Adavosertib (MK-1775)

Catalog No.S1525

Adavosertib (MK-1775) Chemical Structure

Molecular Weight(MW): 500.6

MK-1775 is a potent and selective Wee1 inhibitor with IC50 of 5.2 nM in a cell-free assay; hinders G2 DNA damage checkpoint. Phase 2.

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In DMSO USD 238 In stock
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Cited by 13 Publications

7 Customer Reviews

  • Panobinostat enhances the antitumor activity of MK-1775 in a BxPC-3 xenograft model. Tumor specimens were fixed in 10% formalin, embedded in paraffin, and cut into 4 μM-thick slides for H&E staining.

    Cancer Letters, 2015, 356(200): 656–668 . Adavosertib (MK-1775) purchased from Selleck.

    Diagnostic AML blasts from patients either at first diagnosis or at relapse are equally sensitive to MK-1775. Freshly isolated cells from patient AML#10 were purified by standard Ficoll-Hypaque density centrifugation. AML#10, HL-60, and HL-60/Ara-C cells were treated with MK-1775 for 48 h. Whole cell lysates were subjected to Western blotting and probed with anti-p-CDK1, -CDK1, -p-CDK2, -CDK2, -γH2AX, or -β-actin antibody.

    J Hematol Oncol 2014 7:53. Adavosertib (MK-1775) purchased from Selleck.

  • Front Oncol, 2018, 8:143. Adavosertib (MK-1775) purchased from Selleck.

    (C) Nude mice bearing MDA-MB-231 xenograft tumors were treated with vehicle, MK-1775, cisplatin, or a combination of cisplatin and MK-1775 for 28 days and tumor volumes were measured. Data are presented as the mean of 8 tumors for each group ± SEM.

    Sci Rep, 2017, 7:43517. Adavosertib (MK-1775) purchased from Selleck.

  • GH activates STAT5 and ERK in breast cancer cells. T47D cells were pretreated for 2 hours with vehicle (dimethylsulfoxide) or inhibitors for EGFR (AG1478, 15 uM) or JAK2 (AZD1480, 1 uM), followed by treatment with GH+E2 for 30 minutes.

    Endocrinology 2013 154(9), 3219-27. Adavosertib (MK-1775) purchased from Selleck.

    AZD1480 inhibits the JAK2/STAT3 pathway in vitro. HT29 cells were cultured in 24-well plates overnight and then treated with 1 uM AZD1480 for 2 h followed by 4 ng/ml, IL-6 for 2 h and the distribution of phosphorylated STAT3 was analyzed by immunofluorescence.

    Oncol Rep 2014 32(5), 1991-8. Adavosertib (MK-1775) purchased from Selleck.

  • Histopathological assessment of tumor response to MK-1775 alone and in combination with gemcitabine in a patient-derived osteosarcoma mouse model. A. H&E-stained paraffin sections were prepared to assess microscopic features of cell death and differentiation representative micrographs of B. Ki67 shows high immunoreactivity in the control, MK-1775, and combination treatments compared to gemcitabine treatment. C. Cleaved-caspase 3 images show high immunoreactivity in the MK-1775 and combination treatments compared to vehicle and gemcitabine treatment. D. Slides stained for γH2AX show high immunoreactivity in gemcitabine, MK-1775, and combination treatments compared to controls. E. Slides stained for Cyclin A show higher immunoreactivity in gemcitabine but not in control, MK-1775 alone or in combination treatments.

    PLoS One 2013 8(3), e57523. Adavosertib (MK-1775) purchased from Selleck.

