CAM2602
Based on 1 publication(s) in Google Scholar
CAM2602 is an orally active Aurora A-TPX2 protein−protein interaction inhibitor with a human Kd of 19 nM for Aurora A. CAM2602 increases the proportion of PH3 positive cells while reducing P-T288 Aurora A levels. CAM2602 arrests tumor xenograft growth in mice. CAM2602 can be used for the research of cancer, such as acute T cell leukemia.
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- Pureza : 99.85%
- No. CAS: 3056388-47-4
- Fòrmula: C23H21ClN4O4S
- Peso molecular:484.96
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Almacenamiento:Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month
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Actividad biológica
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Chemical Information
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Solvente y solubilidad
- Protocolo
- Pureza y Documentación
- Referencias
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Help & FAQs
Publications Citing Use of MedChemExpress (MCE) CAM2602
MoreVer todos los productos específicos de isoformas Aurora Kinase
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Actividad biológica
Descripciòn
IC50 & Target
[1]|
Aurora A 19 nM (Kd) |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
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| HeLa | GI50 |
21.8 μM
Compound: CAM2602
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Growth inhibition of human HeLa cells incubated for 72 hrs by sulforhodamine B assay
Growth inhibition of human HeLa cells incubated for 72 hrs by sulforhodamine B assay
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[PMID: 39190548] |
| Jurkat | GI50 |
10.3 μM
Compound: CAM2602
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Growth inhibition of human Jurkat cells incubated for 72 hrs by CellTiter-Blue assay
Growth inhibition of human Jurkat cells incubated for 72 hrs by CellTiter-Blue assay
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[PMID: 39190548] |
In Vitro
CAM2602 binds to purified human Aurora A kinase domain with a Kd of 19 nM, inhibiting the Aurora A-TPX2 protein-protein interaction[1].
CAM2602 (0.1-100 μM; 2 h) induces mislocalization of Aurora A from the mitotic spindle in mitotic HeLa cells with an EC50 of 6.1 μM[1].
CAM2602 (0.1-100 μM; 2 h) induces dephosphorylation of Aurora A at Thr288 in mitotic HeLa cells with an EC50 of 3.9 μM[1].
CAM2602 (1-1000 μM; 72 h) inhibits the viability of Jurkat acute T cell leukemia cells with a GI50 of 10.3 μM[1].
CAM2602 (1-1000 μM; 72 h) inhibits the viability of HeLa cervical adenocarcinoma cells with a GI50 of 21.8 μM[1].
CAM2602 (20 μM; 8 h) induces Aurora A inhibition in Jurkat acute T cell leukemia cells, marked by increased PH3-positive mitotic cells and reduced P-T288 Aurora A levels[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:Jurkat acute T cell leukemia cells；HeLa cervical adenocarcinoma cells
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Concentration:1-1000 μM
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Incubation Time:72 h
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Result:Reduced Jurkat cell viability in a dose-dependent manner, with a half-maximal growth inhibition concentration (GI50) of 10.3 μM.
Reduced HeLa cell viability in a dose-dependent manner, with a GI50 of 21.8 μM.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:NOD-SCID gamma (NSG) mice (female, 5−7 weeks old for biomarker study; female, 6−8 weeks old for efficacy study)[1]
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Dosage:200 mg/kg (biomarker study); 100 mg/kg (efficacy study); 150 mg/kg (efficacy study)
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Administration:p.o.; single dose (biomarker study); daily; 26 days (efficacy study)
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Result:Showed fold-increases in phosphorylated histone H3 (PH3) over vehicle controls at 8 and 12 h post single 200 mg/kg dose.
Decreased levels of Aurora A phosphorylated at Thr288 (P-Thr288) at 8 and 12 h post single 200 mg/kg dose.
Reached plasma concentrations of 350 μM at 8 h and 150 μM at 12 h post single 200 mg/kg dose.
Reached tumor concentrations of 70 μM at 8 h and 54 μM at 12 h post single 200 mg/kg dose.
Suppressed tumor growth relative to vehicle-treated mice with daily dosing of 100 mg/kg or 150 mg/kg for 26 days, with 150 mg/kg showing greater efficacy.
Caused no overt toxicity or body weight loss in treated mice.
Chemical Information
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No. CAS 3056388-47-4
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Appearance Solid
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Peso molecular 484.96
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Fòrmula C23H21ClN4O4S
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Color White to off-white
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SMILES
O=C(C1=CC(C2=CC=C(C(OC3=CC=CC=N3)=C2)Cl)=C4C(NC=C4)=C1C)NS(=O)(N(C)C)=O
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Envío
Room temperature in continental US; may vary elsewhere.
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Almacenamiento
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month
Publications (1)
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Journal Impact Factor
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Most Recent
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J Biol Chem
CEP55 promotes prostate cancer progression via TPX2-dependent activation of AURKA-PI3K-AKT signaling and inhibition of ferroptosis. [Abstract]2026 Mar;302(3):111218. PMID: 41617029
Solvente y solubilidad
In Vitro:
DMSO : 200 mg/mL (412.41 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
In Vivo:
Select the appropriate dissolution method based on your experimental animal and administration route.
