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rsk family kinase inhibitor brd7389  (MedChemExpress)


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    MedChemExpress rsk family kinase inhibitor brd7389
    FAM65A promotes CRC tumor progression is dependent on RSK phosphorylation (A) Results from protein kinase microarray analysis of HCT116-MCS and HCT116-FAM65A cells. (B) Quantitative assessment of the protein kinase microarray data, n = 2. (C) Western blot analysis demonstrating the expression levels of p -RSK and total RSK in HCT116-MCS and HCT116-FAM65A cells. (D) Western blot analysis of p -RSK and RSK expression in HCT116-FAM65A cells treated with 4 and 8 μM <t>BRD7389</t> or without treatment. (E) Results from the CCK8 cell proliferation assay conducted on HCT116-FAM65A cells with and without the application of BRD7389, n = 3, ∗∗ p < 0.01, ∗∗∗ p < 0.001. (F) Outcomes of the colony formation assay performed on HCT116-FAM65A cells treated with BRD7389 or without treatment. (G) Quantitative analysis of the colony formation assay results, n = 3, ∗∗∗ p < 0.001. (H) Results from the EdU assay conducted on HCT116-FAM65A cells with and without the application of BRD7389. Scale bars, 100 μm. (I) Quantitative analysis of the EdU assay results, n = 3, ∗∗∗ p < 0.001. (J) Western blot analysis of Ki-67 expression in HCT116-FAM65A cells treated with BRD7389 or not. (K) Results from the apoptosis assay conducted on HCT116-FAM65A cells treated with BRD7389 or not. Scale bars, 50 μm. (L) Quantitative analysis of the apoptosis experiments, n = 3, ∗∗∗ p < 0.001. (M) Western blot analysis of the expression levels of cleaved Caspase 3, Bcl-2, and Bax in HCT116-FAM65A cells treated with BRD7389 or not. (N) Results from the Transwell migration assay conducted on HCT116-FAM65A cells with and without the application of BRD7389. Scale bars, 50 μm. (O) Quantitative analysis of the Transwell migration assay results, n = 3, ∗∗∗ p < 0.001. (P) Results from the wound healing assay performed on HCT116-FAM65A cells treated with BRD7389 or not. Scale bars, 50 μm. (Q) Quantitative analysis of the wound healing assay results, n = 3, ∗∗ p < 0.01, ∗∗∗ p < 0.001. (R) Western blot analysis the expression of EMT markers in HCT116-FAM65A cells treated with BRD7389 or not. Data are presented as mean ± SEM of biologically independent experiments.
    Rsk Family Kinase Inhibitor Brd7389, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rsk family kinase inhibitor brd7389/product/MedChemExpress
    Average 93 stars, based on 4 article reviews
    rsk family kinase inhibitor brd7389 - by Bioz Stars, 2026-03
    93/100 stars

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    1) Product Images from "FAM65A, as a potential predictor of prognosis, promotes colorectal cancer progression via activating Ras/ERK/RSK signaling"

    Article Title: FAM65A, as a potential predictor of prognosis, promotes colorectal cancer progression via activating Ras/ERK/RSK signaling