Purity & Quality Control

Choose Selective Wee1 Inhibitors

Biological Activity

Description MK-1775 is a potent and selective Wee1 inhibitor with IC50 of 5.2 nM in a cell-free assay; hinders G2 DNA damage checkpoint. Phase 2.
Features The first reported Wee1 inhibitor.
Targets
Wee1 [1]
(Cell-free assay)
5.2 nM
In vitro

MK-1775 inhibits Wee1 kinase in an ATP-competitive manner. Compared to Wee1, MK-1775 displays 2- to 3-fold less potency against Yes with IC50 of 14 nM, 10-fold less potency against seven other kinases with >80% inhibition at 1 μM, and >100-fold selectivity over human Myt 1, another kinase that inhibits cyclin-dependent kinase 1 (CDC2) by phosphorylation at an alternative site (Thr14). By abrogating the DNA damage checkpoint via blockade of Wee1 activity in WiDr cells bearing mutated p53, MK-1775 treatment inhibits the basal phosphorylation of CDC2 at Tyr15 (CDC2Y15) with EC50 of 49 nM, and suppresses gemcitabine-, carboplatin- or cisplatin-induced phosphorylation of CDC2 and cell cycle arrest in a dose-dependent manner, with EC50 of 82 nM and 81 nM, 180 nM and 163 nM, as well as 159 nM and 160 nM, respectively. MK-1775 treatment alone at 30-100 nM has no significant antiproliferative effect in WiDr and H1299 cells, whereas MK-1775 at 300 nM, sufficient to inhibit Wee1 by >80%, displays moderate but significant antiproliferative effects by 34.1% in WiDr cells and 28.4% in H1299 cells. [1]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
ASPC-1 NFLWRZJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M33oRWlEPTB;MUOuNkDDuSBzLkGg{txO MmPHNlU1PTh7NUS=
BxPC-3 NGPiN|NIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NF;Ib4xKSzVyPUCuPEDDuSByLkCzJO69VQ>? M{jaXlI2PDV6OUW0
CFPAC-1 NEfkNlRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkHzTWM2OD1|LkOgxtEhOC5{IN88US=> NXHIN2lvOjV2NUi5OVQ>
HPAC MmPVS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NEK4eolKSzVyPUCuOUDDuSByLkCxJO69VQ>? MnPlNlU1PTh7NUS=
MIAPaCa-2 MonQS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYG2RlBFUUN3ME2wMlUhyrFiMD6wOUDPxE1? NYCxcVNpOjV2NUi5OVQ>
PANC-1 M1fQR2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlnKTWM2OD1zMD62JOKyKDFwMTFOwG0> NVvWPHd2OjV2NUi5OVQ>
SK-N-BE (2) MmLoS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3r2SGlEPTB;Mj605qCKyrIkgJmwMlMh|ryP NFexUpMzPTNyOEmxOi=>
SK-N-BE (2), PAN→MK NIr4SpZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYnJR|UxRTJ4LkdihKnDueLCiUmuOkDPxE1? MV6yOVMxQDlzNh?=
