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stat3 agonist ml115  (MedChemExpress)


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    MedChemExpress stat3 agonist ml115
    DOT1L-mediated H3K79me2 regulates immune evasion-related gene expression. (A-D) ChIP-seq profiles showing H3K79me2 enrichment in the gene regions of JAK1, <t>STAT3,</t> STAT1, and RELA in A549 cells. (E-G) Western blot analysis detected DOT1L and H3K79me2 protein levels after treatment with the DOT1L inhibitor SGC0946. GAPDH served as a loading control. (H-J) qPCR validation of STAT3, JAK1, and RELA mRNA downregulation upon SGC0946 treatment in three independent cell lines (* P < 0.05, ** P < 0.01 versus control.).
    Stat3 Agonist Ml115, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/stat3 agonist ml115/product/MedChemExpress
    Average 94 stars, based on 6 article reviews
    stat3 agonist ml115 - by Bioz Stars, 2026-04
    94/100 stars

    Images

    1) Product Images from "DOT1L promotes immune evasion in lung adenocarcinoma through H3K79me2-mediated epigenetic activation of immune checkpoints"

    Article Title: DOT1L promotes immune evasion in lung adenocarcinoma through H3K79me2-mediated epigenetic activation of immune checkpoints

    Journal: Frontiers in Immunology

    doi: 10.3389/fimmu.2026.1719299

    DOT1L-mediated H3K79me2 regulates immune evasion-related gene expression. (A-D) ChIP-seq profiles showing H3K79me2 enrichment in the gene regions of JAK1, STAT3, STAT1, and RELA in A549 cells. (E-G) Western blot analysis detected DOT1L and H3K79me2 protein levels after treatment with the DOT1L inhibitor SGC0946. GAPDH served as a loading control. (H-J) qPCR validation of STAT3, JAK1, and RELA mRNA downregulation upon SGC0946 treatment in three independent cell lines (* P < 0.05, ** P < 0.01 versus control.).
    Figure Legend Snippet: DOT1L-mediated H3K79me2 regulates immune evasion-related gene expression. (A-D) ChIP-seq profiles showing H3K79me2 enrichment in the gene regions of JAK1, STAT3, STAT1, and RELA in A549 cells. (E-G) Western blot analysis detected DOT1L and H3K79me2 protein levels after treatment with the DOT1L inhibitor SGC0946. GAPDH served as a loading control. (H-J) qPCR validation of STAT3, JAK1, and RELA mRNA downregulation upon SGC0946 treatment in three independent cell lines (* P < 0.05, ** P < 0.01 versus control.).

    Techniques Used: Gene Expression, ChIP-sequencing, Western Blot, Control, Biomarker Discovery

    DOT1L promotes immune evasion in LUAD by activating the JAK1/STAT3/PD-L1 axis and inducing T-cell exhaustion. (A-C) Western blot analysis detected protein expression of DOT1L, JAK1, STAT3, p-STAT3 and PD-L1 in A549 and H1975 cells. (D) Flow cytometry analysis of PD-1+ T cell subsets in the co-cultured system of PBMCs with A549 cells(* P < 0.05 versus control).
    Figure Legend Snippet: DOT1L promotes immune evasion in LUAD by activating the JAK1/STAT3/PD-L1 axis and inducing T-cell exhaustion. (A-C) Western blot analysis detected protein expression of DOT1L, JAK1, STAT3, p-STAT3 and PD-L1 in A549 and H1975 cells. (D) Flow cytometry analysis of PD-1+ T cell subsets in the co-cultured system of PBMCs with A549 cells(* P < 0.05 versus control).

    Techniques Used: Western Blot, Expressing, Flow Cytometry, Cell Culture, Control

    Pharmacological inhibition of DOT1L exhibits antitumor effects in a LUAD tail vein lung metastasis model. (A) Bioluminescence imaging shows in vivo evaluation of PD-1 inhibitor (200 μg i.p, twice weekly), SGC0946-L group(20 mg/kg), SGC0946-H group(40 mg/kg), in the tail-vein lung metastasis model. (B) Average weight of mice in in each group, control group(blue line), PD-1 inhibitor group(green line), SGC0946-L group(purple line), SGC0946-H group(Red line). (C) Survival estimates of mice in each group. (D-G) IHC staining of DOT1L, H3K79me2, STAT3 protein expression in tumor tissues in each group. Red scale bar: 20 µm. SGC0946-L, low does group, SGC0946-H, high does group. * P < 0.05.
    Figure Legend Snippet: Pharmacological inhibition of DOT1L exhibits antitumor effects in a LUAD tail vein lung metastasis model. (A) Bioluminescence imaging shows in vivo evaluation of PD-1 inhibitor (200 μg i.p, twice weekly), SGC0946-L group(20 mg/kg), SGC0946-H group(40 mg/kg), in the tail-vein lung metastasis model. (B) Average weight of mice in in each group, control group(blue line), PD-1 inhibitor group(green line), SGC0946-L group(purple line), SGC0946-H group(Red line). (C) Survival estimates of mice in each group. (D-G) IHC staining of DOT1L, H3K79me2, STAT3 protein expression in tumor tissues in each group. Red scale bar: 20 µm. SGC0946-L, low does group, SGC0946-H, high does group. * P < 0.05.