    Journal: iScience

    doi: 10.1016/j.isci.2026.114662

    FAM65A promotes CRC tumor progression is dependent on RSK phosphorylation (A) Results from protein kinase microarray analysis of HCT116-MCS and HCT116-FAM65A cells. (B) Quantitative assessment of the protein kinase microarray data, n = 2. (C) Western blot analysis demonstrating the expression levels of p -RSK and total RSK in HCT116-MCS and HCT116-FAM65A cells. (D) Western blot analysis of p -RSK and RSK expression in HCT116-FAM65A cells treated with 4 and 8 μM BRD7389 or without treatment. (E) Results from the CCK8 cell proliferation assay conducted on HCT116-FAM65A cells with and without the application of BRD7389, n = 3, ∗∗ p < 0.01, ∗∗∗ p < 0.001. (F) Outcomes of the colony formation assay performed on HCT116-FAM65A cells treated with BRD7389 or without treatment. (G) Quantitative analysis of the colony formation assay results, n = 3, ∗∗∗ p < 0.001. (H) Results from the EdU assay conducted on HCT116-FAM65A cells with and without the application of BRD7389. Scale bars, 100 μm. (I) Quantitative analysis of the EdU assay results, n = 3, ∗∗∗ p < 0.001. (J) Western blot analysis of Ki-67 expression in HCT116-FAM65A cells treated with BRD7389 or not. (K) Results from the apoptosis assay conducted on HCT116-FAM65A cells treated with BRD7389 or not. Scale bars, 50 μm. (L) Quantitative analysis of the apoptosis experiments, n = 3, ∗∗∗ p < 0.001. (M) Western blot analysis of the expression levels of cleaved Caspase 3, Bcl-2, and Bax in HCT116-FAM65A cells treated with BRD7389 or not. (N) Results from the Transwell migration assay conducted on HCT116-FAM65A cells with and without the application of BRD7389. Scale bars, 50 μm. (O) Quantitative analysis of the Transwell migration assay results, n = 3, ∗∗∗ p < 0.001. (P) Results from the wound healing assay performed on HCT116-FAM65A cells treated with BRD7389 or not. Scale bars, 50 μm. (Q) Quantitative analysis of the wound healing assay results, n = 3, ∗∗ p < 0.01, ∗∗∗ p < 0.001. (R) Western blot analysis the expression of EMT markers in HCT116-FAM65A cells treated with BRD7389 or not. Data are presented as mean ± SEM of biologically independent experiments.
    Figure Legend Snippet: FAM65A promotes CRC tumor progression is dependent on RSK phosphorylation (A) Results from protein kinase microarray analysis of HCT116-MCS and HCT116-FAM65A cells. (B) Quantitative assessment of the protein kinase microarray data, n = 2. (C) Western blot analysis demonstrating the expression levels of p -RSK and total RSK in HCT116-MCS and HCT116-FAM65A cells. (D) Western blot analysis of p -RSK and RSK expression in HCT116-FAM65A cells treated with 4 and 8 μM BRD7389 or without treatment. (E) Results from the CCK8 cell proliferation assay conducted on HCT116-FAM65A cells with and without the application of BRD7389, n = 3, ∗∗ p < 0.01, ∗∗∗ p < 0.001. (F) Outcomes of the colony formation assay performed on HCT116-FAM65A cells treated with BRD7389 or without treatment. (G) Quantitative analysis of the colony formation assay results, n = 3, ∗∗∗ p < 0.001. (H) Results from the EdU assay conducted on HCT116-FAM65A cells with and without the application of BRD7389. Scale bars, 100 μm. (I) Quantitative analysis of the EdU assay results, n = 3, ∗∗∗ p < 0.001. (J) Western blot analysis of Ki-67 expression in HCT116-FAM65A cells treated with BRD7389 or not. (K) Results from the apoptosis assay conducted on HCT116-FAM65A cells treated with BRD7389 or not. Scale bars, 50 μm. (L) Quantitative analysis of the apoptosis experiments, n = 3, ∗∗∗ p < 0.001. (M) Western blot analysis of the expression levels of cleaved Caspase 3, Bcl-2, and Bax in HCT116-FAM65A cells treated with BRD7389 or not. (N) Results from the Transwell migration assay conducted on HCT116-FAM65A cells with and without the application of BRD7389. Scale bars, 50 μm. (O) Quantitative analysis of the Transwell migration assay results, n = 3, ∗∗∗ p < 0.001. (P) Results from the wound healing assay performed on HCT116-FAM65A cells treated with BRD7389 or not. Scale bars, 50 μm. (Q) Quantitative analysis of the wound healing assay results, n = 3, ∗∗ p < 0.01, ∗∗∗ p < 0.001. (R) Western blot analysis the expression of EMT markers in HCT116-FAM65A cells treated with BRD7389 or not. Data are presented as mean ± SEM of biologically independent experiments.