SK-N-BE (2), MK→PAN MWnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NEfVc2pKSzVyPUKuOQKBkcLz4pEJNE4{KM7:TR?= NEXhZZAzPTNyOEmxOi=>
SK-N-AS M4jBVWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NIPhdZdKSzVyPUCuOVDjiIoEsfMAjVAvODJizszN M13mTlI2OzB6OUG2
SK-N-DZ MWLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWm2OGs6UUN3ME2wMlM36oDLwsJihKkxNjBzIN88US=> MmHhNlU{ODh7MU[=
SK-N-AS MlnhRZBweHSxc3nzJGF{e2G7 M2\HN|UxOCCwTR?= M3zqclQ5KGh? NWX6Ro9CcW6mdXPld{Bk\WyuIHHwc5B1d3Orcx?= NHvhNlkzPTNyOEmxOi=>
SK-N-DZ NVyybnFqSXCxcITvd4l{KEG|c3H5 NETad2k2ODBibl2= NF7Y[Gc1QCCq MkLCbY5lfWOnczDj[YxtKGGyb4D0c5Nqew>? MlHTNlU{ODh7MU[=
THP-1 NIe4RpRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVvZWHNWOTJ3L{K1NE82ODBibl2= M4e1eFQ5KGh? NFXXOmVqdmO{ZXHz[ZMh[2WubDDk[YF1cCCrbjDhJINwdmOnboTyZZRqd25vZHXw[Y5l\W62IH3hco5meg>? M1i4TlI2ODh2NkG0
MV4-11 NY\mRWJFT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NIDweW0yOjVxMkWwM|UxOCCwTR?= NWjV[mVxPDhiaB?= NYjQNIE4cW6lcnXhd4V{KGOnbHyg[IVifGhiaX6gZUBkd26lZX70doF1cW:wLXTldIVv\GWwdDDtZY5v\XJ? MVyyOVA5PDZzNB?=
U937 NUfFSFJZT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3HQdVEzPS9{NUCvOVAxKG6P M2XYS|Q5KGh? MYrpcoNz\WG|ZYOgZ4VtdCCmZXH0bEBqdiCjIHPvcoNmdnS{YYTpc44u\GWyZX7k[Y51KG2jbn7ldi=> MkK0NlUxQDR4MUS=
HL-60 NXS0d49KT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mly5NVI2NzJ3MD:1NFAhdk1? MYq0PEBp MmnEbY5kemWjc3XzJINmdGxiZHXheIghcW5iYTDjc45k\W62cnH0bY9vNWSncHXu[IVvfCCvYX7u[ZI> MU[yOVA5PDZzNB?=
OCI-AML3 MXzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MknKNVI2NzJ3MD:1NFAhdk1? MkXJOFghcA>? NFi3cGlqdmO{ZXHz[ZMh[2WubDDk[YF1cCCrbjDhJINwdmOnboTyZZRqd25vZHXw[Y5l\W62IH3hco5meg>? NFLrVXAzPTB6NE[xOC=>
MOLM-13 MkLzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXPaWHJCOTJ3L{K1NE82ODBibl2= MUG0PEBp NHLSSFBqdmO{ZXHz[ZMh[2WubDDk[YF1cCCrbjDhJINwdmOnboTyZZRqd25vZHXw[Y5l\W62IH3hco5meg>? M3XueFI2ODh2NkG0
CMK M1XyOWNmdGxiVnnhZoltcXS7IFHzd4F6 MXGxNE0yODByMDDuUS=> M37WblczKGh? MVzy[YR2[2W|IHPlcIwhfmmjbHnibZR6KGmwIHGgZ49v[2WwdILheIlwdi2mZYDlcoRmdnRibXHucoVz M4fleFI1QTZ{M{Ox
CMY MU\D[YxtKF[rYXLpcIl1gSCDc4PhfS=> MoTXNVAuOTByMECgcm0> NGHjfI04OiCq MULy[YR2[2W|IHPlcIwhfmmjbHnibZR6KGmwIHGgZ49v[2WwdILheIlwdi2mZYDlcoRmdnRibXHucoVz NVPHT3Q3OjR7NkKzN|E>
Dayo M3PQVmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3rVdmlEPTB;MUWwJI5O M{LCblI1PjZzOUGw
UW228 Mnq0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MoT6TWM2OD1{M{Kgcm0> MV2yOFY3OTlzMB?=
IST-MES1 MlXzR4VtdCCYaXHibYxqfHliQYPzZZk> MWCxOVAwOjVyIH7N MX63NkBp M4TROoVvcGGwY3XzJJRp\SClaYPwcIF1cW5iY4n0c5RwgGmlIHXm[oVkfCCrbjDhJINwdmOnboTyZZRqd25vZHXw[Y5l\W62IH3hco5meg>? NGDBTHAzPDN4NUe4Ni=>
