PROTAC CDK9 degrader-11
PROTAC CDK9 degrader-11 is an orally active, selective CDK9 PROTAC degrader with a DC50 of 1.09 nM. PROTAC CDK9 degrader-11 recruits CRBN to form a ternary complex and degrades CDK9 via the ubiquitin-proteasome pathway, thereby inhibiting RNA polymerase II phosphorylation and downregulating the expression of anti-apoptotic and pro-oncogenic genes, ultimately inducing apoptosis. PROTAC CDK9 degrader-11 is suitable for research on small-cell lung cancer (SCLC).
(Pink: CDK9 ligand (HY-170979); Blue: Cereblon ligand (HY-W247437); Black: linker).
For research use only. We do not sell to patients.
- CAS No.: 3039540-19-4
- Formula: C39H48Cl2N10O5
- Molecular Weight:807.77
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
CDK9 1.09 nM (DC50) |
PARP-1 |
Caspase 3 |
Cellular Effect
|
Cell Line
|
Type | Value | Description | References |
|---|---|---|---|---|
| NCI-H69 | IC50 |
1.027 mM
|
Significantly inhibits cell viability.
Significantly inhibits cell viability.
|
39895086 |
| NCI-H446 | IC50 |
1.008 nM
|
Significantly inhibits cell viability.
Significantly inhibits cell viability.
|
39895086 |
| BEAS-2B | IC50 |
412.8 nM
|
Does not affect cell viability.
Does not affect cell viability.
|
39895086 |
| L02 | IC50 |
69.94 nM
|
Does not affect cell viability.
Does not affect cell viability.
|
39895086 |
| HEK-293T | IC50 |
95.47 nM
|
Does not affect cell viability.
Does not affect cell viability.
|
39895086 |
In Vitro
PROTAC CDK9 degrader-11 (Compound C3) (0.5-10.0 nM; 8 h) induces the degradation of CDK9 protein in a concentration-dependent manner in NCI-H69 and NCI-H446 cells[1].
PROTAC CDK9 degrader-11 (10 nM; 0.5-12 h) induces the time-dependent degradation of CDK9 protein and promotes CDK9 ubiquitination in NCI-H69 and NCI-H446 cells[1].
PROTAC CDK9 degrader-11 (0.5-10.0 nM; 24 h) inhibits RNA Pol II phosphorylation (at Ser2 and Ser5 sites) and downregulates c-Myc protein expression in NCI-H69 cells[1].
PROTAC CDK9 degrader-11 (1 pM-10 μM; 72 h) significantly inhibits cell viability in NCI-H69 (IC50 = 1.027 nM), NCI-H146, NCI-H446 (IC50 = 1.008 nM), NCI-H524, and DMS114 cells, while showing lower cytotoxicity in normal cells such as MCF10A (IC50 = 126.3 nM), Beas-2b (IC50 = 412.8 nM), LO2 (IC50 = 69.94 nM), and 293T (IC50 = 95.47 nM)[1].
PROTAC CDK9 degrader-11 (2-4 nM; 8-21 days) inhibits colony formation in NCI-H69, NCI-H446, and DMS114 cells[1].
PROTAC CDK9 degrader-11 (0.5-4 nM; 36 h) induces cell cycle arrest at the G0/G1 phase and apoptosis in NCI-H69 and NCI-H446 cells[1].
PROTAC CDK9 degrader-11 (0.5-5.0 nM; 36 h) downregulates the expression of MCL-1 and BCL-2 and upregulates the expression of Cleaved-PARP and Cleaved-Caspase-3 in NCI-H69 cells[1].
PROTAC CDK9 degrader-11 (2-4 nM; 48 h) inhibits cell invasion in DMS114 and DMS53 cells[1].
PROTAC CDK9 degrader-11 (0.3-30 μM; 18 h) demonstrates a low risk of cardiotoxicity (IC50 > 30 μM) in an in vitro hERG binding assay using HEK-293 cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:NCI-H69, NCI-H446
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Concentration:0.5, 1.0, 2.5, 5.0, 7.5, 10.0 nM
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Incubation Time:8 h
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Result:Decreased CDK9 protein levels in a dose-dependent manner.
