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y 27632  (MedChemExpress)


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    Structured Review

    MedChemExpress y 27632
    Y 27632, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 97/100, based on 116 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/y 27632/product/MedChemExpress
    Average 97 stars, based on 116 article reviews
    y 27632 - by Bioz Stars, 2026-01
    97/100 stars

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    BCAT2 inhibitor impedes diabetic atherosclerotic calcification. (A) Docking model <t>of</t> <t>BAY-069</t> (BCAT2 inhibitor) and BCAT2. (B) qRT-PCR analysis of BCAT2 gene expression in the aorta of NC or DM ApoE −/− mice supplemented with DMSO or BAY-069 (0.3 mg/kg). n = 6. (C) Western blot image and analysis showing α-SMA, SM22α, BMP2, RUNX2, and BCAT2 protein expression level in the aorta of NC or DM ApoE −/− mice supplemented with DMSO or BAY-069 (0.3 mg/kg). n = 6. (D) BCAT2 enzyme activity in the aorta of indicated mice. n = 6. (E and F) Biochemical measurement of aortic calcium content and ALP activity for indicated mice. n = 6. (G) Representative images of alizarin red S staining in the whole aorta for indicated mice. (H) Micro-CT was used to detect aortic calcification for indicated mice. (I) Representative images and quantification of von Kossa staining in aortic arch and aortic root tissue sections, and immunohistochemistry staining of RUNX2 in aortic root tissue sections. Scale bars, 200 μm for von Kossa staining and 50 μm for immunohistochemistry staining. n = 6. (J) Western blot image and analysis showing α-SMA, SM22α, BMP2, RUNX2, and BCAT2 protein expression level in Movas supplemented with DMSO or BAY-069 under NM or OM treatment for 14 d. n = 6. (K) Representative images of alizarin red S staining. Scale bars, 200 μm. n = 6. (L) Quantification of calcium deposits. n = 6. Data are presented as mean ± SD. ** P < 0.01, *** P < 0.001, **** P < 0.0001 versus DMSO.
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    Functions of PEAK1 on the <t>HIF-1α/STAT3/NF-κB</t> pathway activation in PCa cells. A WB was conducted to test the protein levels of HIF-1α, PD-L1, p -STAT3, and p –p65 in PC3 and DU145 cells with PEAK1 overexpression. B , C WB was conducted to test the protein levels of HIF-1α, PD-L1, p -STAT3, and p –p65 in PC3 and DU145 cells with PEAK1 knocking down. D WB was conducted to test the protein levels of HIF-1α, PD-L1, p -STAT3, and p –p65 in PC3 cells with PEAK1 overexpression and co-culturing with THP1 cells. E , F WB was conducted to test the protein levels of HIF-1α, PD-L1, p -STAT3, and p –p65 in PC3 and DU145 cells with PEAK1 overexpression and LW6, Stattic or <t>Bay</t> <t>11–7082</t> treatment. N = 3. * stands for p < 0.05, ** stands for p < 0.01, *** stands for p < 0.001
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    Functions of PEAK1 on the <t>HIF-1α/STAT3/NF-κB</t> pathway activation in PCa cells. A WB was conducted to test the protein levels of HIF-1α, PD-L1, p -STAT3, and p –p65 in PC3 and DU145 cells with PEAK1 overexpression. B , C WB was conducted to test the protein levels of HIF-1α, PD-L1, p -STAT3, and p –p65 in PC3 and DU145 cells with PEAK1 knocking down. D WB was conducted to test the protein levels of HIF-1α, PD-L1, p -STAT3, and p –p65 in PC3 cells with PEAK1 overexpression and co-culturing with THP1 cells. E , F WB was conducted to test the protein levels of HIF-1α, PD-L1, p -STAT3, and p –p65 in PC3 and DU145 cells with PEAK1 overexpression and LW6, Stattic or <t>Bay</t> <t>11–7082</t> treatment. N = 3. * stands for p < 0.05, ** stands for p < 0.01, *** stands for p < 0.001
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    Functions of PEAK1 on the <t>HIF-1α/STAT3/NF-κB</t> pathway activation in PCa cells. A WB was conducted to test the protein levels of HIF-1α, PD-L1, p -STAT3, and p –p65 in PC3 and DU145 cells with PEAK1 overexpression. B , C WB was conducted to test the protein levels of HIF-1α, PD-L1, p -STAT3, and p –p65 in PC3 and DU145 cells with PEAK1 knocking down. D WB was conducted to test the protein levels of HIF-1α, PD-L1, p -STAT3, and p –p65 in PC3 cells with PEAK1 overexpression and co-culturing with THP1 cells. E , F WB was conducted to test the protein levels of HIF-1α, PD-L1, p -STAT3, and p –p65 in PC3 and DU145 cells with PEAK1 overexpression and LW6, Stattic or <t>Bay</t> <t>11–7082</t> treatment. N = 3. * stands for p < 0.05, ** stands for p < 0.01, *** stands for p < 0.001
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    Functions of PEAK1 on the <t>HIF-1α/STAT3/NF-κB</t> pathway activation in PCa cells. A WB was conducted to test the protein levels of HIF-1α, PD-L1, p -STAT3, and p –p65 in PC3 and DU145 cells with PEAK1 overexpression. B , C WB was conducted to test the protein levels of HIF-1α, PD-L1, p -STAT3, and p –p65 in PC3 and DU145 cells with PEAK1 knocking down. D WB was conducted to test the protein levels of HIF-1α, PD-L1, p -STAT3, and p –p65 in PC3 cells with PEAK1 overexpression and co-culturing with THP1 cells. E , F WB was conducted to test the protein levels of HIF-1α, PD-L1, p -STAT3, and p –p65 in PC3 and DU145 cells with PEAK1 overexpression and LW6, Stattic or <t>Bay</t> <t>11–7082</t> treatment. N = 3. * stands for p < 0.05, ** stands for p < 0.01, *** stands for p < 0.001
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    Image Search Results