    Techniques Used: Phospho-proteomics, Microarray, Western Blot, Expressing, Proliferation Assay, Colony Assay, EdU Assay, Apoptosis Assay, Transwell Migration Assay, Wound Healing Assay



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    rsk family kinase inhibitor brd7389  (MedChemExpress)
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    MedChemExpress rsk family kinase inhibitor brd7389
    FAM65A promotes CRC tumor progression is dependent on RSK phosphorylation (A) Results from protein kinase microarray analysis of HCT116-MCS and HCT116-FAM65A cells. (B) Quantitative assessment of the protein kinase microarray data, n = 2. (C) Western blot analysis demonstrating the expression levels of p -RSK and total RSK in HCT116-MCS and HCT116-FAM65A cells. (D) Western blot analysis of p -RSK and RSK expression in HCT116-FAM65A cells treated with 4 and 8 μM <t>BRD7389</t> or without treatment. (E) Results from the CCK8 cell proliferation assay conducted on HCT116-FAM65A cells with and without the application of BRD7389, n = 3, ∗∗ p < 0.01, ∗∗∗ p < 0.001. (F) Outcomes of the colony formation assay performed on HCT116-FAM65A cells treated with BRD7389 or without treatment. (G) Quantitative analysis of the colony formation assay results, n = 3, ∗∗∗ p < 0.001. (H) Results from the EdU assay conducted on HCT116-FAM65A cells with and without the application of BRD7389. Scale bars, 100 μm. (I) Quantitative analysis of the EdU assay results, n = 3, ∗∗∗ p < 0.001. (J) Western blot analysis of Ki-67 expression in HCT116-FAM65A cells treated with BRD7389 or not. (K) Results from the apoptosis assay conducted on HCT116-FAM65A cells treated with BRD7389 or not. Scale bars, 50 μm. (L) Quantitative analysis of the apoptosis experiments, n = 3, ∗∗∗ p < 0.001. (M) Western blot analysis of the expression levels of cleaved Caspase 3, Bcl-2, and Bax in HCT116-FAM65A cells treated with BRD7389 or not. (N) Results from the Transwell migration assay conducted on HCT116-FAM65A cells with and without the application of BRD7389. Scale bars, 50 μm. (O) Quantitative analysis of the Transwell migration assay results, n = 3, ∗∗∗ p < 0.001. (P) Results from the wound healing assay performed on HCT116-FAM65A cells treated with BRD7389 or not. Scale bars, 50 μm. (Q) Quantitative analysis of the wound healing assay results, n = 3, ∗∗ p < 0.01, ∗∗∗ p < 0.001. (R) Western blot analysis the expression of EMT markers in HCT116-FAM65A cells treated with BRD7389 or not. Data are presented as mean ± SEM of biologically independent experiments.
    Rsk Family Kinase Inhibitor Brd7389, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rsk family kinase inhibitor brd7389/product/MedChemExpress
    Average 93 stars, based on 1 article reviews
    rsk family kinase inhibitor brd7389 - by Bioz Stars, 2026-03
    93/100 stars
    		  Buy from Supplier
    rsk family kinase inhibitor 700 brd7389  (MedChemExpress)
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    MedChemExpress rsk family kinase inhibitor 700 brd7389
    FAM65A promotes CRC tumor progression is dependent on RSK phosphorylation (A) Results from protein kinase microarray analysis of HCT116-MCS and HCT116-FAM65A cells. (B) Quantitative assessment of the protein kinase microarray data, n = 2. (C) Western blot analysis demonstrating the expression levels of p -RSK and total RSK in HCT116-MCS and HCT116-FAM65A cells. (D) Western blot analysis of p -RSK and RSK expression in HCT116-FAM65A cells treated with 4 and 8 μM <t>BRD7389</t> or without treatment. (E) Results from the CCK8 cell proliferation assay conducted on HCT116-FAM65A cells with and without the application of BRD7389, n = 3, ∗∗ p < 0.01, ∗∗∗ p < 0.001. (F) Outcomes of the colony formation assay performed on HCT116-FAM65A cells treated with BRD7389 or without treatment. (G) Quantitative analysis of the colony formation assay results, n = 3, ∗∗∗ p < 0.001. (H) Results from the EdU assay conducted on HCT116-FAM65A cells with and without the application of BRD7389. Scale bars, 100 μm. (I) Quantitative analysis of the EdU assay results, n = 3, ∗∗∗ p < 0.001. (J) Western blot analysis of Ki-67 expression in HCT116-FAM65A cells treated with BRD7389 or not. (K) Results from the apoptosis assay conducted on HCT116-FAM65A cells treated with BRD7389 or not. Scale bars, 50 μm. (L) Quantitative analysis of the apoptosis experiments, n = 3, ∗∗∗ p < 0.001. (M) Western blot analysis of the expression levels of cleaved Caspase 3, Bcl-2, and Bax in HCT116-FAM65A cells treated with BRD7389 or not. (N) Results from the Transwell migration assay conducted on HCT116-FAM65A cells with and without the application of BRD7389. Scale bars, 50 μm. (O) Quantitative analysis of the Transwell migration assay results, n = 3, ∗∗∗ p < 0.001. (P) Results from the wound healing assay performed on HCT116-FAM65A cells treated with BRD7389 or not. Scale bars, 50 μm. (Q) Quantitative analysis of the wound healing assay results, n = 3, ∗∗ p < 0.01, ∗∗∗ p < 0.001. (R) Western blot analysis the expression of EMT markers in HCT116-FAM65A cells treated with BRD7389 or not. Data are presented as mean ± SEM of biologically independent experiments.
    Rsk Family Kinase Inhibitor 700 Brd7389, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rsk family kinase inhibitor 700 brd7389/product/MedChemExpress
    Average 93 stars, based on 1 article reviews
    rsk family kinase inhibitor 700 brd7389 - by Bioz Stars, 2026-03
    93/100 stars
    		  Buy from Supplier

