33H46BNO8

CAS No.
SMILES

O=C(N[C@H](B1OC(C)(C)C(C)(C)O1)CC2=COC3=CC=CC=C23)C[C@@H]4[C@H](C)[C@]5([H])CC[C@@H](C)[C@]6([H])CC[C@@](O7)(C)OO[C@]65[C@]7([H])O4

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DQ-9
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HY-183683
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