2. Cell Cycle/DNA Damage Epigenetics Apoptosis
  3. HDAC Apoptosis Caspase
  4. HDAC1-IN-13

HDAC1-IN-13 is an orally active HDAC1 inhibitor with IC50 values of 91, 185, 170, and 280 nM against HDAC1, HDAC2, HDAC3, and HDAC10, respectively, and shows no activity against HDAC4, HDAC5, HDAC6, HDAC7, and HDAC9. HDAC1-IN-13 induces extrinsic apoptosis by activating the caspase-8 pathway and triggers G0/G1 cell cycle arrest. HDAC1-IN-13 can be used for the research of leukemia.

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

HDAC1-IN-13

HDAC1-IN-13 Chemical Structure

CAS No. : 3053289-22-5

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HDAC1-IN-13 Related Antibodies

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HDAC HDAC1 HDAC2 HDAC3 HDAC4 HDAC5 HDAC6 HDAC7 HDAC8 HDAC9 HDAC10 HDAC11 HD1 HD2

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Caspase 1 Caspase 2 Caspase 3 Caspase 4 Caspase 5 Caspase 6 Caspase 7 Caspase 8 Caspase 9 Caspase 10 Caspase 12 Caspase Caspase 11 Caspase-13

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Description

HDAC1-IN-13 is an orally active HDAC1 inhibitor with IC50 values of 91, 185, 170, and 280 nM against HDAC1, HDAC2, HDAC3, and HDAC10, respectively, and shows no activity against HDAC4, HDAC5, HDAC6, HDAC7, and HDAC9. HDAC1-IN-13 induces extrinsic apoptosis by activating the caspase-8 pathway and triggers G0/G1 cell cycle arrest. HDAC1-IN-13 can be used for the research of leukemia[1].

IC50 & Target[1]

HDAC1

91 nM (IC50)

HDAC2

181 nM (IC50)

HDAC3

170 nM (IC50)

HDAC10

280 nM (IC50)

Caspase-8

 

In Vitro

HDAC1-IN-13 (Compound 6B) potently inhibits HDAC1 (IC50 = 91 nM), HDAC2 (IC50 = 185 nM), HDAC3 (IC50 = 170 nM), and HDAC10 (IC50 = 280 nM) enzymes, with no activity against HDAC4, HDAC5, HDAC7, HDAC8, or HDAC9[1].
HDAC1-IN-13 (Compound 6B) (72 h) potently inhibits the proliferation of HL-60 (IC50 = 0.31 μM), CCRF-CEM (IC50 = 0.36 μM), and HepG2 (IC50 = 1.01 μM) cancer cells in vitro[1].
HDAC1-IN-13 (Compound 6B) (72 h) has low cytotoxicity to LO2 normal human hepatocytes (IC50 = 5.67 μM) and a high selectivity index of 18.3 relative to HL-60 cancer cells[1].
HDAC1-IN-13 (Compound 6B) (0.1-2.5 μM; 48 h) concentration-dependently increases histone H3 acetylation, downregulates Rb/p-Rb and caspase-8 precursor, and modulates BAX, BAK, and BCL-2 expression in HL-60 cells after 48 h of treatment[1].
HDAC1-IN-13 (Compound 6B) (0-2.5 μM; 48 h) concentration-dependently induces apoptosis in HL-60 cells, with a 46.1% apoptosis rate following 48 h treatment with 2.5 μM[1].
HDAC1-IN-13 (Compound 6B) (0-2.5 μM; 48 h) concentration-dependently induces G0/G1 phase cell cycle arrest in HL-60 cells, with 76.5% of cells arrested in G0/G1 following 48 h treatment with 2.5 μM[1].

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

HDAC1-IN-13 Related Antibodies

Western Blot Analysis[1]

Cell Line: HL-60 promyelocytic leukemia cells
Concentration: 0.1 μM, 0.5 μM, 2.5 μM
Incubation Time: 48 h
Result: Induced a concentration-dependent increase in acetylated histone H3 (Ac-H3) levels, while total histone H3 levels remained unchanged.
Downregulated expression of Rb, phosphorylated Rb (p-Rb), and caspase-8 precursor in a concentration-dependent manner.
Downregulated BAX, BAK, and BCL-2 expression.

Apoptosis Analysis[1]

Cell Line: HL-60 promyelocytic leukemia cells
Concentration: 0 μM, 0.1 μM, 0.5 μM, 2.5 μM
Incubation Time: 48 h
Result: Induced apoptosis in a concentration-dependent manner, with apoptosis rates of 13.87% (0 μM), 25.6% (0.1 μM), 27.6% (0.5 μM), and 46.1% (2.5 μM).
Reached a late apoptotic cell proportion of 22.7% at the highest concentration.

Cell Cycle Analysis[1]

Cell Line: HL-60 promyelocytic leukemia cells
Concentration: 0 μM, 0.1 μM, 0.5 μM, 2.5 μM
Incubation Time: 48 h
Result: Induced G0/G1 phase cell cycle arrest in a concentration-dependent manner, with the proportion of cells in G0/G1 phase increasing from 56.4% (0 μM) to 76.5% (2.5 μM).
Parmacokinetics
Species Dose Route T1/2 Tmax Cmax AUC AUC0-∞ MRT Vd CL
Rat[1] 14 mg/kg i.p. 10.88 h 0.67 h 3085.04 μg/L 9195.38 μg/L·h 9455.28 μg/L·h 6.67 h 23.25 L/kg 1.48 L/h/kg
Rat[1] 14 mg/kg i.g. 5.01 h 1.50 h 511.88 μg/L 4332.53 μg/L·h 4350.86 μg/L·h 6.05 h 23.25 L/kg 3.22 L/h/kg
In Vivo

HDAC1-IN-13 (Compound 6B) (15-30 mg/kg; p.o.; once daily; 18 days) exhibits significant in vivo anti-leukemic activity in mouse models after oral administration, with no obvious toxicity[1].
HDAC1-IN-13 (20 mg/kg; i.p.; once daily; for 7 consecutive days) exhibits potent in vivo anti-leukemia activity with no obvious toxicity in mouse models following intraperitoneal administration[1].

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

Animal Model: BALB/c nude (male, 6-8 weeks old, 18-22 g, subcutaneous xenograft model)[1]
Dosage: 15 mg/kg; 30 mg/kg
Administration: i.g.; daily; 18 days
Result: Achieved a tumor growth inhibition (TGI) rate of 20.72% at 30 mg/kg.
Showed no obvious pathological changes in heart, liver, spleen, lung, or kidney tissue.
Maintained stable mouse body weights throughout the study.
Animal Model: BALB/c nude (male, 6-8 weeks old, 18-22 g, subcutaneous xenograft model)[1]
Dosage: 20 mg/kg
Administration: i.p.; daily; 7 days
Result: Reduced tumor volume by 58.4% after 7 days.
Showed no changes in mouse body weight during the study, indicating low in vivo toxicity.
Molecular Weight

368.43

Formula

C23H20N4O
CAS No.
SMILES

O=C(NC1=CC=CC=C1N)C(C=C2)=CC=C2CNC3=CC=NC4=CC=CC=C43
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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HDAC1-IN-13 Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

HDAC1-IN-133053289-22-5HDACApoptosisCaspaseHistone deacetylasesHL-60HDAC1histone H3HDAC3G0/G1 phaseHDAC2HepG2HDAC10CCRF-CEMcaspase-8 pathwayInhibitorinhibitorinhibit

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