标签归档：cyc

CDK1/Cyc B-IN-1

发表于由
回复

上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白，专注于信号通路和疾病研究领域。

CDK1/Cyc B-IN-1 

CDK1/Cyc B-IN-1 (Compound 5) 是一种选择性的 CDK1/Cyc B 复合体抑制剂，IC50 为 97 nM。CDK1/Cyc B-IN-1 诱导细胞凋亡 (apoptosis) 和 G2/M 细胞期阻滞。CDK1/Cyc B-IN-1 对癌细胞具有广谱的细胞毒性。

CDK1/Cyc B-IN-1

CDK1/Cyc B-IN-1 Chemical Structure

CAS No. : 2459916-56-2

规格 是否有货
100 mg   询价  
250 mg   询价  
500 mg   询价  

* Please select Quantity before adding items.

生物活性

CDK1/Cyc B-IN-1 (Compound 5) is a selective CDK1/Cyc B complex inhibitor with an IC50 of 97 nM. CDK1/Cyc B-IN-1 triggers apoptosis and G2/M cell cycle arrest. CDK1/Cyc B-IN-1 shows broad-spectrum cytotoxic action against cancer cell lines[1].

IC50 & Target

CDK1-Cyclin B

97 nM (IC50)

体外研究
(In Vitro)

CDK1/Cyc B-IN-1 (Compound 5) shows cytotoxic activity with IC50 values of 5.33 ± 0.69 µM and 21.69 ± 1.04 µM against HCT-116 and WI-38, respectively[1].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量

353.85

Formula

C14H12ClN3O2S2
CAS 号

2459916-56-2
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献

  • [1]. Mohamed SH, et al. An investigative study of antitumor properties of a novel thiazolo[4,5-d]pyrimidine small molecule revealing superior antitumor activity with CDK1 selectivity and potent pro-apoptotic properties. Bioorg Med Chem. 2020 Sep 1;28(17):115633.

所有产品仅用作科学研究或药证申报，我们不为任何个人用途提供产品和服务

CYC-116

发表于由

上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白，专注于信号通路和疾病研究领域。

CYC-116  纯度: 98.17%

CYC-116是有效的极光激酶A和B (aurora A/B) 的抑制剂，Ki 值分别为8和9 nM。

CYC-116

CYC-116 Chemical Structure

CAS No. : 693228-63-6

规格 价格 是否有货 数量
5 mg ￥710 In-stock
10 mg ￥921 In-stock
50 mg ￥2753 In-stock
100 mg ￥4850 In-stock
200 mg   询价  
500 mg   询价  

* Please select Quantity before adding items.

CYC-116 相关产品

•相关化合物库:

  • Clinical Compound Library Plus
  • Bioactive Compound Library Plus
  • Cell Cycle/DNA Damage Compound Library
  • Epigenetics Compound Library
  • Kinase Inhibitor Library
  • Anti-Cancer Compound Library
  • Clinical Compound Library
  • Autophagy Compound Library
  • Anti-Aging Compound Library
  • Cytoskeleton Compound Library
  • Anti-Blood Cancer Compound Library

生物活性

CYC-116 is a potent aurora A and aurora B inhibitor with Kis of 8 and 9 nM, respectively.

IC50 & Target[1]

Aurora A

8 nM (Ki)

Aurora B

9.2 nM (Ki)

体外研究
(In Vitro)

CYC-116 also inhibits VEGFR2, Src, Lck AND FLT3 with with Kis of 44, 82, 280, 44 nM, respectively. CYC-116 may have broad-spectrum antitumor activity. CYC-116 shows potent antiproliferative activity against cancer cell lines with with IC50s of 0.599, 0.59, 0.241, 0.34, 0.725, 1.375, 0.471, 0.034, 0.372, 0.681, 0.151, 1.626, 0.775, 0.308, 0.110, 0.09 for MCF7, HeLa, Colo205, HCT-116, HT29, K562, CCRF-CEM, MV4-11, HL60, NCI-H460, A2780, BxPC3, HuPT4, Mia-Paca-2, Saos-2, Messa cells. Treatment with 1.25 μM CYC-116 for 7 h results in complete inhibition of histone H3 phosphorylation in HeLa cell lysates[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究
(In Vivo)

