CDK9/HDAC1/HDAC3-IN-1

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CDK9/HDAC1/HDAC3-IN-1 is dual-functional inhibitor of CDK9 and HDAC. CDK9/HDAC1/HDAC3-IN-1 inhibits the protein activity of CDK9/HDAC/HDAC3 with IC₅₀s of 0.17  μM, 1.73  μM and 1.11 μM for CDK9, HDAC1, and HDAC3, respectively. CDK9/HDAC1/HDAC3-IN-1 inhibits cancer cells by inducing cell apoptosis and cell cycle arrest in the G2/M phase, as well as tumor growth in a murine TNBC MDA-MB-231 xenograft model. CDK9/HDAC1/HDAC3-IN-1 has a broad-spectrum anti-cancer activity, such as breast cancer, cervical cancer, and liver cancer.

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CDK9/HDAC1/HDAC3-IN-1 Chemical Structure

CAS No. : 2197029-81-3

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•Related Small Molecules:

•Related Proteins:

View All CDK Isoform Specific Products:

View All Isoforms

CDK1 CDK2 CDK3 CDK4 CDK5 CDK6 CDK7 CDK8 CDK9 CDK11 CDK12 CDK13 CDK14 CDK16 CDK19 CDC CLK Pho85

View All HDAC Isoform Specific Products:

View All Isoforms

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

Biological Activity
Purity & Documentation
References
Customer Review

Description

IC₅₀ & Target

CDK9

0.17 μM (EC₅₀)

HDAC1

1.73 μM (IC₅₀)

HDAC3

1.11 μM (IC₅₀)

In Vitro

CDK9/HDAC1/HDAC3-IN-1 (Compound 13EA) (24h) shows potent anti-proliferative activities in various cancer cell lines (eg：IC₅₀s of 1.51 μM, 2.47 μM and 4,52 μM for HeLa, MDA-MB-231 and HepG2, respectively) ^[1].
CDK9/HDAC1/HDAC3-IN-1 (MDA-MB-231 cells: 0.625-5 μM, HeLa: 0.625-1.25 μM, 24 h) time- and dose-dependently inhibits p-Ser2 mRNA expression in MDA-MB-231 cells^[1].
CDK9/HDAC1/HDAC3-IN-1 (MDA-MB-231 cells: 0.625-5 μM, 24 h) significantly decreases protein expression of p-Ser2 (substrate of CDK9) and simultaneously increases protein expression of Ac-H3 (substrate of HDAC) in MDA-MB-231 cells and Hela cells^[1].
CDK9/HDAC1/HDAC3-IN-1 (0.625-5 μM, 24 h) concentration-dependently induces mitochondrion-related cell apoptosis, escalates the expression of cleaved PARP, and arrests cell cycle in the G2/M phase in MDA-MB-231 cells and Hela cells^[1].

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

Western Blot Analysis^[1]

Cell Line:	MDA-MB-231 cells, HeLa cells
Concentration:	MDA-MB-231 cells (0.625, 1.25, 2.5, 5 μM), HeLa cells (0.625, 1.25 μM)
Incubation Time:	24 h
Result:	Dose-dependently suppressed p-Ser2 (substrate of CDK9) level and upregulated Ac-H3 (substrate of HDAC) level.

Real Time qPCR^[1]

Cell Line:	MDA-MB-231 cells
Concentration:	0.625, 1.25, 2.5, 5 μM
Incubation Time:	3, 6, 12, 24 h
Result:	Time- and dose-dependently downregulated CDK9 mRNA with maximal suppression at 24 h.

Immunofluorescence^[1]

Cell Line:	MDA-MB-231 cells, HeLa cells
Concentration:	3  μM
Incubation Time:	24 h
Result:	Diminished p-Ser2 level and upregulated Ac-H3 level in both HeLa and MDA-MB-231 cells.

Apoptosis Analysis^[1]

Cell Line:	MDA-MB-231 cells, HeLa cells
Concentration:	2.5 μM/3  μM
Incubation Time:	24 h
Result:	Dose-dependently decreased protein expression of Bcl-2 and Mcl-1 in MDA-MB-231 cells, and escalated protein expression of cleaved PARP in MDA-MB-231 cells and Hela cells. Dose-dependently increased the percentage of apoptotic cells induced, ranging from 11.30 % (0.31 μM) up to 77.38 % (2.5  μM) by Annexin V-FITC/PI staining assay (HY-K1073). Concentration-dependently decreased the mitochondrial membrane potential (MMP, Δψ) in the MDA-MB-231 cells with 17.06 %, 26.83 %, 41.97 %, and 52.73 % loss of Δψ for concentrations of 0.31, 0.63, 1.35, and 2.5  μM, respectively.

Cell Cycle Analysis^[1]

Cell Line:	MDA-MB-231 cells
Concentration:	0.31, 0.63, 1.35, and 2.5 μM
Incubation Time:	24 h
Result:	Significant increased the number of cells in the G2/M phase [ (27.43 % (0.31 μM), 79.47 % (0.63 μM), 47.58 % (1.25 μM), and 42.20 % (2.5 μM) ], and gradually promoted cells in the sub-G1 phase [(3.00 % (0.31 μM), 7.64 % (0.63 μM), 23.89 % (1.25 μM), and 27.94 % (2.5 μM)].

In Vivo

CDK9/HDAC1/HDAC3-IN-1 (30  mg/kg, i.p., daily for 10 days) significantly inhibits tumor growth in the MDA-MB-231 mouse xenograft model^[1].

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

Animal Model:	female BALB/c nude mice (6 weeks old) were injected subcutaneously with log growth-phase of MDA-MB-231 cells (3 × 10⁷ cells/mouse) ^[1].
Dosage:	30 mg/kg
Administration:	i.p., once a day for 10 days after tumors reaching approximately 100 mm³.
Result:	Time-dependently inhibited MDA-MB-231 xenograft tumor growth and remarkably reduced the tumor volume. Notably increased cleaved caspase-3 level, and decreased PCNA level in the tumor tissue with IHC staining.

Molecular Weight

470.55

Formula

C₂₄H₂₂N₈OS

CAS No.

2197029-81-3

SMILES

CNC1=NC(C)=C(S1)C2=NC(NC3=CC=C4C(C=C(C(NC5=CC=CC=C5N)=O)N4)=C3)=NC=C2

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

Handling Instructions (2659 KB)

References

[1]. Chen X, et al. Design, synthesis, and biological evaluation of N-(2-amino-phenyl)-5-(4-aryl-pyrimidin-2-yl) amino)-1H-indole-2-carboxamide derivatives as novel inhibitors of CDK9 and class I HDACs for cancer treatment[J]. Bioorganic Chemistry, 2025: 108577.