Ro 3306

目录号: GC12348纯度: >98.00%同义词: 2-[[(噻吩-2-基)甲基]氨基]-5-[1-(喹啉-6-基)甲-(Z)-亚基]噻唑-4-酮

Ro 3306是一种ATP竞争性抑制剂，主要靶向CDK1/cyclin B1（K_i值为35nmol/L）和CDK1/cyclin A复合物（K_i值为110nmol/L）。

Cas No.: 872573-93-8

规格	价格	库存	数量
5mg	¥525.00	现货	1
10mg	¥720.00	现货	1
50mg	¥2,240.00	现货	1
100mg	¥3,640.00	现货	1
10mM (in 1mL DMSO)	¥577.00	现货	1

电话: 400-920-5774Email: sales@glpbio.cn

文献被引

本产品暂无引用记录;以下为 GlpBio 产品在 Nature / Cell / Science 等顶刊的客户引用样例

Nature
641, 529–536 (2025)
Nature
628, 630–638 (2024)
Nature
632, 686–694 (2024)
Nature
618, 1017–1023 (2023)
Nature
610, 366–372 (2022)
Cell
187(9):2288-2304 (2024)
Cell
183(7):1867-1883 (2020)
Science
388(6745) (2025)
Science
387(6739) (2025)
Science
387(6734) (2025)
Cell Research
35, 97–116 (2025)
Cell Research
34, 683–706 (2024)
Cell Research
33, 273–287 (2023)
Cell Research
33, 546–561 (2023)
Cell Research
33, 904–922 (2023)
Cell Research
31, 1291–1307 (2021)

产品描述 Description

Ro 3306 functions as the ATP-competitive inhibitor targeting CDK1/cyclin B1 with K_i value of 35nmol/L, and targeting CDK1/cyclin A complexes with K_i value of 110nmol/L^[1]. Ro 3306 has been widely used in cell cycle studies and anti-tumor assays^[2].

In vitro, Ro 3306 exhibited an IC₅₀ of 1.8μmol/L for WAC2 cell lines and the IC₅₀ of 2.3μmol/L for NB69 cell lines after 48h treatment^[3]. Ro 3306 treatment (5μmol/L, 24h) caused G2/M-phase cell cycle arrest and apoptosis in OCI-AML-3 cells, and reduced the levels of the antiapoptotic proteins Bcl-2 and survivin^[4]. Ro 3306 treatment (10μmol/L, 20h) arrested immature porcine oocytes at the germinal vesicle (GV) stage^[5].

In vivo, Ro 3306 treatment (Intraperitoneal injection) at a dose of 2mg/kg/day, every other day, for a week attenuated angiotensin II-mediated cardiac hypertrophy and cardiac fibrosis in male C57BL/6J mice^[6]. Treatment with Ro 3306 at a dose of 1.5mg/kg/day for 5 days through intranasal administration inhibited infection with the influenza A PR/8 strain, prolonged the survival of infected mice, and significantly reduced viral load in BALB/c mice^[7].

References:
[1] Vassilev L T, Tovar C, Chen S, et al. Selective small-molecule inhibitor reveals critical mitotic functions of human CDK1[J]. Proceedings of the National Academy of Sciences, 2006, 103(28): 10660-10665.
[2] Sunada S, Saito H, Zhang D, et al. CDK1 inhibitor controls G2/M phase transition and reverses DNA damage sensitivity[J]. Biochemical and biophysical research communications, 2021, 550: 56-61.
[3] Schwermer M, Lee S, Köster J, et al. Sensitivity to cdk1-inhibition is modulated by p53 status in preclinical models of embryonal tumors[J]. Oncotarget, 2015, 6(17): 15425.
[4] Kojima K, Shimanuki M, Shikami M, et al. Cyclin‐dependent kinase 1 inhibitor RO‐3306 enhances p53‐mediated Bax activation and mitochondrial apoptosis in AML[J]. Cancer science, 2009, 100(6): 1128-1136.
[5] Jang W I, Lin Z L, Lee S H, et al. A specific inhibitor of CDK1, RO-3306, reversibly arrests meiosis during in vitro maturation of porcine oocytes[J]. Animal reproduction science, 2014, 144(3-4): 102-108.
[6] Yamamoto T, Matsushima S, Okabe K, et al. Cyclin dependent kinase 1 (CDK1) positively regulates cardiac hypertrophy and fibrosis via TGF-beta pathway[J]. European Heart Journal, 2020, 41(Supplement_2): ehaa946. 3743.
[7] Zhao L, Yan Y, Dai Q, et al. The CDK1 inhibitor, Ro-3306, is a potential antiviral candidate against influenza virus infection[J]. Antiviral Research, 2022, 201: 105296.