Oral administration of CYC-116 at dose levels of 75 and 100 mg/kg q.d. causes tumor growth delays of 2.3 and 5.8 days, which translates into specific growth delays of 0.32 and 0.81, respectively. The mean relative tumor volumes of mice receiving CYC-116 at both dose levels are less than those of vehicle-treated mice for the duration of the study period. At 100 mg/kg po q.d., the reduction in growth is statistically significant on days 6 and 9[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Clinical Trial

分子量

368.46

Formula

C18H20N6OS
CAS 号

693228-63-6
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
溶解性数据
In Vitro: 

DMSO : 15 mg/mL (40.71 mM; Need ultrasonic)

H2O : < 0.1 mg/mL (insoluble)

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 2.7140 mL 13.5700 mL 27.1400 mL
5 mM 0.5428 mL 2.7140 mL 5.4280 mL
10 mM 0.2714 mL 1.3570 mL 2.7140 mL

*

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, 6 months; -20°C, 1 month。-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。

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：

——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

  • 1.

    请依序添加每种溶剂： 10% DMSO    40% PEG300    5% Tween-80    45% saline

    Solubility: 1.5 mg/mL (4.07 mM); Suspended solution; Need ultrasonic

    此方案可获得 1.5 mg/mL (4.07 mM) 的均匀悬浊液，悬浊液可用于口服和腹腔注射。

    以 1 mL 工作液为例，取 100 μL 15.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

    将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液

  • 2.

    请依序添加每种溶剂： 10% DMSO    90% (20% SBE-β-CD in saline)

    Solubility: ≥ 1.5 mg/mL (4.07 mM); Clear solution

    此方案可获得 ≥ 1.5 mg/mL (4.07 mM，饱和度未知) 的澄清溶液。

    以 1 mL 工作液为例，取 100 μL 15.0 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。

    将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
*以上所有助溶剂都可在 上海金畔生物科技有限公司 网站选购。
参考文献

  • [1]. Wang S, et al. Discovery of N-phenyl-4-(thiazol-5-yl)pyrimidin-2-amine aurora kinase inhibitors. J Med Chem. 2010 Jun 10;53(11):4367-78.

Kinase Assay
[1]

Aurora A kinase assays are performed using a 25 μL reaction volume (25 mM β-glycerophosphate, 20 mM Tris/HCl, pH 7.5, 5 mM EGTA, 1 mM DTT, 1 mM Na3VO4, 10 μg of kemptide (peptide substrate)), and recombinant aurora A kinase is diluted in 20 mM Tris/HCl, pH 8, containing 0.5 mg/mL BSA, 2.5% glycerol, and 0.006% Brij-35. Reactions are started by the addition of 5 μL Mg/ATP mix (15 mM MgCl4, 100 μM ATP, with 18.5 kBq γ-32P-ATP per well) and incubated at 30°C for 30 min before terminating by the addition of 25 μL of 75 mM H3PO4. Aurora B kinase assays are performed as for aurora A except that prior to use, aurora B is activated in a separate reaction at 30°C for 60 min with inner centromeres protein[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Assay

CYC-116 is prepared in DMSO and diluted in cell medium[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration
[1]

Mice: Mice implanted intraperitoneally with P388/0 cells are treated with CYC-116, and the antitumor activity is measured as an increase in lifespan of the treated animals versus the vehicle control group[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献

  • [1]. Wang S, et al. Discovery of N-phenyl-4-(thiazol-5-yl)pyrimidin-2-amine aurora kinase inhibitors. J Med Chem. 2010 Jun 10;53(11):4367-78.

