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MK-1775 {[allProObj[0].p_purity_real_show]}

货号：A399066 同义名： Adavosertib; AZD1775

Adavosertib (AZD-1775; MK-1775) 具有强效的Wee1抑制作用，IC50为5.2 nM。

MK-1775 化学结构 CAS号：955365-80-7
MK-1775 化学结构
CAS号：955365-80-7
MK-1775 3D分子结构
CAS号：955365-80-7
MK-1775 化学结构 CAS号：955365-80-7
MK-1775 3D分子结构 CAS号：955365-80-7
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MK-1775 纯度/质量文件 产品仅供科研

货号：A399066 标准纯度： {[allProObj[0].p_purity_real_show]}
批次查询： 批次纯度:

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产品名称 Wee1 ↓ 其他靶点 纯度
MK-1775 +++

Wee1, IC50: 5.2 nM

 		98%
PD0166285 ++

Wee1, IC50: 24 nM

 		99%+
1. 鼠标悬停在“+”上可以显示相关IC50的具体数值。"+"越多，抑制作用越强。2. "✔"表示该化合物对相应的亚型有抑制作用，但抑制强度暂时没有相关数据。

MK-1775 生物活性

靶点

  • Wee1

    Wee1, IC50:5.2 nM
描述 Wee1 is a cellular protein kinase which inhibits Cdc2 activity, thereby preventing cells from proceeding through mitosis by maintaining G2 arrest. MK-1775 (AZD1775) is a first-in-class, pyrazolo-pyrimidine derivative and potent small-molecule inhibitor of Wee1 kinase with IC50 of 5.2 nM and blocks G2 DNA damage checkpoint[3]. In vitro, MK-1775 treatment at 500 nM for 48h caused S arrest or both S and G2/M arrest in human pancreatic cancer cell lines AsPC-1, BxPC-3, CFPAC-1, HPAC, MIAPaCa-2 and PANC-1[4]. In vivo, MK-1775 (20 mg/kg) twice daily combined with and panobinostat (10 mg/kg) once daily treatment in mice bearing BxPC-3 xenograft tumors, resulted in significant delay of tumor growth during the treatment period compared to single drug treatment, with 58.7% tumor growth inhibition on day 20[5]. The combination of gemcitabine (100 mg/kg, i.p., twice weekly on days 1 and 4, for 4 weeks) with MK-1775 (30 mg/kg. p.o., once daily for 4 weeks) produced robust antitumor activity and remarkably enhanced tumor regression response (4.01-fold) compared to gemcitabine treatment in p53-deficient tumors[6].

