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cdk4 6i abemaciclib  (MedChemExpress)


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    Structured Review

    MedChemExpress cdk4 6i abemaciclib
    ( A ) Representative flow cytometry plots showing surface expression of indicated NK cell-activating and inhibiting signals in a PDO158 treated with 1 μM abemaciclib or vehicle control for 5 days. ( B ) Quantification of surface marker expression across 11 PDOs treated as in (A). n=3. ***p < 0.001, ****p < 0.0001 (two-way ANOVA). ( C ) Pie chart showing the proportion of PDOs that upregulated stress ligands and ICAM-1 <t>after</t> <t>CDK4/6i</t> treatment based on data in (B).
    Cdk4 6i Abemaciclib, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "CDK4/6 inhibition sensitizes breast cancer to NK cell therapy by inducing immune-interactive surface proteins"

    Article Title: CDK4/6 inhibition sensitizes breast cancer to NK cell therapy by inducing immune-interactive surface proteins

    Journal: bioRxiv

    doi: 10.64898/2026.04.19.719504

    ( A ) Representative flow cytometry plots showing surface expression of indicated NK cell-activating and inhibiting signals in a PDO158 treated with 1 μM abemaciclib or vehicle control for 5 days. ( B ) Quantification of surface marker expression across 11 PDOs treated as in (A). n=3. ***p < 0.001, ****p < 0.0001 (two-way ANOVA). ( C ) Pie chart showing the proportion of PDOs that upregulated stress ligands and ICAM-1 after CDK4/6i treatment based on data in (B).
    Figure Legend Snippet: ( A ) Representative flow cytometry plots showing surface expression of indicated NK cell-activating and inhibiting signals in a PDO158 treated with 1 μM abemaciclib or vehicle control for 5 days. ( B ) Quantification of surface marker expression across 11 PDOs treated as in (A). n=3. ***p < 0.001, ****p < 0.0001 (two-way ANOVA). ( C ) Pie chart showing the proportion of PDOs that upregulated stress ligands and ICAM-1 after CDK4/6i treatment based on data in (B).

    Techniques Used: Flow Cytometry, Expressing, Control, Marker

    ( A, B ) Schematic of in vivo experiments administering CDK4/6i and NK cells sequentially (A) or concurrently (B). For sequential treatment (experiments 1 and 2, C-F), mice were pretreated with abemaciclib for 7-11 days, followed by a single NK cell infusion (10×10⁶ cells/injection). For concurrent treatment (experiment 3, G-H), mice were pretreated with abemaciclib for one week, and abemaciclib and NK cells (10×10⁶ cells/injection, weekly) were administered simultaneously. ( C ) Experiment 1, sequential treatment. Tumor growth curves in PDX-bearing mice treated with abemaciclib (75 mg/kg, daily) and NK92 cells. The treatment schedule is as shown in (A). n = 5 mice/group. Statistical significance calculated using 2-way ANOVA with Tukey’s post-test. ( D ) Corresponding survival curves for the experiment in (C). The Log-rank (Mantel-Cox) test was used to compare the combo and vehicle groups. ( E-F ) Tumor growth and survival in Experiment 2 with sequential treatment. The treatment scheme is shown in (A). Doses and analyses as in (C-D). n = 5 mice/group. ( G-H ) Tumor growth and survival in Experiment 3 with concurrent treatment. The treatment scheme is shown in (B). Doses and analyses as in (C-D). n = 5 mice/group.
    Figure Legend Snippet: ( A, B ) Schematic of in vivo experiments administering CDK4/6i and NK cells sequentially (A) or concurrently (B). For sequential treatment (experiments 1 and 2, C-F), mice were pretreated with abemaciclib for 7-11 days, followed by a single NK cell infusion (10×10⁶ cells/injection). For concurrent treatment (experiment 3, G-H), mice were pretreated with abemaciclib for one week, and abemaciclib and NK cells (10×10⁶ cells/injection, weekly) were administered simultaneously. ( C ) Experiment 1, sequential treatment. Tumor growth curves in PDX-bearing mice treated with abemaciclib (75 mg/kg, daily) and NK92 cells. The treatment schedule is as shown in (A). n = 5 mice/group. Statistical significance calculated using 2-way ANOVA with Tukey’s post-test. ( D ) Corresponding survival curves for the experiment in (C). The Log-rank (Mantel-Cox) test was used to compare the combo and vehicle groups. ( E-F ) Tumor growth and survival in Experiment 2 with sequential treatment. The treatment scheme is shown in (A). Doses and analyses as in (C-D). n = 5 mice/group. ( G-H ) Tumor growth and survival in Experiment 3 with concurrent treatment. The treatment scheme is shown in (B). Doses and analyses as in (C-D). n = 5 mice/group.

