Ro 3306

Manufactured by MedChemExpress

Sourced in United States

RO-3306 is a selective small-molecule inhibitor of cyclin-dependent kinase 1 (CDK1). CDK1 is a key regulator of the cell cycle and plays a crucial role in the G2/M transition and mitotic progression. RO-3306 inhibits CDK1 activity, thereby arresting cells in the G2/M phase of the cell cycle.

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Lab products found in correlation

8 protocols using ro 3306

Cell Cycle Regulation Inhibitors

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A Cdc7/Cdk9 inhibitor, PHA-767491, was used at 10 µM or 2 µM. Another Cdc7 inhibitor, XL413 (BioVision, BMS-863233), was used at 2 µM. Aurora B inhibitor (AZD1152, Sigma) was used at 100 nM. Nocodazole was used at 30, 50 or 100 ng/ml. Paclitaxel was used at 10 nM. RO-3306 (CDK1 inhibitor; MedChemexpress) was used at 10 µM. Auxin was used at 0.5 µM. Doxycycline was used at 1 µg/ml.

Ito S., Goto H., Kuniyasu K., Shindo M., Yamada M., Tanaka K., Toh G.T., Sawa M., Inagaki M., Bartek J, & Masai H. (2019). Cdc7 kinase stimulates Aurora B kinase in M-phase. Scientific Reports, 9, 18622.

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Antibodies and Inhibitors for TRABID Study

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The antibodies against TRABID were described previously^{37 (link)}. Other antibodies used in this study are listed in Supplementary Table 1. MG132 was purchased from Calbiochem. Rapamycin, Cycloheximide, Bafilomycin A1, and TRABID inhibitor NSC112200 were purchased from Sigma-Aldrich. Lovastatin, aphidicolin, RO-3306, nocodazole, cGAS inhibitor G140 and STING inhibitor C176 were obtained from MedChemExpress. Adenoviruses AdCre and AdLuc were obtained from Baylor College of Medicine Vector Develop Laboratory.

Chen Y.H., Chen H.H., Wang W.J., Chen H.Y., Huang W.S., Kao C.H., Lee S.R., Yeat N.Y., Yan R.L., Chan S.J., Wu K.P, & Chen R.H. (2023). TRABID inhibition activates cGAS/STING-mediated anti-tumor immunity through mitosis and autophagy dysregulation. Nature Communications, 14, 3050.

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In vitro Culture of Human Osteosarcoma Cell Lines

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The human osteosarcoma cell lines SJSA, SAOS2, 143B, U2OS and HOS were cultured in high glucose Dulbecco’s Modified Eagle Medium (DMEM; Gibco, United States) supplemented with 10% fetal bovine serum (FBS; Wisent, Canada) and 1% Penicillin-Streptomycin-Glutamine (Wisent Inc., Cañada) in a humidified atmosphere of 5% CO2 and 95% air at 37°C. Cells were dissociated by TrypLETM Express (Gibco, Thermo Fisher Scientific Inc., United States) and passaged when they are 90%–100% confluent. Cell line authentication was performed on cells that used for in vitro and in vivo studies using Short Tandem Repeat (STR) DNA profiling and all cell lines were preserved at Shanghai Bone Tumor Institute (Shanghai, China). Reagents used in the study included: Ro-3306 (#HY-12529, MCE/MedChemExpress, United States), Doxorubicin hydrochloride (#HY-15142, MCE/MedChemExpress, United States). The antibodies used in this study were purchased as follows: anti-MYC (#ab78318, 1:1000), anti-GAPDH (#ab263962, 1:1000). HRP-conjugated goat anti-rabbit IgG (#L3042, 1:5000) and goat anti-mouse IgG (#101, 1:5000) secondary antibodies for Western blot were purchased from Signalway Antibody.

Tao Y., Li L., Yang X., Yin S., Zhang Z., Wang H., Pu R., Wang Z., Zhang Q., Mu H., Wu C., He J, & Yang L. (2024). Magnetic-driven hydrogel microrobots for promoting osteosarcoma chemo-therapy with synthetic lethality strategy. Frontiers in Chemistry, 12, 1386076.

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Small Molecule Compound Purchases

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Chemical compounds were purchased from Selleckchem (LY2603618), ThermoFisher Scientific (puromycin, doxycycline, and geneticin), and MedChemExpress (AZD1775, AZD6738, RO-3306, roscovitine, VX-970, NSC663284, and GDC-0575).

Koppenhafer S.L., Goss K.L., Terry W.W, & Gordon D.J. (2019). Inhibition of the ATR-CHK1 pathway in Ewing sarcoma cells causes DNA damage and apoptosis via the CDK2-mediated degradation of RRM2. Molecular cancer research : MCR, 18(1), 91-104.