MK-1775 细胞实验

Cell Line
Concentration Treated Time Description References
SKM-1 100 nM 72 h MK-1775 increased cytotoxicity in SKM-1 cells Cancer Cell Int. 2023 Jun 27;23(1):128.
SKM-1 100 nM 72 h MK-1775 inhibited the proliferation of SKM-1 cells Cancer Cell Int. 2023 Jun 27;23(1):128.
NB4 cells 75 nM 2 h MK-1775 inhibited the phosphorylation of CDK1. Leukemia. 2015 Jan;29(1):27-37.
NB4 cells 75 nM 2 h MK-1775 suppressed phosphorylation of cdc2 (CDK1) Leukemia. 2015 Jan;29(1):27-37.
LASCPC-01 0.38 μM 4 days AZD1775 inhibited the growth of LASCPC tumor spheroids Oncogene. 2024 Mar;43(11):789-803.
NCI-H660 1.14 μM 96 hours AZD1775 showed time-dependent cell killing in NCI-H660 cells Oncogene. 2024 Mar;43(11):789-803.
PC3 1.21 μM 96 hours AZD1775 showed time-dependent cell killing in PC3 cells Oncogene. 2024 Mar;43(11):789-803.
C4-2B 0.58 μM 96 hours AZD1775 showed time-dependent cell killing in C4-2B cells Oncogene. 2024 Mar;43(11):789-803.
22Rv1 0.71 μM 96 hours AZD1775 showed time-dependent cell killing in 22Rv1 cells Oncogene. 2024 Mar;43(11):789-803.
DU145 0.38 μM 96 hours AZD1775 at lower concentrations (≤0.38 μM) stimulated cell proliferation, while at higher concentrations (>0.38 μM) decreased cell viability/proliferation Oncogene. 2024 Mar;43(11):789-803.
SKM-1 100 nM 24 h MK-1775 increased caspase 3 and PARP activity in SKM-1 cells Cancer Cell Int. 2023 Jun 27;23(1):128.
AML cell lines 200-400 nM 72 h MK-1775 induced apoptosis in AML cells, accompanied by decreased phosphorylation of CDK1 and CDK2 and increased DNA double-strand breaks. J Hematol Oncol. 2014 Aug 1;7:53.
CTS and U937 cell lines 500 nM 48 h MK-1775 treatment abrogated the G2/M cell cycle checkpoint, accompanied by increased γH2AX and decreased p-CDK1 and p-CDK2. J Hematol Oncol. 2014 Aug 1;7:53.
MCF7 cells 200 nM 72 h MK-1775 in combination with Alisertib selectively induced apoptosis in RB-deficient cells by inhibiting WEE1 and AURK. Oncogene. 2022 Jul;41(27):3524-3538.
T47D cells 200 nM 48 h MK-1775 in combination with Alisertib selectively induced apoptosis in RB-deficient cells by inhibiting WEE1 and AURK. Oncogene. 2022 Jul;41(27):3524-3538.
PCI-13 cells 0.25 μM 48 h MK-1775 significantly enhanced the cytotoxic effect of cisplatin in p53-deficient HNSCC cells, as evidenced by the shift in the cisplatin response curve and a significant reduction in IC values. Mol Cancer Ther. 2015 Feb;14(2):608-19.
SKM-1 100 nM 72 h MK-1775 alone inhibited the proliferation of SKM-1 cells, increased cellular cytotoxicity and caspase 3/7 activity. Cancer Cell Int. 2023 Jun 27;23(1):128.
Ba/F3-NRAS-G12D cells 75 nM 2 h MK-1775 combined with mTOR inhibitors inhibited the phosphorylation of AKT, 4E-BP1, and S6K. Leukemia. 2015 Jan;29(1):27-37.
Ba/F3-KRAS-G12D cells 75 nM 2 h MK-1775 combined with mTOR inhibitors inhibited the phosphorylation of AKT, 4E-BP1, and S6K. Leukemia. 2015 Jan;29(1):27-37.
Ba/F3-NRAS-G12D cells 75 nM 2 h MK-1775 combined with mTOR inhibitors suppressed phosphorylation of AKT, 4E-BP1, and S6K Leukemia. 2015 Jan;29(1):27-37.
Ba/F3-KRAS-G12D cells 75 nM 2 h MK-1775 combined with mTOR inhibitors suppressed phosphorylation of AKT, 4E-BP1, and S6K Leukemia. 2015 Jan;29(1):27-37.
ASPC-1 13.2 μM 48 h MK-1775 treatment caused S phase or both S and G2/M phase arrest, accompanied by increased H2AX phosphorylation, indicating increased DNA double-strand breaks, and activation of CHK1 Cancer Lett. 2015 Jan 28;356(2 Pt B):656-68.
BxPC-3 0.8 μM 48 h MK-1775 treatment caused S phase or both S and G2/M phase arrest, accompanied by increased H2AX phosphorylation, indicating increased DNA double-strand breaks, and activation of CHK1 Cancer Lett. 2015 Jan 28;356(2 Pt B):656-68.
CFPAC-1 3.3 μM 48 h MK-1775 treatment caused S phase or both S and G2/M phase arrest, accompanied by increased H2AX phosphorylation, indicating increased DNA double-strand breaks, and activation of CHK1 Cancer Lett. 2015 Jan 28;356(2 Pt B):656-68.
HPAC 0.5 μM 48 h MK-1775 treatment caused S phase or both S and G2/M phase arrest, accompanied by increased H2AX phosphorylation, indicating increased DNA double-strand breaks, and activation of CHK1 Cancer Lett. 2015 Jan 28;356(2 Pt B):656-68.
MIAPaCa-2 0.5 μM 48 h MK-1775 treatment caused S phase or both S and G2/M phase arrest, accompanied by increased H2AX phosphorylation, indicating increased DNA double-strand breaks, and activation of CHK1 Cancer Lett. 2015 Jan 28;356(2 Pt B):656-68.
PANC-1 10.6 μM 48 h MK-1775 treatment caused S phase or both S and G2/M phase arrest, accompanied by increased H2AX phosphorylation, indicating increased DNA double-strand breaks, and activation of CHK1 Cancer Lett. 2015 Jan 28;356(2 Pt B):656-68.
Ba/F3-KRAS-G12D cells 75 nM 2 h Evaluate the effect of MK-1775 combined with mTOR inhibitors on mutant KRAS-expressing cells Leukemia. 2015 Jan;29(1):27-37.