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    FAM65A promotes CRC tumor progression is dependent on RSK phosphorylation (A) Results from protein kinase microarray analysis of HCT116-MCS and HCT116-FAM65A cells. (B) Quantitative assessment of the protein kinase microarray data, n = 2. (C) Western blot analysis demonstrating the expression levels of p -RSK and total RSK in HCT116-MCS and HCT116-FAM65A cells. (D) Western blot analysis of p -RSK and RSK expression in HCT116-FAM65A cells treated with 4 and 8 μM BRD7389 or without treatment. (E) Results from the CCK8 cell proliferation assay conducted on HCT116-FAM65A cells with and without the application of BRD7389, n = 3, ∗∗ p < 0.01, ∗∗∗ p < 0.001. (F) Outcomes of the colony formation assay performed on HCT116-FAM65A cells treated with BRD7389 or without treatment. (G) Quantitative analysis of the colony formation assay results, n = 3, ∗∗∗ p < 0.001. (H) Results from the EdU assay conducted on HCT116-FAM65A cells with and without the application of BRD7389. Scale bars, 100 μm. (I) Quantitative analysis of the EdU assay results, n = 3, ∗∗∗ p < 0.001. (J) Western blot analysis of Ki-67 expression in HCT116-FAM65A cells treated with BRD7389 or not. (K) Results from the apoptosis assay conducted on HCT116-FAM65A cells treated with BRD7389 or not. Scale bars, 50 μm. (L) Quantitative analysis of the apoptosis experiments, n = 3, ∗∗∗ p < 0.001. (M) Western blot analysis of the expression levels of cleaved Caspase 3, Bcl-2, and Bax in HCT116-FAM65A cells treated with BRD7389 or not. (N) Results from the Transwell migration assay conducted on HCT116-FAM65A cells with and without the application of BRD7389. Scale bars, 50 μm. (O) Quantitative analysis of the Transwell migration assay results, n = 3, ∗∗∗ p < 0.001. (P) Results from the wound healing assay performed on HCT116-FAM65A cells treated with BRD7389 or not. Scale bars, 50 μm. (Q) Quantitative analysis of the wound healing assay results, n = 3, ∗∗ p < 0.01, ∗∗∗ p < 0.001. (R) Western blot analysis the expression of EMT markers in HCT116-FAM65A cells treated with BRD7389 or not. Data are presented as mean ± SEM of biologically independent experiments.