所有产品仅用作科学研究或药证申报，我们不为任何个人用途提供产品和服务

Fadraciclib(Synonyms: CYC065)

发表于由

上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白，专注于信号通路和疾病研究领域。

Fadraciclib (Synonyms: CYC065) 纯度: 99.78%

Fadraciclib (CYC065) 是第二代口服有效的 ATP 竞争性的 CDK2/CDK9 激酶抑制剂，IC50 分别为 5 和 26 nM。

Fadraciclib(Synonyms: CYC065)

Fadraciclib Chemical Structure

CAS No. : 1070790-89-4

规格 价格 是否有货 数量
10 mM * 1 mL in DMSO ￥3935 In-stock
1 mg ￥1500 In-stock
5 mg ￥4500 In-stock
10 mg ￥7500 In-stock
50 mg ￥19500 In-stock
100 mg ￥28000 In-stock
200 mg   询价  
500 mg   询价  

* Please select Quantity before adding items.

Fadraciclib 相关产品

•相关化合物库:

  • Drug Repurposing Compound Library Plus
  • Clinical Compound Library Plus
  • Bioactive Compound Library Plus

生物活性

Fadraciclib (CYC065) is a second-generation, orally available ATP-competitive inhibitor of CDK2/CDK9 kinases[1] with IC50s of 5 and 26 nM, respectively[2].

IC50 & Target[1]

CDK2

 

CDK9

 

体外研究
(In Vitro)

Fadraciclib blocks cells in the G1 phase of the cell cycle and inhibits cell growth specifically in cyclin E1 (CCNE1)-overexpressing uterine serous carcinomas (USCs). USC cell lines expressing high CCNE1 mRNA and protein levels to be significantly more sensitive to treatment with Fadraciclib in vitro when compared with low CCNE1-expressing cell lines (IC50: mean±s.d.=124.1±57.8 nM in CCNE1-overexpressing USC cell lines vs 415±117.5 nM in CCNE1 low expressors, respectively; P=0.0003). Importantly, low concentrations of Fadraciclib (i.e., 100 nM) causes an arrest in the G1 phase of the cell cycle only in the CCNE1-overexpressing USC cell lines (i.e., USC-ARK-2, USC-ARK-7) [1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究
(In Vivo)

To evaluate the therapeutic potential of Fadraciclib as a single agent, USC-ARK-2-derived xenografts are treated daily with Fadraciclib (22.5 mg/kg) for a 3-week period. Tumor size and mouse weight are recorded two times a week. The daily administration of Fadraciclib results in a significant reduction of tumor growth compared with the vehicle-treated mice (P=0.012 starting at day 9 of the treatment). No significant weight loss is reported during the entire treatment period[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Clinical Trial

分子量

397.52

Formula

C21H31N7O
CAS 号

1070790-89-4
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
溶解性数据
In Vitro: 

DMSO : ≥ 100 mg/mL (251.56 mM)

* “≥” means soluble, but saturation unknown.

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 2.5156 mL 12.5780 mL 25.1560 mL
5 mM 0.5031 mL 2.5156 mL 5.0312 mL
10 mM 0.2516 mL 1.2578 mL 2.5156 mL

*

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, 6 months; -20°C, 1 month。-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。

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：

——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

  • 1.

    请依序添加每种溶剂： 10% DMSO    40% PEG300    5% Tween-80    45% saline

    Solubility: ≥ 2.5 mg/mL (6.29 mM); Clear solution

    此方案可获得 ≥ 2.5 mg/mL (6.29 mM，饱和度未知) 的澄清溶液。

    以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

    将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液

  • 2.

    请依序添加每种溶剂： 10% DMSO    90% (20% SBE-β-CD in saline)

    Solubility: ≥ 2.5 mg/mL (6.29 mM); Clear solution

    此方案可获得 ≥ 2.5 mg/mL (6.29 mM，饱和度未知) 的澄清溶液。

    以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。

    将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
  • 3.