    BCAT2 inhibitor impedes diabetic atherosclerotic calcification. (A) Docking model of BAY-069 (BCAT2 inhibitor) and BCAT2. (B) qRT-PCR analysis of BCAT2 gene expression in the aorta of NC or DM ApoE −/− mice supplemented with DMSO or BAY-069 (0.3 mg/kg). n = 6. (C) Western blot image and analysis showing α-SMA, SM22α, BMP2, RUNX2, and BCAT2 protein expression level in the aorta of NC or DM ApoE −/− mice supplemented with DMSO or BAY-069 (0.3 mg/kg). n = 6. (D) BCAT2 enzyme activity in the aorta of indicated mice. n = 6. (E and F) Biochemical measurement of aortic calcium content and ALP activity for indicated mice. n = 6. (G) Representative images of alizarin red S staining in the whole aorta for indicated mice. (H) Micro-CT was used to detect aortic calcification for indicated mice. (I) Representative images and quantification of von Kossa staining in aortic arch and aortic root tissue sections, and immunohistochemistry staining of RUNX2 in aortic root tissue sections. Scale bars, 200 μm for von Kossa staining and 50 μm for immunohistochemistry staining. n = 6. (J) Western blot image and analysis showing α-SMA, SM22α, BMP2, RUNX2, and BCAT2 protein expression level in Movas supplemented with DMSO or BAY-069 under NM or OM treatment for 14 d. n = 6. (K) Representative images of alizarin red S staining. Scale bars, 200 μm. n = 6. (L) Quantification of calcium deposits. n = 6. Data are presented as mean ± SD. ** P < 0.01, *** P < 0.001, **** P < 0.0001 versus DMSO.

    Journal: Research

    Article Title: Vascular Smooth Muscle Cell-Specific BCAT2 Deficiency Attenuates Diabetic Atherosclerotic Calcification via Histone Propionylation

    doi: 10.34133/research.1052

    Figure Lengend Snippet: BCAT2 inhibitor impedes diabetic atherosclerotic calcification. (A) Docking model of BAY-069 (BCAT2 inhibitor) and BCAT2. (B) qRT-PCR analysis of BCAT2 gene expression in the aorta of NC or DM ApoE −/− mice supplemented with DMSO or BAY-069 (0.3 mg/kg). n = 6. (C) Western blot image and analysis showing α-SMA, SM22α, BMP2, RUNX2, and BCAT2 protein expression level in the aorta of NC or DM ApoE −/− mice supplemented with DMSO or BAY-069 (0.3 mg/kg). n = 6. (D) BCAT2 enzyme activity in the aorta of indicated mice. n = 6. (E and F) Biochemical measurement of aortic calcium content and ALP activity for indicated mice. n = 6. (G) Representative images of alizarin red S staining in the whole aorta for indicated mice. (H) Micro-CT was used to detect aortic calcification for indicated mice. (I) Representative images and quantification of von Kossa staining in aortic arch and aortic root tissue sections, and immunohistochemistry staining of RUNX2 in aortic root tissue sections. Scale bars, 200 μm for von Kossa staining and 50 μm for immunohistochemistry staining. n = 6. (J) Western blot image and analysis showing α-SMA, SM22α, BMP2, RUNX2, and BCAT2 protein expression level in Movas supplemented with DMSO or BAY-069 under NM or OM treatment for 14 d. n = 6. (K) Representative images of alizarin red S staining. Scale bars, 200 μm. n = 6. (L) Quantification of calcium deposits. n = 6. Data are presented as mean ± SD. ** P < 0.01, *** P < 0.001, **** P < 0.0001 versus DMSO.

    Article Snippet: BAY-069 (catalog no. HY-148242) and C646 (catalog no. HY-13823) were obtained from MedChemExpress (New Jersey, USA).

