Antitumor agent-101
Antitumor agent-101 is a selective covalent inhibitor of lysine methyltransferases G9a/GLP, with IC50s of 8.5 nM and 5.5 nM for G9a and GLP, respectively. Antitumor agent-101 shows antitumor efficacy in the PANC-1 xenograft model.
For research use only. We do not sell to patients.
- CAS No.: 2848632-52-8
- Formula: C26H38N6O3
- Molecular Weight:482.62
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Histone Methyltransferase Isoforms
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Biological Activity
Description
IC50 & Target
[1]|
G9a 8.5 nM (IC50) |
GLP 5.5 nM (IC50) |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| MDA-MB-231 | IC50 |
2.88 μM
Compound: 27
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Antiproliferative activity against human MDA-MB-231 cells assessed as cell viability measured after 24 hrs by CCK-8 assay
Antiproliferative activity against human MDA-MB-231 cells assessed as cell viability measured after 24 hrs by CCK-8 assay
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[PMID: 37268593] |
| PANC-1 | IC50 |
2.68 μM
Compound: 27
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Antiproliferative activity against human PANC-1 cells assessed as cell viability measured after 24 hrs by CCK-8 assay
Antiproliferative activity against human PANC-1 cells assessed as cell viability measured after 24 hrs by CCK-8 assay
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[PMID: 37268593] |
In Vitro
Antitumor agent-101 (Compound 27) ( 0-5 μM; 48 hours) significantly exhibits proliferation and colony formation of PANC-1 and MDA-MB-231 cells with IC50s of 2.68 and 2.88 μM, respectively[1].
Antitumor agent-101 (0-10 μM; 0-96 hours) effectively reduces H3K9me2 in PANC-1 and MDA-MB-231 cells in a concentration- and time-dependent manner[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:PANC-1 and MDA-MB-231 cells
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Concentration:0, 1.25, 2.5, 5 μM
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Incubation Time:48 hours
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Result:Ihibited proliferation of PANC-1 and MDA-MB-231 cells with IC50s of 2.68 and 2.88 μM, respectively.
Significantly suppressed the colony formation in MDA-MB-231 and PANC-1 cell lines at 2.5 μM.
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Cell Line:PANC-1 and MDA-MB-231 cells
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Concentration:2.5, 5, 10 μM
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Incubation Time:4, 48, 72, or 96 hours
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Result:Effectively reduced H3K9me2 in PANC-1 and MDA-MB-231 cells in a concentration- and time-dependent manner.
Still significantly inhibited the levels of H3K9me2 in the cells treated with compound 27 were still significantly inhibited within 24h after Antitumor agent-101 was washed out, and the levels of H3K9me2 were recovered after 48h.
In Vivo
Antitumor agent-101 (2 mg/kg for p.o.) shows a Cmax of 316 ng/mL, and mean residence time (MRT) of 0.61 hour[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:PANC-1 xenograft tumor models in male Balb/c nu/nu mice[1]
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Dosage:2 mg/kg
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Administration:Intraperitoneal injection (i.p.), 5 days a week (5 days on and 2 days off).
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Result:Exhibited potent antitumor activity with a tumor growth inhibition (TGI) rate of 52.2% with no obvious toxicity.
Showed lower levels of H3K9me2 than the vehicle group.
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Animal Model:Male ICR Mice (Pharmacokinetic assay)[1]
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Dosage:2 mg/kg
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Administration:Intraperitoneal injection (i.p.)