    请依序添加每种溶剂： 10% DMSO    90% corn oil

    Solubility: ≥ 2.5 mg/mL (6.29 mM); Clear solution

    此方案可获得 ≥ 2.5 mg/mL (6.29 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

    以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

  • 4.

    请依序添加每种溶剂： 5% DMSO    40% PEG300    5% Tween-80    50% saline

    Solubility: ≥ 2.5 mg/mL (6.29 mM); Clear solution

*以上所有助溶剂都可在 上海金畔生物科技有限公司 网站选购。
参考文献

  • [1]. Cocco E, et al. Dual CCNE1/PIK3CA targeting is synergistic in CCNE1-amplified/PIK3CA-mutated uterine serous carcinomas in vitro and in vivo. Br J Cancer. 2016 Jul 26;115(3):303-11.

    [2]. Sumana Devata, et al. Molecular markers and venous thromboembolism (VTE) in acute myelogenous leukemia (AML)
Cell Assay
[1]

The effect of CYC065 on the viability and IC50 of USC-ARK-1, USC-ARK-2, USC-ARK-7, USC-ARK-4 and USC-ARK-6 USC primary cell lines is determined in flow-cytometry assay. Briefly, tumour cells are plated in six-well plates and treated with a titration of CYC065 concentrations (i.e., ranging from 100 to 500 nM). After 72 h, cells are harvested, washed and stained with propidium iodide (PI; 5 μg/mL) for flow cytometric counts. The percentage of viable cells is then normalised considering the vehicle-treated cells as 100% viable. Half-maximal inhibitory concentration values are determined using GraphPad Prism5 version 6. For drug combination studies, USC-ARK-1 and USC-ARK-2 cell lines are incubated with the combination of Taselisib and CYC065 at multiple paired concentrations including the IC50, the IC50/2 and the IC50*2 of each cell line to the corresponding drug (i.e., 10 nM of Taselisib and 198 nM of CYC065 for USC-ARK-1 and 50 nM of Taselisib and 62.5 nM of CYC065 for USC-ARK-2). Synergism is assessed by the combination index (CI). CI values <1 define a synergistic activity of the combination treatment. ci values are calculated using compusyn software[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration
[1]

Mice[1]
The in vivo efficacy of CYC065 used as a single agent is evaluated on xenograft mouse models derived from the CCNE1-amplified USC-ARK-2 USC cell line. Xenografts derived from the CCNE1-amplified, PIK3CA-mutated USC-ARK-1 cell line are used for evaluating the in vivo combination of CYC065 and Taselisib. Briefly, 5-7-week-old SCID mice are injected into the subcutaneous region with USC cells. A minimum of five animals per group are used. Treatments are administrated by oral gavage starting 1 week after tumor implantation when the size of the tumor is 0.125-0.150 cm3. Uterine serous carcinoma-ARK-2-derived xenografts are divided into two groups: one group of animal receive the vehicle, whereas the experimental group receive CYC065 (22.5 mg/kg daily for 3 weeks). Uterine serous carcinoma-ARK-1-derived xenografts are instead divided into four groups: one group receive the vehicle (0.5% methylcellulose-0.2% Tween-80), one group receive CYC065 (22.5 mg/kg daily for 3 weeks), one group receive Taselisib (10 mg/kg daily, 5 days per week per 3 weeks) and the last group receive the combination of CYC065 and Taselisib. The size of the tumor at the initiation of treatment is 0.125-0.150 cm3. Mouse weight and tumor size is recorded two times a week for the entire experimental period. Tumor volume is calculated.

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献

  • [1]. Cocco E, et al. Dual CCNE1/PIK3CA targeting is synergistic in CCNE1-amplified/PIK3CA-mutated uterine serous carcinomas in vitro and in vivo. Br J Cancer. 2016 Jul 26;115(3):303-11.

    [2]. Sumana Devata, et al. Molecular markers and venous thromboembolism (VTE) in acute myelogenous leukemia (AML)

所有产品仅用作科学研究或药证申报，我们不为任何个人用途提供产品和服务