    Techniques Used: Inhibition, Imaging, In Vivo, Control, Immunohistochemistry, Expressing

    Clinical association of DOT1L expression with metastatic progression and immune checkpoint regulation in LUAD. (A, B) IHC analysis of DOT1L and associated markers (H3K79me2, STAT3, PD-L1, PD-1, CD276, and LAG3) in LUAD tissues stratified by DOT1L expression levels. (C) Comparison of DOT1L expression between tumor and adjacent normal tissues. (D) DOT1L expression in stage IV metastatic LUAD compared to non-metastatic cases. (E-J) Pearson correlation analysis between DOT1L and immune checkpoint/epigenetic markers. (K) Pearson correlation analysis between DOT1L expression and TMB.
    Figure Legend Snippet: Clinical association of DOT1L expression with metastatic progression and immune checkpoint regulation in LUAD. (A, B) IHC analysis of DOT1L and associated markers (H3K79me2, STAT3, PD-L1, PD-1, CD276, and LAG3) in LUAD tissues stratified by DOT1L expression levels. (C) Comparison of DOT1L expression between tumor and adjacent normal tissues. (D) DOT1L expression in stage IV metastatic LUAD compared to non-metastatic cases. (E-J) Pearson correlation analysis between DOT1L and immune checkpoint/epigenetic markers. (K) Pearson correlation analysis between DOT1L expression and TMB.

    Techniques Used: Expressing, Comparison



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    DOT1L-mediated H3K79me2 regulates immune evasion-related gene expression. (A-D) ChIP-seq profiles showing H3K79me2 enrichment in the gene regions of JAK1, <t>STAT3,</t> STAT1, and RELA in A549 cells. (E-G) Western blot analysis detected DOT1L and H3K79me2 protein levels after treatment with the DOT1L inhibitor SGC0946. GAPDH served as a loading control. (H-J) qPCR validation of STAT3, JAK1, and RELA mRNA downregulation upon SGC0946 treatment in three independent cell lines (* P < 0.05, ** P < 0.01 versus control.).
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    DOT1L-mediated H3K79me2 regulates immune evasion-related gene expression. (A-D) ChIP-seq profiles showing H3K79me2 enrichment in the gene regions of JAK1, <t>STAT3,</t> STAT1, and RELA in A549 cells. (E-G) Western blot analysis detected DOT1L and H3K79me2 protein levels after treatment with the DOT1L inhibitor SGC0946. GAPDH served as a loading control. (H-J) qPCR validation of STAT3, JAK1, and RELA mRNA downregulation upon SGC0946 treatment in three independent cell lines (* P < 0.05, ** P < 0.01 versus control.).
    P Stat3 Agonist Ml115, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    DOT1L-mediated H3K79me2 regulates immune evasion-related gene expression. (A-D) ChIP-seq profiles showing H3K79me2 enrichment in the gene regions of JAK1, STAT3, STAT1, and RELA in A549 cells. (E-G) Western blot analysis detected DOT1L and H3K79me2 protein levels after treatment with the DOT1L inhibitor SGC0946. GAPDH served as a loading control. (H-J) qPCR validation of STAT3, JAK1, and RELA mRNA downregulation upon SGC0946 treatment in three independent cell lines (* P < 0.05, ** P < 0.01 versus control.).

    Journal: Frontiers in Immunology

    Article Title: DOT1L promotes immune evasion in lung adenocarcinoma through H3K79me2-mediated epigenetic activation of immune checkpoints

    doi: 10.3389/fimmu.2026.1719299

    Figure Lengend Snippet: DOT1L-mediated H3K79me2 regulates immune evasion-related gene expression. (A-D) ChIP-seq profiles showing H3K79me2 enrichment in the gene regions of JAK1, STAT3, STAT1, and RELA in A549 cells. (E-G) Western blot analysis detected DOT1L and H3K79me2 protein levels after treatment with the DOT1L inhibitor SGC0946. GAPDH served as a loading control. (H-J) qPCR validation of STAT3, JAK1, and RELA mRNA downregulation upon SGC0946 treatment in three independent cell lines (* P < 0.05, ** P < 0.01 versus control.).

    Article Snippet: To rescue STAT3 activity, cells were co-treated with 2 nM STAT3 agonist ML115 (MedChemExpress, HY-111152) for 48 hours.

    Techniques: Gene Expression, ChIP-sequencing, Western Blot, Control, Biomarker Discovery

    DOT1L promotes immune evasion in LUAD by activating the JAK1/STAT3/PD-L1 axis and inducing T-cell exhaustion. (A-C) Western blot analysis detected protein expression of DOT1L, JAK1, STAT3, p-STAT3 and PD-L1 in A549 and H1975 cells. (D) Flow cytometry analysis of PD-1+ T cell subsets in the co-cultured system of PBMCs with A549 cells(* P < 0.05 versus control).