MK-1775 动物实验

Species
Animal Model
Administration Dosage Frequency Description References
Mice MCF7 xenograft models Oral 30 mg/kg Every other day for 3 weeks MK-1775 in combination with Alisertib significantly inhibited the growth of RB-deficient tumors, while having limited effect on RB-proficient tumors. Oncogene. 2022 Jul;41(27):3524-3538.
Nude mice Oral tongue cancer model Oral 30 mg/kg Twice weekly for 4 weeks MK-1775 significantly enhanced the antitumor efficacy of cisplatin in high-risk TP53 mutant HNSCC tumors, as evidenced by significant delay in tumor growth. Mol Cancer Ther. 2015 Feb;14(2):608-19.
Mice Inducible mutant Kras lung cancer model Oral 10 mg/kg Once daily for one week The combination of MK-1775 and Torin 2 significantly suppressed tumor growth. Leukemia. 2015 Jan;29(1):27-37.
BALB/c nude mice BxPC-3 xenograft model Oral gavage 20 mg/kg Twice a week for three weeks MK-1775 alone had modest delay of tumor growth, while combination with panobinostat significantly delayed tumor growth with 58.7% inhibition Cancer Lett. 2015 Jan 28;356(2 Pt B):656-68.

MK-1775 临床研究

NCT号 适应症或疾病 临床期 招募状态 预计完成时间 地点
NCT03385655 Prostate Cancer Phase 2 Recruiting December 31, 2020 Canada, Alberta ... 展开 >> Cross Cancer Institute Recruiting Edmonton, Alberta, Canada, T6G 1Z2 Contact: Michael Kolinsky    780 432-8762       Canada, British Columbia BCCA - Vancouver Cancer Centre Recruiting Vancouver, British Columbia, Canada, V5Z 4E6 Contact: Kim Chi    604 877-6000 ext 2746       Canada, Nova Scotia QEII Health Sciences Centre Recruiting Halifax, Nova Scotia, Canada, B3H 1V7 Contact: Robyn J. Macfarlane    902 473-6106       Canada, Ontario Juravinski Cancer Centre at Hamilton Health Sciences Recruiting Hamilton, Ontario, Canada, L8V 5C2 Contact: Som Mukherjee    905 387-9495 ext 64605       London Regional Cancer Program Recruiting London, Ontario, Canada, N6A 5W9 Contact: Eric W. Winquist    519 685-8261       Ottawa Hospital Research Institute Recruiting Ottawa, Ontario, Canada, K1H 8L6 Contact: Michael Ong    613 737-7700 ext 75051       University Health Network Recruiting Toronto, Ontario, Canada, M5G 2M9 Contact: Adrian Sacher    416 946-4501 ext 3550       Canada, Quebec CHUM-Centre Hospitalier de l'Universite de Montreal Recruiting Montreal, Quebec, Canada, H2X 3E4 Contact: Fred Saad    514 890-8000 ext 27466       The Jewish General Hospital Recruiting Montreal, Quebec, Canada, H3T 1E2 Contact: Cristiano Ferrario    514 398-8307       Canada, Saskatchewan Allan Blair Cancer Centre Recruiting Regina, Saskatchewan, Canada, S4T 7T1 Contact: Muhammad Salim    306 766-2691       Saskatoon Cancer Centre Recruiting Saskatoon, Saskatchewan, Canada, S7N 4H4 Contact: Nayyer Iqbal    306 655-2710 收起 <<
NCT02546661 Muscle Invasive Bladder Cancer Phase 1 Recruiting March 27, 2020 -
NCT02813135 Children, Adolescents and Youn... 展开 >>g Adults With Refractory or Recurrent Malignancies 收起 << Phase 1 Phase 2 Recruiting January 2022 France ... 展开 >> Gustave Roussy Recruiting Villejuif, Val De Marne, France, 94805 Contact: Birgit Geoerger, MD    1 42 11 4661 ext +33    birgit.geoerger@gustaveroussy.fr    Contact: Xavier Paoletti, MD    1 42 11 6564 ext +33    xavier.paoletti@gustaveroussy.fr    Principal Investigator: Birgit Geoerger, MD          Germany University Children's Hospitalermany Not yet recruiting Heidelberg, Germany Contact: Olaf Witt, MD    6221 56 4555 ext +49    O.Witt@Dkfz-Heidelberg.de    Italy Fondazione IRCCS Istituto Nazionale dei Tumori Not yet recruiting Milan, Italy Contact: Michela Casanova, MD    02 23 90 25 94 ext +39    Michela.Casanova@istitutotumori.mi.it    Netherlands Erasmus MC, Sophia Children's Hospital Not yet recruiting Rotterdam, Netherlands Contact: Michel Zwaan, MD    10 703 6691 ext +31    c.m.zwaan@erasmusmc.nl    Spain Unidad de Oncología Pediátrica Hospital Niño Jesús Not yet recruiting Madrid, Spain, 28009 Contact: Francisco Bautista, MD    915 035 900 ext +43    franciscojose.bautista@salud.madrid.org    United Kingdom Pediatric and Adolescent Oncology The Royal Marsden Hospital Not yet recruiting Sutton, United Kingdom Contact: Lynley Marshall, MD    208 661 3678 ext +44    Lynley.Marshall@icr.ac.uk 收起 <<