    Techniques Used: In Vivo, Injection



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    ( A ) Representative flow cytometry plots showing surface expression of indicated NK cell-activating and inhibiting signals in a PDO158 treated with 1 μM abemaciclib or vehicle control for 5 days. ( B ) Quantification of surface marker expression across 11 PDOs treated as in (A). n=3. ***p < 0.001, ****p < 0.0001 (two-way ANOVA). ( C ) Pie chart showing the proportion of PDOs that upregulated stress ligands and ICAM-1 <t>after</t> <t>CDK4/6i</t> treatment based on data in (B).
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    A. Representative time-lapse images of PC3-FUCCI undergoing mitotic bypass and endoreplication during 72h treatment with CDK1i. Scale bar, 10μm. B. Scatter plots of DNA content vs. geminin abundance in individual PC3 after 72h treatment with DMSO, CDK1i, <t>CDK4/6i,</t> or CDK2i. Points colored based on their relative density. Dotted lines represent cut-off values for determining DNA content and geminin positivity. Data shown are combined from 3 independent experiments. 1000 individual nuclei shown for each condition. C. Quantification of percent of cells in each cell cycle phase in each condition from ( B ). Data shown are mean percentages from 3 independent experiments. D. Experimental outline for determining the effects of CDK4/6i or CDK2i on cisplatin-, etoposide-, or CDK1i- induced mitotic bypass. E. Percent of PC3 in each cell cycle phase after treatment as in ( D ). Data shown are mean percentages from ≥ 5 independent experiments.
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    A. Representative time-lapse images of PC3-FUCCI undergoing mitotic bypass and endoreplication during 72h treatment with CDK1i. Scale bar, 10μm. B. Scatter plots of DNA content vs. geminin abundance in individual PC3 after 72h treatment with DMSO, CDK1i, <t>CDK4/6i,</t> or CDK2i. Points colored based on their relative density. Dotted lines represent cut-off values for determining DNA content and geminin positivity. Data shown are combined from 3 independent experiments. 1000 individual nuclei shown for each condition. C. Quantification of percent of cells in each cell cycle phase in each condition from ( B ). Data shown are mean percentages from 3 independent experiments. D. Experimental outline for determining the effects of CDK4/6i or CDK2i on cisplatin-, etoposide-, or CDK1i- induced mitotic bypass. E. Percent of PC3 in each cell cycle phase after treatment as in ( D ). Data shown are mean percentages from ≥ 5 independent experiments.
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    A. Representative time-lapse images of PC3-FUCCI undergoing mitotic bypass and endoreplication during 72h treatment with CDK1i. Scale bar, 10μm. B. Scatter plots of DNA content vs. geminin abundance in individual PC3 after 72h treatment with DMSO, CDK1i, <t>CDK4/6i,</t> or CDK2i. Points colored based on their relative density. Dotted lines represent cut-off values for determining DNA content and geminin positivity. Data shown are combined from 3 independent experiments. 1000 individual nuclei shown for each condition. C. Quantification of percent of cells in each cell cycle phase in each condition from ( B ). Data shown are mean percentages from 3 independent experiments. D. Experimental outline for determining the effects of CDK4/6i or CDK2i on cisplatin-, etoposide-, or CDK1i- induced mitotic bypass. E. Percent of PC3 in each cell cycle phase after treatment as in ( D ). Data shown are mean percentages from ≥ 5 independent experiments.
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    A. Representative time-lapse images of PC3-FUCCI undergoing mitotic bypass and endoreplication during 72h treatment with CDK1i. Scale bar, 10μm. B. Scatter plots of DNA content vs. geminin abundance in individual PC3 after 72h treatment with DMSO, CDK1i, <t>CDK4/6i,</t> or CDK2i. Points colored based on their relative density. Dotted lines represent cut-off values for determining DNA content and geminin positivity. Data shown are combined from 3 independent experiments. 1000 individual nuclei shown for each condition. C. Quantification of percent of cells in each cell cycle phase in each condition from ( B ). Data shown are mean percentages from 3 independent experiments. D. Experimental outline for determining the effects of CDK4/6i or CDK2i on cisplatin-, etoposide-, or CDK1i- induced mitotic bypass. E. Percent of PC3 in each cell cycle phase after treatment as in ( D ). Data shown are mean percentages from ≥ 5 independent experiments.