    Journal: Frontiers in Immunology

    Article Title: DOT1L promotes immune evasion in lung adenocarcinoma through H3K79me2-mediated epigenetic activation of immune checkpoints

    doi: 10.3389/fimmu.2026.1719299

    Figure Lengend Snippet: DOT1L promotes immune evasion in LUAD by activating the JAK1/STAT3/PD-L1 axis and inducing T-cell exhaustion. (A-C) Western blot analysis detected protein expression of DOT1L, JAK1, STAT3, p-STAT3 and PD-L1 in A549 and H1975 cells. (D) Flow cytometry analysis of PD-1+ T cell subsets in the co-cultured system of PBMCs with A549 cells(* P < 0.05 versus control).

    Article Snippet: To rescue STAT3 activity, cells were co-treated with 2 nM STAT3 agonist ML115 (MedChemExpress, HY-111152) for 48 hours.

    Techniques: Western Blot, Expressing, Flow Cytometry, Cell Culture, Control

    Pharmacological inhibition of DOT1L exhibits antitumor effects in a LUAD tail vein lung metastasis model. (A) Bioluminescence imaging shows in vivo evaluation of PD-1 inhibitor (200 μg i.p, twice weekly), SGC0946-L group(20 mg/kg), SGC0946-H group(40 mg/kg), in the tail-vein lung metastasis model. (B) Average weight of mice in in each group, control group(blue line), PD-1 inhibitor group(green line), SGC0946-L group(purple line), SGC0946-H group(Red line). (C) Survival estimates of mice in each group. (D-G) IHC staining of DOT1L, H3K79me2, STAT3 protein expression in tumor tissues in each group. Red scale bar: 20 µm. SGC0946-L, low does group, SGC0946-H, high does group. * P < 0.05.

    Journal: Frontiers in Immunology

    Article Title: DOT1L promotes immune evasion in lung adenocarcinoma through H3K79me2-mediated epigenetic activation of immune checkpoints

    doi: 10.3389/fimmu.2026.1719299

    Figure Lengend Snippet: Pharmacological inhibition of DOT1L exhibits antitumor effects in a LUAD tail vein lung metastasis model. (A) Bioluminescence imaging shows in vivo evaluation of PD-1 inhibitor (200 μg i.p, twice weekly), SGC0946-L group(20 mg/kg), SGC0946-H group(40 mg/kg), in the tail-vein lung metastasis model. (B) Average weight of mice in in each group, control group(blue line), PD-1 inhibitor group(green line), SGC0946-L group(purple line), SGC0946-H group(Red line). (C) Survival estimates of mice in each group. (D-G) IHC staining of DOT1L, H3K79me2, STAT3 protein expression in tumor tissues in each group. Red scale bar: 20 µm. SGC0946-L, low does group, SGC0946-H, high does group. * P < 0.05.

    Article Snippet: To rescue STAT3 activity, cells were co-treated with 2 nM STAT3 agonist ML115 (MedChemExpress, HY-111152) for 48 hours.

    Techniques: Inhibition, Imaging, In Vivo, Control, Immunohistochemistry, Expressing

    Clinical association of DOT1L expression with metastatic progression and immune checkpoint regulation in LUAD. (A, B) IHC analysis of DOT1L and associated markers (H3K79me2, STAT3, PD-L1, PD-1, CD276, and LAG3) in LUAD tissues stratified by DOT1L expression levels. (C) Comparison of DOT1L expression between tumor and adjacent normal tissues. (D) DOT1L expression in stage IV metastatic LUAD compared to non-metastatic cases. (E-J) Pearson correlation analysis between DOT1L and immune checkpoint/epigenetic markers. (K) Pearson correlation analysis between DOT1L expression and TMB.

    Journal: Frontiers in Immunology

    Article Title: DOT1L promotes immune evasion in lung adenocarcinoma through H3K79me2-mediated epigenetic activation of immune checkpoints

    doi: 10.3389/fimmu.2026.1719299

    Figure Lengend Snippet: Clinical association of DOT1L expression with metastatic progression and immune checkpoint regulation in LUAD. (A, B) IHC analysis of DOT1L and associated markers (H3K79me2, STAT3, PD-L1, PD-1, CD276, and LAG3) in LUAD tissues stratified by DOT1L expression levels. (C) Comparison of DOT1L expression between tumor and adjacent normal tissues. (D) DOT1L expression in stage IV metastatic LUAD compared to non-metastatic cases. (E-J) Pearson correlation analysis between DOT1L and immune checkpoint/epigenetic markers. (K) Pearson correlation analysis between DOT1L expression and TMB.

    Article Snippet: To rescue STAT3 activity, cells were co-treated with 2 nM STAT3 agonist ML115 (MedChemExpress, HY-111152) for 48 hours.

    Techniques: Expressing, Comparison