    Journal: iScience

    Article Title: FAM65A, as a potential predictor of prognosis, promotes colorectal cancer progression via activating Ras/ERK/RSK signaling

    doi: 10.1016/j.isci.2026.114662

    Figure Lengend Snippet: FAM65A promotes CRC tumor progression is dependent on RSK phosphorylation (A) Results from protein kinase microarray analysis of HCT116-MCS and HCT116-FAM65A cells. (B) Quantitative assessment of the protein kinase microarray data, n = 2. (C) Western blot analysis demonstrating the expression levels of p -RSK and total RSK in HCT116-MCS and HCT116-FAM65A cells. (D) Western blot analysis of p -RSK and RSK expression in HCT116-FAM65A cells treated with 4 and 8 μM BRD7389 or without treatment. (E) Results from the CCK8 cell proliferation assay conducted on HCT116-FAM65A cells with and without the application of BRD7389, n = 3, ∗∗ p < 0.01, ∗∗∗ p < 0.001. (F) Outcomes of the colony formation assay performed on HCT116-FAM65A cells treated with BRD7389 or without treatment. (G) Quantitative analysis of the colony formation assay results, n = 3, ∗∗∗ p < 0.001. (H) Results from the EdU assay conducted on HCT116-FAM65A cells with and without the application of BRD7389. Scale bars, 100 μm. (I) Quantitative analysis of the EdU assay results, n = 3, ∗∗∗ p < 0.001. (J) Western blot analysis of Ki-67 expression in HCT116-FAM65A cells treated with BRD7389 or not. (K) Results from the apoptosis assay conducted on HCT116-FAM65A cells treated with BRD7389 or not. Scale bars, 50 μm. (L) Quantitative analysis of the apoptosis experiments, n = 3, ∗∗∗ p < 0.001. (M) Western blot analysis of the expression levels of cleaved Caspase 3, Bcl-2, and Bax in HCT116-FAM65A cells treated with BRD7389 or not. (N) Results from the Transwell migration assay conducted on HCT116-FAM65A cells with and without the application of BRD7389. Scale bars, 50 μm. (O) Quantitative analysis of the Transwell migration assay results, n = 3, ∗∗∗ p < 0.001. (P) Results from the wound healing assay performed on HCT116-FAM65A cells treated with BRD7389 or not. Scale bars, 50 μm. (Q) Quantitative analysis of the wound healing assay results, n = 3, ∗∗ p < 0.01, ∗∗∗ p < 0.001. (R) Western blot analysis the expression of EMT markers in HCT116-FAM65A cells treated with BRD7389 or not. Data are presented as mean ± SEM of biologically independent experiments.

    Article Snippet: The phosphorylation of RSK was inhibited by the selective RSK family kinase inhibitor BRD7389 (Cat. # HY-12185, MedChemExpress, USA).

    Techniques: Phospho-proteomics, Microarray, Western Blot, Expressing, Proliferation Assay, Colony Assay, EdU Assay, Apoptosis Assay, Transwell Migration Assay, Wound Healing Assay