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    A. Representative time-lapse images of PC3-FUCCI undergoing mitotic bypass and endoreplication during 72h treatment with CDK1i. Scale bar, 10μm. B. Scatter plots of DNA content vs. geminin abundance in individual PC3 after 72h treatment with DMSO, CDK1i, <t>CDK4/6i,</t> or CDK2i. Points colored based on their relative density. Dotted lines represent cut-off values for determining DNA content and geminin positivity. Data shown are combined from 3 independent experiments. 1000 individual nuclei shown for each condition. C. Quantification of percent of cells in each cell cycle phase in each condition from ( B ). Data shown are mean percentages from 3 independent experiments. D. Experimental outline for determining the effects of CDK4/6i or CDK2i on cisplatin-, etoposide-, or CDK1i- induced mitotic bypass. E. Percent of PC3 in each cell cycle phase after treatment as in ( D ). Data shown are mean percentages from ≥ 5 independent experiments.
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    A. Representative time-lapse images of PC3-FUCCI undergoing mitotic bypass and endoreplication during 72h treatment with CDK1i. Scale bar, 10μm. B. Scatter plots of DNA content vs. geminin abundance in individual PC3 after 72h treatment with DMSO, CDK1i, <t>CDK4/6i,</t> or CDK2i. Points colored based on their relative density. Dotted lines represent cut-off values for determining DNA content and geminin positivity. Data shown are combined from 3 independent experiments. 1000 individual nuclei shown for each condition. C. Quantification of percent of cells in each cell cycle phase in each condition from ( B ). Data shown are mean percentages from 3 independent experiments. D. Experimental outline for determining the effects of CDK4/6i or CDK2i on cisplatin-, etoposide-, or CDK1i- induced mitotic bypass. E. Percent of PC3 in each cell cycle phase after treatment as in ( D ). Data shown are mean percentages from ≥ 5 independent experiments.
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    A. Representative time-lapse images of PC3-FUCCI undergoing mitotic bypass and endoreplication during 72h treatment with CDK1i. Scale bar, 10μm. B. Scatter plots of DNA content vs. geminin abundance in individual PC3 after 72h treatment with DMSO, CDK1i, <t>CDK4/6i,</t> or CDK2i. Points colored based on their relative density. Dotted lines represent cut-off values for determining DNA content and geminin positivity. Data shown are combined from 3 independent experiments. 1000 individual nuclei shown for each condition. C. Quantification of percent of cells in each cell cycle phase in each condition from ( B ). Data shown are mean percentages from 3 independent experiments. D. Experimental outline for determining the effects of CDK4/6i or CDK2i on cisplatin-, etoposide-, or CDK1i- induced mitotic bypass. E. Percent of PC3 in each cell cycle phase after treatment as in ( D ). Data shown are mean percentages from ≥ 5 independent experiments.
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    A. Representative time-lapse images of PC3-FUCCI undergoing mitotic bypass and endoreplication during 72h treatment with CDK1i. Scale bar, 10μm. B. Scatter plots of DNA content vs. geminin abundance in individual PC3 after 72h treatment with DMSO, CDK1i, <t>CDK4/6i,</t> or CDK2i. Points colored based on their relative density. Dotted lines represent cut-off values for determining DNA content and geminin positivity. Data shown are combined from 3 independent experiments. 1000 individual nuclei shown for each condition. C. Quantification of percent of cells in each cell cycle phase in each condition from ( B ). Data shown are mean percentages from 3 independent experiments. D. Experimental outline for determining the effects of CDK4/6i or CDK2i on cisplatin-, etoposide-, or CDK1i- induced mitotic bypass. E. Percent of PC3 in each cell cycle phase after treatment as in ( D ). Data shown are mean percentages from ≥ 5 independent experiments.
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    Image Search Results