- For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
- To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
- The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline
Solubility: ≥ 5 mg/mL (10.31 mM); Clear solution
This protocol yields a clear solution of ≥ 5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (50.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%Saline +
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Working solution concentration: 0.22 mg/mL
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL.
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Protocolo
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Pull-down
The pull-down assay is an in vitro technique used to detect physical interactions between two or more proteins and an invaluable tool for confirming a predicted protein-protein interaction or identifying novel interacting partners. This method typically involves the use of affinity purification with various wash and elution steps.
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Immunoprecipitation
Immunoprecipitation (IP) is an experimental method that uses the principle of antibody specific binding to purify and enrich target proteins.
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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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Protocol for Bimolecular Fluorescence Complementation (BiFC) Assay
Bimolecular fluorescence complementation detects protein-protein proximity in living or fixed cells by fusing two candidate interaction partners to nonfluorescent N- and C-terminal fragments of a fluorescent protein; when the partners interact or remain close enough, the fluorescent fragments complement, mature, and generate a fluorescent signal at the site of the protein complex. The BiFC readout is fluorescence intensity and subcellular localization of the reconstituted fluorophore, which reflects formation or stabilization of a protein complex rather than direct biochemical binding kinetics; BiFC is therefore useful for mapping where interactions occur in cancer cells, neurons, macrophages, organoid-derived cells, or drug-screening systems, but results should be validated by independent assays such as co-IP or Western blot. BiFC signal formation is delayed by fluorophore maturation and can stabilize otherwise transient complexes, so it is not a real-time reversible interaction assay
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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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Research Protocol for Cancer Immunology
Cancer immunology studies how the immune system recognizes, suppresses, edits, or fails to eliminate malignant cells through tumor antigen release, antigen presentation, T-cell priming, immune trafficking, tumor-cell killing, and feedback inhibition in the tumor microenvironment. The cancer-immunity cycle links tumor antigenicity, dendritic-cell priming, CD8+ T-cell infiltration, cytotoxic function, and immune-checkpoint regulation to tumor rejection or immune escape. Immune-checkpoint pathways such as PD-1/PD-L1 and CTLA-4 suppress antitumor T-cell activity and can be therapeutically blocked, but many tumors remain resistant because of poor antigen presentation, weak T-cell infiltration, suppressive myeloid cells, regulatory T cells, and tumor-intrinsic immune-exclusion programs. Unresolved questions include which immune-cell states predict response, how tumor-intrinsic pathways exclude immune cells, how myeloid suppression limits checkpoint blockade, and which combination strategies
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Co-Immunoprecipitation
Co-immunoprecipitation technology can verify protein interaction based on the specific immune reaction between antibodies and antigens.
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Protocol for Yeast Two-Hybrid (Y2H) Assay
The yeast two-hybrid assay detects binary protein-protein interactions by separating a transcription factor into a DNA-binding domain fused to a "bait" protein and a transcriptional activation domain fused to a "prey" protein; if bait and prey interact in yeast, the transcription factor is reconstituted and activates reporter genes such as HIS3, ADE2, lacZ, MEL1, or other selectable/readable reporters. The readout is yeast growth on selective medium and/or reporter activity, which reflects proximity-dependent transcriptional activation in the yeast nucleus rather than direct biochemical binding in the original mammalian, tumor, neuronal, macrophage, or organoid context. Because yeast two-hybrid can generate false positives and false negatives, interaction claims should be validated using independent assays such as co-immunoprecipitation, Western blot, immunofluorescence colocalization, BiFC, pull-down, or mammalian two-hybrid assays.
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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.
Pureza y Documentación
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Ficha de datos (283 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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Instrucciones de manejo (2659 KB)
Referencias
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| DMSO | 1 mM | 2.0620 mL | 10.3101 mL | 20.6203 mL | 51.5506 mL |
| 5 mM | 0.4124 mL | 2.0620 mL | 4.1241 mL | 10.3101 mL | |
| 10 mM | 0.2062 mL | 1.0310 mL | 2.0620 mL | 5.1551 mL | |
| 15 mM | 0.1375 mL | 0.6873 mL | 1.3747 mL | 3.4367 mL | |
| 20 mM | 0.1031 mL | 0.5155 mL | 1.0310 mL | 2.5775 mL | |
| 25 mM | 0.0825 mL | 0.4124 mL | 0.8248 mL | 2.0620 mL | |
| 30 mM | 0.0687 mL | 0.3437 mL | 0.6873 mL | 1.7184 mL | |
| 40 mM | 0.0516 mL | 0.2578 mL | 0.5155 mL | 1.2888 mL | |
| 50 mM | 0.0412 mL | 0.2062 mL | 0.4124 mL | 1.0310 mL | |
| 60 mM | 0.0344 mL | 0.1718 mL | 0.3437 mL | 0.8592 mL | |
| 80 mM | 0.0258 mL | 0.1289 mL | 0.2578 mL | 0.6444 mL | |
| 100 mM | 0.0206 mL | 0.1031 mL | 0.2062 mL | 0.5155 mL |
CAM2602 Related Classifications
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