IST-MES2 NIP0XJpE\WyuIG\pZYJqdGm2eTDBd5NigQ>? NVjO[VBNOTVyL{K1NEBvVQ>? NXzDUHJGPzJiaB?= NWHFNGwz\W6qYX7j[ZMhfGinIHPpd5Bt[XSrbjDjfZRwfG:6aXOg[YZn\WO2IHnuJIEh[2:wY3XueJJifGmxbj3k[ZBmdmSnboSgcYFvdmW{ NFXxS5czPDN4NUe4Ni=>
REN MX7D[YxtKF[rYXLpcIl1gSCDc4PhfS=> Mn;6NVUxNzJ3MDDuUS=> MUC3NkBp NYrzfpps\W6qYX7j[ZMhfGinIHPpd5Bt[XSrbjDjfZRwfG:6aXOg[YZn\WO2IHnuJIEh[2:wY3XueJJifGmxbj3k[ZBmdmSnboSgcYFvdmW{ M{e3R|I1OzZ3N{iy
NCI-H2452 MlLVR4VtdCCYaXHibYxqfHliQYPzZZk> NEP4d|YyPTBxMkWwJI5O NFXSfmM4OiCq NHPT[o9mdmijbnPld{B1cGViY3nzdIxifGmwIHP5eI91d3irYzDl[oZm[3RiaX6gZUBkd26lZX70doF1cW:wLXTldIVv\GWwdDDtZY5v\XJ? MVqyOFM3PTd6Mh?=
MSTO-211H MUjD[YxtKF[rYXLpcIl1gSCDc4PhfS=> NYTiVYRNOTVyL{K1NEBvVQ>? NIfnZnU4OiCq M1Pub4VvcGGwY3XzJJRp\SClaYPwcIF1cW5iY4n0c5RwgGmlIHXm[oVkfCCrbjDhJINwdmOnboTyZZRqd25vZHXw[Y5l\W62IH3hco5meg>? MYmyOFM3PTd6Mh?=
NCI-H2052 NEjENG1E\WyuIG\pZYJqdGm2eTDBd5NigQ>? NVXYXllWOTVyL{K1NEBvVQ>? MkXSO|IhcA>? NVzSbmQ{\W6qYX7j[ZMhfGinIHPpd5Bt[XSrbjDjfZRwfG:6aXOg[YZn\WO2IHnuJIEh[2:wY3XueJJifGmxbj3k[ZBmdmSnboSgcYFvdmW{ MlvSNlQ{PjV5OEK=
WEE1 MmXhS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NX\LcWFuUUN3ME21MlIhdk1? NIrIdXEzOzZ7OU[1OS=>
CDC2 MnXBS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHHncI1KSzVy78{eNVAxOCCwTR?= MU[yN|Y6QTZ3NR?=
CDK7 M{S1Zmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUPJR|Ux97zgMUCwNEBvVQ>? MkHwNlM3QTl4NUW=
MYT1 NYrs[XFsT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFvqNFVKSzVyPUWzNEBvVQ>? MVWyN|Y6QTZ3NR?=
T98G  NXztXJBKSXCxcITvd4l{KEG|c3H5 NX3kdI43OTByL{K1NEBvVQ>? NHT0NYY3KGh? NHu0bFhmdmijbnPld{Bz[WSrYYTpc44ucW6mdXPl[EBk\WyuIHvpcIxqdmd? MV:yNVk6Ojd7Mx?=
A549 NULwb4lYSXCxcITvd4l{KEG|c3H5 MkLCNlAxKG6P NIDlN2syKGh? NXjaNJNHemGmaX;z[Y5{cXSrenXzJG5US0yFIHPlcIx{KGmwIHGgdFU{NWSncHXu[IVvfCCvYX7u[ZI> NYn3VY1kOjF5OUmwN|M>
H460 M4rN[GFxd3C2b4Ppd{BCe3OjeR?= MVSyNFAhdk1? MknUNUBp MWLyZYRqd3OnboPpeIl7\XNiTmPDUGMh[2WubIOgbY4h[SCyNUOt[IVx\W6mZX70JI1idm6nch?= M4fEcVIyPzl7MEOz
H1299 MWHBdI9xfG:|aYOgRZN{[Xl? NFPUc5UzODBibl2= NVvS[4JwOSCq M2\lXZJi\Gmxc3Xud4l1cXqnczDOV2NNSyClZXzsd{BqdiCjIIC1N{1l\XCnbnTlcpQhdWGwbnXy MV6yNVc6QTB|Mx?=
Calu-6  NHLPNFFCeG:ydH;zbZMhSXO|YYm= MYmyNFAhdk1? NE[zZ4IyKGh? M{jKS5Ji\Gmxc3Xud4l1cXqnczDOV2NNSyClZXzsd{BqdiCjIIC1N{1l\XCnbnTlcpQhdWGwbnXy NYXqOmh5OjF5OUmwN|M>
WiDr NW\oUphYU2mwYYPlJGF{e2G7cx?= M1K0bVExNTFyMECwJI5O MmfKPEBp M4SzPIlvcGmkaYTzJJBpd3OyaH;yfYxifGmxbjDv[kBETEN{IHH0JHR6ejF3IIfpeIgh[W5iRVO1NOKhfmGudXWgc4YhQDVibn3vcE9NKHC{ZYTy[YF1\WRid3n0bEBo\W2laYThZolv\Q>? NUXyXVc4OTl6OEe1OFU>