    ( A ) Representative flow cytometry plots showing surface expression of indicated NK cell-activating and inhibiting signals in a PDO158 treated with 1 μM abemaciclib or vehicle control for 5 days. ( B ) Quantification of surface marker expression across 11 PDOs treated as in (A). n=3. ***p < 0.001, ****p < 0.0001 (two-way ANOVA). ( C ) Pie chart showing the proportion of PDOs that upregulated stress ligands and ICAM-1 after CDK4/6i treatment based on data in (B).

    Journal: bioRxiv

    Article Title: CDK4/6 inhibition sensitizes breast cancer to NK cell therapy by inducing immune-interactive surface proteins

    doi: 10.64898/2026.04.19.719504

    Figure Lengend Snippet: ( A ) Representative flow cytometry plots showing surface expression of indicated NK cell-activating and inhibiting signals in a PDO158 treated with 1 μM abemaciclib or vehicle control for 5 days. ( B ) Quantification of surface marker expression across 11 PDOs treated as in (A). n=3. ***p < 0.001, ****p < 0.0001 (two-way ANOVA). ( C ) Pie chart showing the proportion of PDOs that upregulated stress ligands and ICAM-1 after CDK4/6i treatment based on data in (B).

    Article Snippet: Small molecule inhibitors, including CDK4/6i abemaciclib and ribociclib, PI3K/mTORi gedatolisib, and NFkB inhibitor BMS-345541 were purchased from AdooQ, MedChemExpress, and Selleckchem.

    Techniques: Flow Cytometry, Expressing, Control, Marker

    ( A, B ) Schematic of in vivo experiments administering CDK4/6i and NK cells sequentially (A) or concurrently (B). For sequential treatment (experiments 1 and 2, C-F), mice were pretreated with abemaciclib for 7-11 days, followed by a single NK cell infusion (10×10⁶ cells/injection). For concurrent treatment (experiment 3, G-H), mice were pretreated with abemaciclib for one week, and abemaciclib and NK cells (10×10⁶ cells/injection, weekly) were administered simultaneously. ( C ) Experiment 1, sequential treatment. Tumor growth curves in PDX-bearing mice treated with abemaciclib (75 mg/kg, daily) and NK92 cells. The treatment schedule is as shown in (A). n = 5 mice/group. Statistical significance calculated using 2-way ANOVA with Tukey’s post-test. ( D ) Corresponding survival curves for the experiment in (C). The Log-rank (Mantel-Cox) test was used to compare the combo and vehicle groups. ( E-F ) Tumor growth and survival in Experiment 2 with sequential treatment. The treatment scheme is shown in (A). Doses and analyses as in (C-D). n = 5 mice/group. ( G-H ) Tumor growth and survival in Experiment 3 with concurrent treatment. The treatment scheme is shown in (B). Doses and analyses as in (C-D). n = 5 mice/group.