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Cell Line:NCI-H69, NCI-H446
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Concentration:10 nM
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Incubation Time:0.5, 1, 3, 6, 12 h
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Result:Decreased CDK9 protein levels in a time-dependent manner.
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Cell Line:NCI-H69, NCI-H446
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Concentration:0.5, 1.0, 2.5, 5.0, 7.5, 10.0 nM
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Incubation Time:3 h
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Result:Significantly increased the ubiquitination levels of CDK9 protein.
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Cell Line:NCI-H69
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Concentration:0.5, 1.0, 2.5, 5.0, 7.5, 10.0 nM
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Incubation Time:24 h
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Result:Decreased the phosphorylation levels of RNA Pol II (Ser2 and Ser5) in a dose-dependent manner.
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Cell Line:NCI-H69
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Concentration:2.5, 5, 10 nM
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Incubation Time:24 h
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Result:Decreased the expression of c-Myc protein in a dose-dependent manner.
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Cell Line:NCI-H69, NCI-H146, NCI-H446, NCI-H524, DMS114
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Concentration:1 pM, 10 pM, 100 pM, 1 nM, 10 nM, 100 nM, 1 μM, 10 μM
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Incubation Time:72 h
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Result:Significantly decreased cell viability.
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Cell Line:NCI-H69, NCI-H446, DMS114
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Concentration:2, 4 nM
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Incubation Time:8 to 21 days
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Result:Significantly decreased the number of malignant colonies formed.
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Cell Line:NCI-H69, NCI-H446
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Concentration:0.5, 1, 2, 4 nM
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Incubation Time:36 h
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Result:Increased the proportion of cells in the G1 phase in a dose-dependent manner.
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Cell Line:NCI-H69, NCI-H446
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Concentration:1, 2, 4 nM
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Incubation Time:36 h
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Result:Increased cell apoptosis rates in a dose-dependent manner.
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Cell Line:NCI-H69
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Concentration:0.5, 1.0, 2.5, 5.0 nM
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Incubation Time:36 h
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Result:Upregulated the expression of pro-apoptotic proteins (Cleaved-PARP, Cleaved-Caspase-3) and downregulated anti-apoptotic proteins (MCL-1, BCL-2).
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Cell Line:DMS114, DMS53
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Concentration:2, 4 nM
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Incubation Time:48 h
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Result:Significantly decreased the number of invading cells migrating through the upper chamber.
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Cell Line:MCF10A, Beas-2b, LO2, 293T
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Concentration:100 nM, 1 μM, 10 μM, 100 μM
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Incubation Time:72 h
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Result:Normal cell viability was less affected, exhibiting low cytotoxicity.
Parmacokinetics
| Species | Dose | Route | T1/2 | Cmax | AUC0-24 | AUC0-∞ | F |
|---|---|---|---|---|---|---|---|
| Mice | 25 mg/kg | p.o. | 4.7 h | 277 ng/mL | 951 ng·h/mL | 977 ng·h/mL | 6.8 % |
| Mice | 5 mg/kg | i.v. | 8.2 h | 2603 ng/mL | 2660 ng·h/mL | 2857 ng·h/mL | / |
| Rat | 25 mg/kg | p.o. | 5.4 h | 179 ng/mL | 714 ng·h/mL | 893 ng·h/mL | 6.5 % |
| Rat | 5 mg/kg | i.v. | 2.8 h | 2003 ng/mL | 2179 ng·h/mL | 2331 ng·h/mL | / |
In Vivo
PROTAC CDK9 degrader-11 (12.5 mg/kg or 25.0 mg/kg; p.o.; once daily; 19 days) significantly reduced systemic metastasis and overall tumor burden in a BALB/c nude mouse model with systemic metastasis induced by tail vein injection of NCI-H446-Luc-GFP cells[1].