... Click to View More Cell Line Experimental Data

In vivo MK-1775 treatment alone at ~20 mg/kg displays minimal antitumor effects against WiDr xenografts in rats with T/C of 69% at day 3. Antitumor efficacy by MK-1775 alone in the nude rat HeLa-luc and TOV21G-shp53 xenograft models is also moderate. [1]

Protocol

Kinase Assay:

[1]

+ Expand

In vitro kinase assays:

Recombinant human Wee1 is used. Kinase reaction is conducted with 10 μM ATP, 1.0 μCi of [γ-33P]ATP, and 2.5 μg of poly(Lys, Tyr) as a substrate in the presence of increasing concentrations of MK-1775 at 30°C for 30 minutes. Radioactivity incorporated into the substrate is trapped on MultiScreen-PH plates and is counted on a liquid scintillation counter.
Cell Research:

[1]

+ Expand
  • Cell lines: WiDr, NCI-H1299, TOV21G, and HeLa
  • Concentrations: Dissolved in DMSO, final concentrations ~10 μM
  • Incubation Time: 24 hours
  • Method:

    Cells are treated with or without gemcitabine for 24 hours, then with MK-1775 for an additional 24 hours. Cell viability is determined with a WST-8 kit using SpectraMax. Cellular caspase-3/7 activities are determined with a Caspase-3/7 Glo kit.


    (Only for Reference)
Animal Research:

[1]

+ Expand
  • Animal Models: Immunodeficient nude rats (F344/NJcl-rnu) bearing WiDr, HeLa-luc, or TOV21G-shp53 tumors
  • Formulation: Prepared in a vehicle of 0.5% methylcellulose solution
  • Dosages: ~20 mg/kg/day
  • Administration: Orally
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 80 mg/mL (159.8 mM)
Ethanol 10 mg/mL (19.97 mM)
Water 0.0001 mg/mL (0.0 mM)
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
2% DMSO+30% PEG 300+5% Tween 80+ddH2O
For best results, use promptly after mixing.
5mg/mL

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 500.6
Formula

C27H32N8O2

CAS No. 955365-80-7
Storage powder
in solvent
Synonyms N/A

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT02037230 Active not recruiting Adenocarcinoma of the Pancreas University of Michigan Rogel Cancer Center January 2014 Phase 1|Phase 2
NCT02037230 Active not recruiting Adenocarcinoma of the Pancreas University of Michigan Rogel Cancer Center January 2014 Phase 1|Phase 2
NCT01748825 Active not recruiting Neoplasms|Lymphoma National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) December 19 2012 Phase 1
NCT01748825 Active not recruiting Neoplasms|Lymphoma National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) December 19 2012 Phase 1
NCT01357161 Completed Ovarian Cancer Merck Sharp & Dohme Corp. July 26 2011 Phase 2
NCT01357161 Completed Ovarian Cancer Merck Sharp & Dohme Corp. July 26 2011 Phase 2

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

Tel: +1-832-582-8158 Ext:3

If you have any other enquiries, please leave a message.

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Frequently Asked Questions

  • Question 1:

    How to prepare MK1775 methylcellulose solution? and how to prepare methylcellulose itself? Once make the MK1775 methylcellulose solution, how should i keep it?

  • Answer:

    MK1775 in 0.5% methylcellulose is a suspension or emulsion, and it is ok to treat mice orally. It is recommended to dissolve methylcellulose in saline. It will take some time to dissolve methylcellulose, and you can vortex it for a while. The MK1775 methylcellulose solution can be stored at 4°C for a week.

Wee1 Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID