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wee1 kinase inhibitor azd1775  (AstraZeneca ltd)

 
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    AstraZeneca ltd wee1 kinase inhibitor azd1775
    Estimates of dose-limiting toxicity (DLT) rates using the time-to-event continual reassessment method (TITE-CRM) and a two-parameter logistic regression model with 90% CI at each dose level of the <t>Wee1</t> inhibitor <t>AZD1775.</t> The target DLT rate was 0.30. Dose level 1 (150 mg AZD1775) was determined to be the maximum tolerated dose and recommended phase II dose.
    Wee1 Kinase Inhibitor Azd1775, supplied by AstraZeneca ltd, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/wee1+kinase+inhibitor/azd1775/pmc07006846-58-23-28
    Average 90 stars, based on 1 article reviews
    wee1 kinase inhibitor azd1775 - by Bioz Stars, 2026-11
    90/100 stars

    Images

    1) Product Images from "Dose Escalation Trial of the Wee1 Inhibitor Adavosertib (AZD1775) in Combination With Gemcitabine and Radiation for Patients With Locally Advanced Pancreatic Cancer"

    Article Title: Dose Escalation Trial of the Wee1 Inhibitor Adavosertib (AZD1775) in Combination With Gemcitabine and Radiation for Patients With Locally Advanced Pancreatic Cancer

    Journal: Journal of Clinical Oncology

    doi: 10.1200/JCO.19.00730

    Estimates of dose-limiting toxicity (DLT) rates using the time-to-event continual reassessment method (TITE-CRM) and a two-parameter logistic regression model with 90% CI at each dose level of the Wee1 inhibitor AZD1775. The target DLT rate was 0.30. Dose level 1 (150 mg AZD1775) was determined to be the maximum tolerated dose and recommended phase II dose.
    Figure Legend Snippet: Estimates of dose-limiting toxicity (DLT) rates using the time-to-event continual reassessment method (TITE-CRM) and a two-parameter logistic regression model with 90% CI at each dose level of the Wee1 inhibitor AZD1775. The target DLT rate was 0.30. Dose level 1 (150 mg AZD1775) was determined to be the maximum tolerated dose and recommended phase II dose.

    Techniques Used:

    Pharmacodynamics of AZD1775 in surrogate tissues. Sequential punch biopsy samples of hair-bearing skin were obtained after gemcitabine infusion but before AZD1775 administration and after AZD1775 administration. Immunohistochemistry on paraffin-embedded specimens was performed using anti–phosphorylation of cyclin-dependent kinase 1 (phospho-CDK1) antibody. (A) Representative images of phospho-CDK1 staining of hair follicles before and after AZD1775 in a patient treated in this study. (B) Mean percentage of phospho-CDK1–positive hair follicles with 95% CI before and after AZD1775 for each dose level.
    Figure Legend Snippet: Pharmacodynamics of AZD1775 in surrogate tissues. Sequential punch biopsy samples of hair-bearing skin were obtained after gemcitabine infusion but before AZD1775 administration and after AZD1775 administration. Immunohistochemistry on paraffin-embedded specimens was performed using anti–phosphorylation of cyclin-dependent kinase 1 (phospho-CDK1) antibody. (A) Representative images of phospho-CDK1 staining of hair follicles before and after AZD1775 in a patient treated in this study. (B) Mean percentage of phospho-CDK1–positive hair follicles with 95% CI before and after AZD1775 for each dose level.

    Techniques Used: Drug discovery, Immunohistochemistry, Phospho-proteomics, Staining

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    Article Snippet: | Genomic profiling of tumours in patients in clinical trials enables rapid testing of multiple hypotheses to confirm which genomic events determine likely responder groups for targeted agents.. A key challenge of this new capability is defining which specific genomic events should be classified as ‘actionable’ (that is, potentially responsive to a targeted therapy), especially when looking for early indications of patient subgroups likely to be responsive to new drugs.. This Opinion article discusses some of the different approaches being taken in early clinical development to define actionable mutations, and describes our strategy to address this challenge in early-stage exploratory clinical trials.

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    Article Snippet: Initially, the umbrella study will consider drugs from the AstraZeneca DDR inhibitor portfolio, given the favourable potential mechanism of synergy and promising results from other tumour sites (e.g. PARP inhibitor, Wee1 Kinase inhibitor, ATR inhibitor, ATM inhibitor) [21].



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    Estimates of dose-limiting toxicity (DLT) rates using the time-to-event continual reassessment method (TITE-CRM) and a two-parameter logistic regression model with 90% CI at each dose level of the <t>Wee1</t> inhibitor <t>AZD1775.</t> The target DLT rate was 0.30. Dose level 1 (150 mg AZD1775) was determined to be the maximum tolerated dose and recommended phase II dose.
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    Image Search Results


    Functional and biological evaluation of WEE inhibitors in oocytes and somatic cells. (A) ELISA analysis for phosphorylation activity of WEE1 and WEE2 in situ. MK-1775 significantly inhibits WEE1 and WEE2, reducing a greater proportion of WEE2 kinase activity. Error bars represent SEM with P > 0.05 by Student t -test. (B) Fertilization rates of bovine oocytes co-cultured with inhibitor or DMSO (control) during IVF ( N = 126). MK-1775 reduced MII exit compared to DMSO by 16%. (C) Somatic cell division activity (mitosis) was tracked over time by flow cytometry analysis. MK-1775 induced a decrease in mitosis at 0.1 and 0.01 μM and arrested the cell culture at 1 μM.

    Journal: Biology of Reproduction

    Article Title: Development of WEE2 kinase inhibitors as novel non-hormonal female contraceptives that target meiosis †

    doi: 10.1093/biolre/ioaa097

    Figure Lengend Snippet: Functional and biological evaluation of WEE inhibitors in oocytes and somatic cells. (A) ELISA analysis for phosphorylation activity of WEE1 and WEE2 in situ. MK-1775 significantly inhibits WEE1 and WEE2, reducing a greater proportion of WEE2 kinase activity. Error bars represent SEM with P > 0.05 by Student t -test. (B) Fertilization rates of bovine oocytes co-cultured with inhibitor or DMSO (control) during IVF ( N = 126). MK-1775 reduced MII exit compared to DMSO by 16%. (C) Somatic cell division activity (mitosis) was tracked over time by flow cytometry analysis. MK-1775 induced a decrease in mitosis at 0.1 and 0.01 μM and arrested the cell culture at 1 μM.

    Article Snippet: Inhibitor activity against WEE1 and WEE2 were assessed using a CycLex WEE1 Kinase Assay/Inhibitor Screening Kit (Cat# CY-1172; MBL International, Woburn, MA) as previously described [ ].

    Techniques: Functional Assay, Enzyme-linked Immunosorbent Assay, Activity Assay, In Situ, Cell Culture, Flow Cytometry

    Estimates of dose-limiting toxicity (DLT) rates using the time-to-event continual reassessment method (TITE-CRM) and a two-parameter logistic regression model with 90% CI at each dose level of the Wee1 inhibitor AZD1775. The target DLT rate was 0.30. Dose level 1 (150 mg AZD1775) was determined to be the maximum tolerated dose and recommended phase II dose.

    Journal: Journal of Clinical Oncology

    Article Title: Dose Escalation Trial of the Wee1 Inhibitor Adavosertib (AZD1775) in Combination With Gemcitabine and Radiation for Patients With Locally Advanced Pancreatic Cancer

    doi: 10.1200/JCO.19.00730

    Figure Lengend Snippet: Estimates of dose-limiting toxicity (DLT) rates using the time-to-event continual reassessment method (TITE-CRM) and a two-parameter logistic regression model with 90% CI at each dose level of the Wee1 inhibitor AZD1775. The target DLT rate was 0.30. Dose level 1 (150 mg AZD1775) was determined to be the maximum tolerated dose and recommended phase II dose.

    Article Snippet: 15 , 16 Our initial preclinical efforts to target the DDR focused on Chk1 inhibitors, 17 , 18 but we ultimately chose the Wee1 kinase inhibitor AZD1775 (adavosertib; AstraZeneca, Cambridge, United Kingdom), which targets the same pathway, for our clinical trial.

    Techniques:

    Pharmacodynamics of AZD1775 in surrogate tissues. Sequential punch biopsy samples of hair-bearing skin were obtained after gemcitabine infusion but before AZD1775 administration and after AZD1775 administration. Immunohistochemistry on paraffin-embedded specimens was performed using anti–phosphorylation of cyclin-dependent kinase 1 (phospho-CDK1) antibody. (A) Representative images of phospho-CDK1 staining of hair follicles before and after AZD1775 in a patient treated in this study. (B) Mean percentage of phospho-CDK1–positive hair follicles with 95% CI before and after AZD1775 for each dose level.

    Journal: Journal of Clinical Oncology

    Article Title: Dose Escalation Trial of the Wee1 Inhibitor Adavosertib (AZD1775) in Combination With Gemcitabine and Radiation for Patients With Locally Advanced Pancreatic Cancer

    doi: 10.1200/JCO.19.00730

    Figure Lengend Snippet: Pharmacodynamics of AZD1775 in surrogate tissues. Sequential punch biopsy samples of hair-bearing skin were obtained after gemcitabine infusion but before AZD1775 administration and after AZD1775 administration. Immunohistochemistry on paraffin-embedded specimens was performed using anti–phosphorylation of cyclin-dependent kinase 1 (phospho-CDK1) antibody. (A) Representative images of phospho-CDK1 staining of hair follicles before and after AZD1775 in a patient treated in this study. (B) Mean percentage of phospho-CDK1–positive hair follicles with 95% CI before and after AZD1775 for each dose level.

    Article Snippet: 15 , 16 Our initial preclinical efforts to target the DDR focused on Chk1 inhibitors, 17 , 18 but we ultimately chose the Wee1 kinase inhibitor AZD1775 (adavosertib; AstraZeneca, Cambridge, United Kingdom), which targets the same pathway, for our clinical trial.

    Techniques: Drug discovery, Immunohistochemistry, Phospho-proteomics, Staining