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Purification of Human NEIL1 Protein

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Endonuclease VIII enzyme was purchased from New England Biolabs. Human NEIL1 was purified in bacteria by expression of the construct pET28hNEIL1 (kind gift from Susan Wallace) in BL21 (DE3) T1R pRARE2 at 18°C overnight. Bacteria were lyzed using sonication and the resulting lysate was centrifuged and filtered. C-terminally His-tagged human NEIL1 was purified using affinity chromatography using HisTrap HP (GE Healthcare). Fractions containing human NEIL1 eluted from the HisTrap column were pooled and protein was further purified using gel filtration on HiLoad 16/60 Superdex 200 (GE Healthcare). The purity of the protein was analyzed using SDS-PAGE.
Proteinase K and RNase A were purchased from Thermo Fisher.
Inhibitors used are as follows: vincristine (Sigma), Colcemid (Gibco), RO-3306 (CDK1 inhibitor, MedChemExpress), Reversine (GSK923295, Axon MedChem), APE1 inhibitor (Sigma, CAS 6960–45–8), PARP inhibitor (olaparib, SelleckChem, 763113–22–0).

Zhao Z., Gad H., Benitez-Buelga C., Sanjiv K., Xiangwei H., Kang H., Feng M., Zhao Z., Berglund U.W., Xia Q, & Helleday T. (2021). NEIL3 Prevents Senescence in Hepatocellular Carcinoma by Repairing Oxidative Lesions at Telomeres during Mitosis. Cancer Research, 81(15), 4079-4093.

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Cell Synchronization at G2/M Boundary

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Cells were synchronized at the G2/M boundary by treatment with thymidine‐thymidine‐Ro‐3306. At first, the cells were treated with 2 mmol/L thymidine (MP Biomedicals, Santa Ana, CA, USA) for 14 hours, and then released to thymidine‐free medium for 10 hours. Subsequently, the cells were treated with 2 mmol/L thymidine for 14 hours, and then released to thymidine‐free medium for 2 hours. Finally, the cells were treated with 10 μmol/L Ro‐3306 (MedChemExpress, Monmouth Junction, NJ, USA) for 16 hours. The medium was replaced with a Ro‐3306‐free medium to allow the cells to re‐enter the cell cycle and progress through mitosis.

Chen A., Wen S., Liu F., Zhang Z., Liu M., Wu Y., He B., Yan M., Kang T., Lam E.W., Wang Z, & Liu Q. (2021). CRISPR/Cas9 screening identifies a kinetochore‐microtubule dependent mechanism for Aurora‐A inhibitor resistance in breast cancer. Cancer Communications, 41(2), 121-139.

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Quantifying Telomere Synthesis in G2-Phase Cells

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ATSA assay was performed according to Zhang et al.^{43 (link)} to detect telomere synthesis in APBs in G2 cells. U2OS or SAOS-2 cells were seeded in chamber slides and treated the next day first with either DMSO or ponatinib, then after 3 h, a CDK1 inhibitor (Ro-3306; MedchemExpress) was added for 15–16 h to synchronize the cells in G2 phase. EdU was then added for 2 h, and cells were fixed with 4% formaldehyde for 10 min, permeabilized for 15 min with PBS Triton-X 0.5% and stained for telomeric DNA (using a TelG-PNA-probe) as per the FISH protocol. After telomere staining, cells were fixed again, permeabilized and EdU was stained using a Click reaction according to the manufacturer’s protocol (Click-&-Go Plus EdU 647; Click Chemistry Tools). The slides were fixed again, permeabilized and stained for PML bodies (using an antibody against SP100, a component of the PML bodies). Images were captured with a LSM710 confocal microscope and APB-positive cells were scored for their total number of APBs as well as the EdU+ APBs.

Kusuma F.K., Prabhu A., Tieo G., Ahmed S.M., Dakle P., Yong W.K., Pathak E., Madan V., Jiang Y.Y., Tam W.L., Kappei D., Dröge P., Koeffler H.P, & Jeitany M. (2023). Signalling inhibition by ponatinib disrupts productive alternative lengthening of telomeres (ALT). Nature Communications, 14, 1919.

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Evaluating Therapeutic Inhibitors in Cancer

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The following drugs were used: ERK5 inhibitors XMD8-92 [31 (link)] and JWG-045 [34 (link)] have been developed in Gray’s laboratory; MEK5 inhibitor BIX02189 [32 (link)], ERK1/2 inhibitor SCH772984 [47 (link)] and BRAFV600E inhibitor vemurafenib [48 (link)] (Selleckchem, Italy, www.selleckchem.com); CDK1 inhibitor RO-3306 (MedChem Express, www.medchemexpress.com) [49 (link)].

Tusa I., Gagliardi S., Tubita A., Pandolfi S., Urso C., Borgognoni L., Wang J., Deng X., Gray N.S., Stecca B, & Rovida E. (2018). ERK5 is activated by oncogenic BRAF and promotes melanoma growth. Oncogene, 37(19), 2601-2614.

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