PROTAC CDK9 degrader-11 (12.5 mg/kg or 25.0 mg/kg; p.o.; once daily; 7 days) demonstrated significant inhibition of primary tumor growth in a small-cell lung cancer Mini-PDX model[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c nude mice (female, 6-week-old) were subcutaneously injected with 5 x 10 6 NCI-H446 cells[1]
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Dosage:12.5 mg/kg and 25.0 mg/kg
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Administration:p.o.; once daily; for 14 days
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Result:Significantly decreased tumor volume and weight, exhibiting dose-dependent tumor growth inhibitory activity.
Animal body weight remained stable throughout the administration period, and no obvious toxic side effects were observed.
Significantly decreased the expression levels of CDK9 and the proliferation marker Ki-67, while the expression level of the apoptosis marker Cleaved-caspase-3 significantly increased.
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Animal Model:BALB/c nude mice (6-week-old) were injected via the tail vein with 5 x 10 6 NCI-H446-Luc-GFP cells[1]
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Dosage:12.5 mg/kg and 25.0 mg/kg
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Administration:p.o.; once daily; for 19 days
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Result:Significantly attenuated the fluorescence signal intensity in vivo, as demonstrated by in vivo imaging.
Significantly decreased systemic metastasis and overall tumor burden.
There was no significant difference in body weight changes among the groups of mice.
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Animal Model:BALB/c nude mice (four-week-old, 15-20 g) were used to establish the model by subcutaneously implanting capsules with primary small-cell lung cancer (three capsules per mouse; capsules were washed with HBSS) [1]
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Dosage:12.5 mg/kg and 25.0 mg/kg
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Administration:p.o.; once daily; for 7 days
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Result:Significantly reduced the relative fluorescence units (RFU) within capsules containing primary samples.
Demonstrated significant tumor growth inhibition across all tested sample models.
Chemical Information
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CAS No. 3039540-19-4
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Molecular Weight 807.77
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Formula C39H48Cl2N10O5
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SMILES
O=C(NC1=CNN=C1C(NC2CCN(CC2)C(CN3CCC(CC3)CN4CCN(CC4)C5=CC(NC6C(NC(CC6)=O)=O)=CC=C5)=O)=O)C7=C(C=CC=C7Cl)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.
Protocols
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Kinase activity and phosphorylation assays
Kinase activity assays measure the ability of kinases to transfer phosphate groups from ATP to specific substrates, while phosphorylation assays detect the presence and levels of phosphorylated proteins. Common methods include radiolabeled ATP incorporation (e. g. ,), ADP release detection via bioluminescence (e. g. ,[3]), enzyme-linked immunosorbent assays (ELISA) for phospho-specific epitopes (e. g. ,[6]), and microtiter-based formats for high-throughput screening (e. g. ,[8]). The ADP-Glo assay quantifies kinase activity by measuring ADP produced during phosphorylation using a luciferase-based system. Radiometric assays involve autoradiography or scintillation counting after incorporation of 32P-labeled ATP into substrate proteins. ELISA-based approaches rely on phospho-specific antibodies to detect activated kinases in cell lysates or purified samples.
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Western Blot
Western blotting (WB) is a commonly used experimental method in molecular biology, biochemistry, and immunogenetics for identifying and quantifying target proteins. It combines gel electrophoresis with immunoassay, enabling researchers to analyze protein expression, post-translational modifications, and molecular weight.
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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
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Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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Protocol for Kinase activity and phosphorylation assays
Kinase activity assays measure transfer of phosphate from ATP to a protein or peptide substrate, generating phosphorylated substrate, ADP, or incorporated radiolabeled phosphate as the readout; phosphorylation assays measure site-specific phosphorylation in cells or tissues as a proxy for kinase-pathway activation, inhibition, or substrate regulation. Phosphorylation can be detected by phospho-specific Western blot, immunoprecipitation kinase assay, phospho-immunofluorescence, phospho-flow cytometry, luminescent ADP detection, radiolabeled ATP incorporation, or reporter-based pathway assays, and these readouts can be applied to cancer cells, primary neurons, mouse tumors, organoids, inflammatory macrophages, ferroptosis studies, and mitophagy studies when the kinase target is biologically relevant.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)