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Result:Pharmacokinetic parameters for antitumor agent-101 (Compound 27) in rats [1]
Route Dose (mg/kg) Cmax (ng/mL) AUC0-t (h•ng/mL) AUC0-Ꝏ (h•ng/mL) MRT (h) i.p. 2 316 208 214 0.61
Chemical Information
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CAS No. 2848632-52-8
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Molecular Weight 482.62
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Formula C26H38N6O3
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SMILES
COC1=CC2=C(N=C(N(C)C(C=C)=O)N=C2NC3CCN(C)CC3)C=C1OCCCN4CCCC4
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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
All Animals and DiseasesMore-
Patient-Derived Xenograft (PDX)
Patient-derived xenograft (PDX) models are generated by engrafting primary human tumor tissue directly into immunodeficient mice, allowing in vivo propagation of patient tumor biology without initial in vitro adaptation. These models are used to preserve key histopathological and molecular characteristics of the original tumor and enable assessment of tumor growth dynamics and therapeutic response in a living organism. The biological readout is tumor engraftment and subsequent growth in the murine host, which reflects the ability of human tumor cells to survive, vascularize, and expand in an immunocompromised microenvironment.
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Splenic/Portal-Vein Liver Metastasis Xenograft
Splenic and portal-vein liver metastasis xenograft models deliver tumor cells into the portal circulation so that cells reach the liver first and form hepatic metastatic lesions; splenic injection uses the spleen as an access route to the portal system, while direct portal-vein injection introduces cells into the portal vein without requiring splenectomy. The assay detects liver colonization, intrahepatic tumor growth, tumor distribution, treatment response, survival, and liver-metastasis microenvironment changes; readouts include bioluminescence or fluorescence imaging, gross liver nodule counts, liver weight or tumor burden, histology, and survival.
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Subcutaneous Cell-Line-Derived Xenograft
Subcutaneous cell-line-derived xenograft (CDX) models are established by implanting cultured human cancer cell lines into immunodeficient mice, where the injected cells form localized tumors that can be monitored in vivo as a measure of tumorigenic potential, growth kinetics, and treatment response. These models are widely used in oncology research because they allow reproducible tumor formation and enable comparative assessment of tumor growth between different cell lines or genetic manipulations in a controlled in vivo microenvironment. Subcutaneous implantation of cancer cells in immunodeficient mice is a standard approach for evaluating tumor growth behavior and therapeutic response across multiple cancer types, including prostate, esophageal, pancreatic, and colon cancer models.
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Orthotopic Cell-Line Xenograft
Orthotopic cell-line xenograft models involve implantation of human cancer cell lines into the anatomically corresponding organ of immunodeficient mice to reproduce tumor growth within a native microenvironment, enabling more clinically relevant tumor behavior compared with subcutaneous models. These models are widely used because orthotopic placement better recapitulates tumor progression, including invasion and metastatic spread, which are often underrepresented in heterotopic implantation systems. Compared with conventional xenografts, orthotopic implantation is described as more technically complex but provides improved simulation of tumor-microenvironment interactions and metastatic behavior, making it particularly valuable for translational oncology research. Surgical orthotopic implantation approaches have been emphasized as enabling faithful reproduction of clinical cancer features, including metastasis and disease progression patterns that align with the tumor’s organ of origi
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Intraperitoneal/Peritoneal Dissemination Xenograft
Intraperitoneal (IP) or peritoneal dissemination xenograft models are based on the introduction of human cancer cells into the peritoneal cavity of immunodeficient mice, where they attach to peritoneal surfaces, form multicellular aggregates or spheroids, and progressively generate disseminated tumor nodules that mimic advanced peritoneal metastatic disease. These models are widely used to study ovarian cancer progression, tumor-microenvironment interactions, and intraperitoneal therapeutic responses, often incorporating bioluminescence or fluorescence imaging to longitudinally monitor tumor burden in vivo. The biological principle relies on the capacity of tumor cells such as SKOV3 or related ovarian carcinoma lines to survive in suspension, aggregate within ascites-like fluid, adhere to mesothelial surfaces, and invade peritoneal organs, thereby recapitulating human peritoneal carcinomatosis patterns observed in advanced disease.
Purity & Documentation
Select Batch:Purity: 99.98%Assay: 99.98%ee.: 99.98%
References
Calculators
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