MK-1775 参考文献

[1]Do K, Wilsker D, Ji J, Zlott J, Freshwater T, Kinders RJ, Collins J, Chen AP, Doroshow JH, Kummar S. Phase I Study of Single-Agent AZD1775 (MK-1775), a Wee1 Kinase Inhibitor, in Patients With Refractory Solid Tumors. J Clin Oncol. 2015 Oct 20;33(30):3409-15. doi: 10.1200/JCO.2014.60.4009. Epub 2015 May 11. PMID: 25964244; PMCID: PMC4606059.

[2]Wang G, Niu X, Zhang W, Caldwell JT, Edwards H, Chen W, Taub JW, Zhao L, Ge Y. Synergistic antitumor interactions between MK-1775 and panobinostat in preclinical models of pancreatic cancer. Cancer Lett. 2015 Jan 28;356(2 Pt B):656-68. doi: 10.1016/j.canlet.2014.10.015. Epub 2014 Oct 18. PMID: 25458954; PMCID: PMC4282784.

[3]Wang G, Niu X, Zhang W, Caldwell JT, Edwards H, Chen W, Taub JW, Zhao L, Ge Y. Synergistic antitumor interactions between MK-1775 and panobinostat in preclinical models of pancreatic cancer. Cancer Lett. 2015 Jan 28;356(2 Pt B):656-68. doi: 10.1016/j.canlet.2014.10.015. Epub 2014 Oct 18. PMID: 25458954; PMCID: PMC4282784.

[4]Rajeshkumar NV, De Oliveira E, Ottenhof N, Watters J, Brooks D, Demuth T, Shumway SD, Mizuarai S, Hirai H, Maitra A, Hidalgo M. MK-1775, a potent Wee1 inhibitor, synergizes with gemcitabine to achieve tumor regressions, selectively in p53-deficient pancreatic cancer xenografts. Clin Cancer Res. 2011 May 1;17(9):2799-806. doi: 10.1158/1078-0432.CCR-10-2580. Epub 2011 Mar 9. PMID: 21389100; PMCID: PMC3307341.

MK-1775 实验方案

计算器
存储液制备 1mg 5mg 10mg

1 mM

5 mM

10 mM

2.00mL

0.40mL

0.20mL

9.99mL

2.00mL

1.00mL

19.98mL

4.00mL

2.00mL

MK-1775 技术信息

CAS号955365-80-7
分子式C27H32N8O2
分子量 500.6
SMILES Code O=C1N(CC=C)N(C2=NC(C(C)(O)C)=CC=C2)C3=NC(NC4=CC=C(N5CCN(C)CC5)C=C4)=NC=C31
MDL No. MFCD17215200
别名 Adavosertib; AZD1775
运输蓝冰
InChI Key BKWJAKQVGHWELA-UHFFFAOYSA-N
Pubchem ID 24856436
存储条件

In solvent -20°C: 3-6个月 -80°C: 12个月

Pure form Keep in dark place, sealed in dry, store in freezer, under -20°C
溶解方案

DMSO: 120 mg/mL(239.71 mM)，配合低频超声助溶，注意：DMSO长时间开封后，会吸水并导致溶解能力下降，请避免使用长期开封的DMSO

请根据您的动物给药指南选择适当的溶解方案。
以下溶解方案都请先按照体外实验的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
方案 一
方案 二
方案 三
方案 四
配制的工作液建议现用现配，短期内尽快用完。 以下溶剂前显示的百分比是指该溶剂在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。
方案 一

Tags: MK-1775 | Wee1 | AmBeed-信号通路专用抑制剂 | MK-1775 纯度/质量文件 | MK-1775 亚型比较 | MK-1775 生物活性 | MK-1775 临床数据 | MK-1775 参考文献 | MK-1775 实验方案 | MK-1775 技术信息

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