    Techniques: Quantitative RT-PCR, Gene Expression, Western Blot, Expressing, Activity Assay, Staining, Micro-CT, Immunohistochemistry

    Functions of PEAK1 on the HIF-1α/STAT3/NF-κB pathway activation in PCa cells. A WB was conducted to test the protein levels of HIF-1α, PD-L1, p -STAT3, and p –p65 in PC3 and DU145 cells with PEAK1 overexpression. B , C WB was conducted to test the protein levels of HIF-1α, PD-L1, p -STAT3, and p –p65 in PC3 and DU145 cells with PEAK1 knocking down. D WB was conducted to test the protein levels of HIF-1α, PD-L1, p -STAT3, and p –p65 in PC3 cells with PEAK1 overexpression and co-culturing with THP1 cells. E , F WB was conducted to test the protein levels of HIF-1α, PD-L1, p -STAT3, and p –p65 in PC3 and DU145 cells with PEAK1 overexpression and LW6, Stattic or Bay 11–7082 treatment. N = 3. * stands for p < 0.05, ** stands for p < 0.01, *** stands for p < 0.001

    Journal: European Journal of Medical Research

    Article Title: PEAK1 promotes prostate cancer progression and docetaxel resistance by mediating the polarization of tumor-associated macrophages

    doi: 10.1186/s40001-025-03568-2

    Figure Lengend Snippet: Functions of PEAK1 on the HIF-1α/STAT3/NF-κB pathway activation in PCa cells. A WB was conducted to test the protein levels of HIF-1α, PD-L1, p -STAT3, and p –p65 in PC3 and DU145 cells with PEAK1 overexpression. B , C WB was conducted to test the protein levels of HIF-1α, PD-L1, p -STAT3, and p –p65 in PC3 and DU145 cells with PEAK1 knocking down. D WB was conducted to test the protein levels of HIF-1α, PD-L1, p -STAT3, and p –p65 in PC3 cells with PEAK1 overexpression and co-culturing with THP1 cells. E , F WB was conducted to test the protein levels of HIF-1α, PD-L1, p -STAT3, and p –p65 in PC3 and DU145 cells with PEAK1 overexpression and LW6, Stattic or Bay 11–7082 treatment. N = 3. * stands for p < 0.05, ** stands for p < 0.01, *** stands for p < 0.001

    Article Snippet: The PC3 and DU145 cells were treated with the HIF-1α inhibitor LW6 (10 μM, #HY-13671, MedChemExpress) [ ]; the STAT3 inhibitor Stattic (10 μM, #HY-13818, MedChemExpress) [ ]; the NF-κB inhibitor Bay 11–7082 (15 μM, #HY-13453, MedChemExpress) [ ]; and increasing doses of enzalutamide (5 μM, 10 μM, 20 μM, and 40 μM, #HY-70002, MedChemExpress) [ ] for 24 h.

    Techniques: Activation Assay, Over Expression

    Mechanistic diagram of PEAK1 in PCa. Summary diagram of the functions and mechanisms of PEAK1 in PCa. Upregulated PEAK1 promotes the HIF-1α/STAT3/NF-κB pathway activation, thus enhancing tumor proliferation, migration, EMT, and reducing apoptosis, docetaxel/enzalutamide sensitivity. PEAK1 enhances CCL2, IL-6 and PD-L1 expression from PCa cells, which mediate “M2” polarization of TAMs and inducing TGF- β expression from TAMs. TGF- β can act on PCa cells and induce PEAK1 upregulation

    Journal: European Journal of Medical Research

    Article Title: PEAK1 promotes prostate cancer progression and docetaxel resistance by mediating the polarization of tumor-associated macrophages

    doi: 10.1186/s40001-025-03568-2

    Figure Lengend Snippet: Mechanistic diagram of PEAK1 in PCa. Summary diagram of the functions and mechanisms of PEAK1 in PCa. Upregulated PEAK1 promotes the HIF-1α/STAT3/NF-κB pathway activation, thus enhancing tumor proliferation, migration, EMT, and reducing apoptosis, docetaxel/enzalutamide sensitivity. PEAK1 enhances CCL2, IL-6 and PD-L1 expression from PCa cells, which mediate “M2” polarization of TAMs and inducing TGF- β expression from TAMs. TGF- β can act on PCa cells and induce PEAK1 upregulation

    Article Snippet: The PC3 and DU145 cells were treated with the HIF-1α inhibitor LW6 (10 μM, #HY-13671, MedChemExpress) [ ]; the STAT3 inhibitor Stattic (10 μM, #HY-13818, MedChemExpress) [ ]; the NF-κB inhibitor Bay 11–7082 (15 μM, #HY-13453, MedChemExpress) [ ]; and increasing doses of enzalutamide (5 μM, 10 μM, 20 μM, and 40 μM, #HY-70002, MedChemExpress) [ ] for 24 h.

    Techniques: Activation Assay, Migration, Expressing