    Journal: bioRxiv

    Article Title: CDK4/6 inhibition sensitizes breast cancer to NK cell therapy by inducing immune-interactive surface proteins

    doi: 10.64898/2026.04.19.719504

    Figure Lengend Snippet: ( A, B ) Schematic of in vivo experiments administering CDK4/6i and NK cells sequentially (A) or concurrently (B). For sequential treatment (experiments 1 and 2, C-F), mice were pretreated with abemaciclib for 7-11 days, followed by a single NK cell infusion (10×10⁶ cells/injection). For concurrent treatment (experiment 3, G-H), mice were pretreated with abemaciclib for one week, and abemaciclib and NK cells (10×10⁶ cells/injection, weekly) were administered simultaneously. ( C ) Experiment 1, sequential treatment. Tumor growth curves in PDX-bearing mice treated with abemaciclib (75 mg/kg, daily) and NK92 cells. The treatment schedule is as shown in (A). n = 5 mice/group. Statistical significance calculated using 2-way ANOVA with Tukey’s post-test. ( D ) Corresponding survival curves for the experiment in (C). The Log-rank (Mantel-Cox) test was used to compare the combo and vehicle groups. ( E-F ) Tumor growth and survival in Experiment 2 with sequential treatment. The treatment scheme is shown in (A). Doses and analyses as in (C-D). n = 5 mice/group. ( G-H ) Tumor growth and survival in Experiment 3 with concurrent treatment. The treatment scheme is shown in (B). Doses and analyses as in (C-D). n = 5 mice/group.

    Article Snippet: Small molecule inhibitors, including CDK4/6i abemaciclib and ribociclib, PI3K/mTORi gedatolisib, and NFkB inhibitor BMS-345541 were purchased from AdooQ, MedChemExpress, and Selleckchem.

    Techniques: In Vivo, Injection

    A. Representative time-lapse images of PC3-FUCCI undergoing mitotic bypass and endoreplication during 72h treatment with CDK1i. Scale bar, 10μm. B. Scatter plots of DNA content vs. geminin abundance in individual PC3 after 72h treatment with DMSO, CDK1i, CDK4/6i, or CDK2i. Points colored based on their relative density. Dotted lines represent cut-off values for determining DNA content and geminin positivity. Data shown are combined from 3 independent experiments. 1000 individual nuclei shown for each condition. C. Quantification of percent of cells in each cell cycle phase in each condition from ( B ). Data shown are mean percentages from 3 independent experiments. D. Experimental outline for determining the effects of CDK4/6i or CDK2i on cisplatin-, etoposide-, or CDK1i- induced mitotic bypass. E. Percent of PC3 in each cell cycle phase after treatment as in ( D ). Data shown are mean percentages from ≥ 5 independent experiments.

    Journal: bioRxiv

    Article Title: Mitotic bypass and endocycling promote cancer cell survival after genotoxic chemotherapy

    doi: 10.1101/2025.11.03.686258

    Figure Lengend Snippet: A. Representative time-lapse images of PC3-FUCCI undergoing mitotic bypass and endoreplication during 72h treatment with CDK1i. Scale bar, 10μm. B. Scatter plots of DNA content vs. geminin abundance in individual PC3 after 72h treatment with DMSO, CDK1i, CDK4/6i, or CDK2i. Points colored based on their relative density. Dotted lines represent cut-off values for determining DNA content and geminin positivity. Data shown are combined from 3 independent experiments. 1000 individual nuclei shown for each condition. C. Quantification of percent of cells in each cell cycle phase in each condition from ( B ). Data shown are mean percentages from 3 independent experiments. D. Experimental outline for determining the effects of CDK4/6i or CDK2i on cisplatin-, etoposide-, or CDK1i- induced mitotic bypass. E. Percent of PC3 in each cell cycle phase after treatment as in ( D ). Data shown are mean percentages from ≥ 5 independent experiments.

    Article Snippet: 1μM WEE1i (Adavosertib, SelleckChem #S1525), 1μM Myt1i (RP-6306, MedChemExpress #HY145817A), 1μM ATRi (Ceralasertib, #S7693), 1μM ATMi (KU-60019, SelleckChem #S1570), 1μM CDK4/6i (Palbociclib, MedChemExpress #HY50767), 500nM CDK2i (INX-315, SelleckChem #E1854), and 5μM CDK1i (Ro-3306, SelleckChem #S7747) were used unless stated otherwise.

    Techniques: