HDAC11-IN-5
HDAC11-IN-5 is a selective, potent and orally active HDAC11 inhibitor with an IC50 of 0.021 μM. HDAC11-IN-5 increases fatty acylation levels of substrate SHMT2 in AML cells. HDAC11-IN-5 induces apoptosis, G1 phase cell cycle arrest, ferroptosis, ROS production and terminal myeloid differentiation in AML cells. HDAC11-IN-5 demonstrates anti-tumor potency in an MLL-AF9-induced mouse AML model. HDAC11-IN-5 can be used for the research of cancer, such as acute myeloid leukemia.
For research use only. We do not sell to patients.
- Formula: C24H25Cl2F3N4O2
- Molecular Weight:529.38
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
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HDAC11 0.021 μM (IC50) |
SHMT2 |
HDAC11-IN-5 (Compound 25) potently inhibits purified HDAC11 protein with an IC50 of 0.021 ± 0.005 μM, and shows no significant inhibition of HDAC1, HDAC6, HDAC7, or HDAC8 at concentrations up to 10 μM[1].
HDAC11-IN-5 (96 h) potently inhibits proliferation of U937, OCI-AML2, THP-1, and MOLM13 AML cell lines with IC50 values of 6.3 μM, 5.7 μM, 5.4 μM, and 6.7 μM, respectively[1].
HDAC11-IN-5 (10-20 μM; 6 h) selectively inhibits intracellular HDAC11 in U937 AML cells, as shown by increased SHMT2 fatty acylation at 10 μM for 6 h and no significant changes in histone H3 or α-tubulin acetylation at 20 μM for 6 h[1].
HDAC11-IN-5 (8 μM; 48 h) strongly induces apoptosis in U937 and OCI-AML2 AML cells[1].
HDAC11-IN-5 (8 μM; 48 h) induces G1-phase cell cycle arrest in U937 AML cells[1].
HDAC11-IN-5 (8 μM; 48 h) promotes myeloid differentiation of U937 AML cells, as shown by increased CD14 and CD11b expression[1].
HDAC11-IN-5 (8 μM; 48 h) induces ferroptosis in U937 AML cells, as shown by increased lipid peroxidation, cellular ROS, and intracellular Fe2+ levels[1].
HDAC11-IN-5 (5-20 μM; 96 h) exhibits strong synergistic antiproliferative activity with ivosidenib in U937, OCI-AML2, and MLL-AF9 mouse AML cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:U937 AML cells
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Concentration:10 μM (SHMT2 fatty acylation analysis); 20 μM (histone H3 and α-tubulin acetylation analysis)
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Incubation Time:6 h
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Result:Significantly increased fatty acylation levels of SHMT2 (a specific HDAC11 substrate) at 10 μM for 6 h.
Had negligible effects on acetylation levels of histone H3 (a class I HDAC substrate) and α-tubulin (an HDAC6 substrate) at 20 μM for 6 h.
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Cell Line:U937, OCI-AML2 AML cell lines
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Concentration:8 μM
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Incubation Time:48 h
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Result:Significantly induced apoptosis in both U937 and OCI-AML2 cells.
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Cell Line:U937 AML cells
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Concentration:8 μM
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Incubation Time:48 h
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Result:Significantly increased expression of the myeloid differentiation markers CD14 and CD11b in U937 cells, with a stronger effect than FT895.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6 (6-week-old female, 20-22 g, tail vein injection of 1×105 MLL-AF9-GFP+ leukemic cells)[1]
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Dosage:50 mg/kg
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Administration:I.g.,; once daily; 14 days
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Result:Reduced the percentage of GFP+ leukemic cells in peripheral blood.
Significantly extended the survival of AML mice compared to vehicle control.
Reduced the percentage of GFP+ leukemic cells when combined with ivosidenib, with greater survival extension than either agent alone.
Caused no significant body weight loss prior to the moribund stage.
Chemical Information
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Molecular Weight 529.38
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Formula C24H25Cl2F3N4O2
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SMILES
O=C(C1=CC=CC2=C1C=C(C#CC3=CC=CC(C(F)(F)F)=C3)N2CCN4CCNCC4)NO.Cl.Cl
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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