Ro 3306是一种ATP竞争性抑制剂，主要靶向CDK1/cyclin B1（K_i值为35nmol/L）和CDK1/cyclin A复合物（K_i值为110nmol/L）^[1]。Ro 3306已被广泛应用于细胞周期研究和抗肿瘤实验^[2]。

在体外，Ro 3306处理48小时后，对WAC2细胞系的IC₅₀值为1.8μmol/L，对 NB69细胞系的IC₅₀值为2.3μmol/L^[3]。使用5μmol/L的Ro 3306处理24小时，可导致OCI-AML-3细胞在G2/M期发生细胞周期阻滞并诱导细胞凋亡，同时降低抗凋亡蛋白Bcl-2和survivin的表达水平^[4]。10μmol/L的Ro 3306处理20小时可使未成熟猪卵母细胞停滞在生发泡（GV）期^[5]。

在体内，腹腔注射Ro 3306（2mg/kg/day，隔日给药，持续一周）可显著减轻由血管紧张素II诱导的雄性C57BL/6J小鼠心肌肥大和心脏纤维化^[6]。鼻内给药Ro 3306（1.5mg/kg/day，连续5天）能有效抑制甲型流感病毒PR/8株的感染，延长感染小鼠的存活时间，并显著降低 BALB/c小鼠肺部的病毒载量^[7]。

实验参考方法 Experimental Reference Method

Cell experiment [1]:
Cell lines	OVCA-429 cells
Preparation Method	OVCA-429 cells were cultured in DMEM medium supplemented with 10% fetal bovine serum (FBS) at 37 °C in an incubator with 5% CO₂. The medium was supplemented with 2mmol/L L-glutamine, 100U/mL penicillin, and 100µg/mL streptomycin. OVCA-429 cells were seeded in 24-well plates at a density of 1×10⁵cells. Each well was transfected with 100μmol/L si-Cdk1 and treated with Ro 3306 (0, 2.5, 5 and 10μmol/L) for 48h. Cells were fixed with 10% acetic acid solution containing 10% methanol, stained with 0.5% crystal violet for 1h, photographed and extracted with 1% SDS solution. The absorbance of the cell crystal violet extract at 595nm was measured using a microplate reader. For consistency, each experiment was performed at least three times.
Reaction Conditions	0, 2.5, 5 and 10μmol/L; 48h
Applications	Ro 3306 significantly increased the proliferation of OVCA-429 cells in a dose-dependent manner.
Animal experiment [2]:
Animal models	KpB (K18-gT^+/− 121; p53^fl/fl; Brca1^fl/fl) transgenic mice (KpB mice)
Preparation Method	Breeding and maintenance Sixty mice of KpB were maintained on a 12h light/dark cycle with ad libitum access to food and water. Mimicking diet-induced obesity (DIO), one-half of the KpB female mice were fed an high-fat diet (HFD, 60% fat-derived calories), and the other one-half were fed a low-fat diet (LFD, fat-derived calories, Research Diets) at 3 weeks of age. All mice were injected with 5µL recombinant adenovirus Ad5-CMV-Cre (2.5×10¹⁰P.F.U) into the left ovarian bursa cavity at six to eight weeks old. The mice were maintained on HFD and LFD chow throughout the course of the treatment and were palpated every week to check for the presence of ovarian tumors. When palpable tumors had grown to a mean size of 0.1×0.1cm in diameter, the mice were randomly allocated to groups of four groups (HFD control, LFD control, HFD+Ro 3306, and LFD+Ro 3306, n=15 mice/group). When the ovarian tumor was about 0.1×0.1cm, KpB mice were injected with Ro 3306 (4mg/kg, i.p., every 3 days) for 4 weeks. Toxicity was evaluated daily according to clinically visible abnormalities and weight measurements were performed weekly during the treatment. Tumor development was followed by palpation twice a week until the tumor reached a size that could be measured with calipers. All mice were euthanized by CO₂ asphyxiation following 4 weeks of treatment. Tumors and serum were obtained. Half of the tumor tissues were stored at −80°C, and the other tissue and serum were fixed in paraffin. Blood serum was collected and frozen at −80°C. The ovarian tumor volume was determined by the formula: (width² × length)/2.
Dosage form	4mg/kg every 3 days for 4 weeks; i.p.
Applications	Ro 3306 treatment significantly reduced tumor volume and tumor weight in KpB mice, and significantly inhibited Bcl-xL expression.
References: [1] Yang W, Cho H, Shin H Y, et al. Accumulation of cytoplasmic Cdk1 is associated with cancer growth and survival rate in epithelial ovarian cancer[J]. Oncotarget, 2016, 7(31): 49481. [2] Huang Y, Fan Y, Zhao Z, et al. Inhibition of CDK1 by RO-3306 exhibits anti-tumorigenic effects in ovarian cancer cells and a transgenic mouse model of ovarian cancer[J]. International journal of molecular sciences, 2023, 24(15): 12375.

产品文档 Product Documents

批次：Purity:>98.00%

化学性质Chemical Properties

CAS 号

872573-93-8

同义词

2-[[(噻吩-2-基)甲基]氨基]-5-[1-(喹啉-6-基)甲-(Z)-亚基]噻唑-4-酮

化学名

(Z)-5-(quinolin-6-ylmethylene)-2-((thiophen-2-ylmethyl)amino)thiazol-4(5H)-one

SMILES

O=C1N=C(NCC2=CC=CS2)S/C1=C\C3=CC=C(N=CC=C4)C4=C3

分子式

C₁₈H₁₃N₃OS₂

分子量

351.45 g/mol

溶解性

≥ 4.39mg/mL in DMSO

保存条件

Store at -20°C

General tips

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。
为了提高溶解度，请将管子加热至 37°C，然后在超声波浴中震荡一段时间。

Shipping Condition

评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备 RT，或根据请求配备蓝冰。

计算工具摩尔浓度 / 稀释 / 分子量 / 单位换算 / 体内配方 / 溶解度

质量 (Mass)

体积 (Volume)

浓度 (Concentration)

分子量 (MW)

g/mol