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Biomol GmbH sta-21
Sta 21, supplied by Biomol GmbH, 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/sta21/sta+21/pm18025205-76-0-14
Average 90 stars, based on 1 article reviews
sta-21 - by Bioz Stars, 2026-10
90/100 stars

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Related Articles

Expressing:

Article Title: STAT3 is required for proliferation and maintenance of multipotency in glioblastoma stem cells
Article Snippet: Inhibitor experiments were performed using 100 μM S3I-201 (NCI) or 30 μM STA-21 (BioMol International, NCI) unless otherwise indicated.

Article Title: Inhibition of glycogen synthase kinase-3 increases NKG2D ligand MICA expression and sensitivity to NK cell-mediated cytotoxicity in multiple myeloma cells: role of STAT3.
Article Snippet: STA-21, a selective inhibitor of STAT3, was purchased from BIOMOL/Enzo Life Sciences (Farmingdale, NY).

Article Title: Caveolin-1 upregulation mediates suppression of primary breast tumor growth and brain metastases by Stat3 inhibition
Article Snippet: STA-21 were obtained from Biomol (Plymouth Meeting, PA).

Article Title: Signal transducer and activator of transcription 3 is a proviral host factor for hepatitis C virus.
Article Snippet: Host factors play an important role in all facets of the hepatitis C virus (HCV) life cycle and one such host factor is signal transducer and activator of transcription 3 (STAT3).. The HCV core protein has been shown to directly interact with and activate STAT3, while oxidative stress generated during HCV replication in a replicon-based model also induced STAT3 activation.. However, despite these findings the precise role of STAT3 in the HCV life cycle remains unknown.

Article Title: Interleukin-10-Induced Neutrophil Gelatinase-Associated Lipocalin Production in Macrophages with Consequences for Tumor Growth
Article Snippet: STA-21 was delivered by Biomol (Hamburg, Germany).

Transfection:

Article Title: STAT3 is required for proliferation and maintenance of multipotency in glioblastoma stem cells
Article Snippet: Inhibitor experiments were performed using 100 μM S3I-201 (NCI) or 30 μM STA-21 (BioMol International, NCI) unless otherwise indicated.

Article Title: Inhibition of glycogen synthase kinase-3 increases NKG2D ligand MICA expression and sensitivity to NK cell-mediated cytotoxicity in multiple myeloma cells: role of STAT3.
Article Snippet: STA-21, a selective inhibitor of STAT3, was purchased from BIOMOL/Enzo Life Sciences (Farmingdale, NY).

Article Title: Caveolin-1 upregulation mediates suppression of primary breast tumor growth and brain metastases by Stat3 inhibition
Article Snippet: STA-21 were obtained from Biomol (Plymouth Meeting, PA).

Article Title: Signal transducer and activator of transcription 3 is a proviral host factor for hepatitis C virus.
Article Snippet: Host factors play an important role in all facets of the hepatitis C virus (HCV) life cycle and one such host factor is signal transducer and activator of transcription 3 (STAT3).. The HCV core protein has been shown to directly interact with and activate STAT3, while oxidative stress generated during HCV replication in a replicon-based model also induced STAT3 activation.. However, despite these findings the precise role of STAT3 in the HCV life cycle remains unknown.

Article Title: Interleukin-10-Induced Neutrophil Gelatinase-Associated Lipocalin Production in Macrophages with Consequences for Tumor Growth
Article Snippet: STA-21 was delivered by Biomol (Hamburg, Germany).

Plasmid Preparation:

Article Title: STAT3 is required for proliferation and maintenance of multipotency in glioblastoma stem cells
Article Snippet: Inhibitor experiments were performed using 100 μM S3I-201 (NCI) or 30 μM STA-21 (BioMol International, NCI) unless otherwise indicated.

Article Title: Inhibition of glycogen synthase kinase-3 increases NKG2D ligand MICA expression and sensitivity to NK cell-mediated cytotoxicity in multiple myeloma cells: role of STAT3.
Article Snippet: STA-21, a selective inhibitor of STAT3, was purchased from BIOMOL/Enzo Life Sciences (Farmingdale, NY).

Article Title: Caveolin-1 upregulation mediates suppression of primary breast tumor growth and brain metastases by Stat3 inhibition
Article Snippet: STA-21 were obtained from Biomol (Plymouth Meeting, PA).

Article Title: Signal transducer and activator of transcription 3 is a proviral host factor for hepatitis C virus.
Article Snippet: Host factors play an important role in all facets of the hepatitis C virus (HCV) life cycle and one such host factor is signal transducer and activator of transcription 3 (STAT3).. The HCV core protein has been shown to directly interact with and activate STAT3, while oxidative stress generated during HCV replication in a replicon-based model also induced STAT3 activation.. However, despite these findings the precise role of STAT3 in the HCV life cycle remains unknown.

Article Title: Interleukin-10-Induced Neutrophil Gelatinase-Associated Lipocalin Production in Macrophages with Consequences for Tumor Growth
Article Snippet: STA-21 was delivered by Biomol (Hamburg, Germany).

Western Blot:

Article Title: STAT3 is required for proliferation and maintenance of multipotency in glioblastoma stem cells
Article Snippet: Inhibitor experiments were performed using 100 μM S3I-201 (NCI) or 30 μM STA-21 (BioMol International, NCI) unless otherwise indicated.

Article Title: Inhibition of glycogen synthase kinase-3 increases NKG2D ligand MICA expression and sensitivity to NK cell-mediated cytotoxicity in multiple myeloma cells: role of STAT3.
Article Snippet: STA-21, a selective inhibitor of STAT3, was purchased from BIOMOL/Enzo Life Sciences (Farmingdale, NY).

Article Title: Caveolin-1 upregulation mediates suppression of primary breast tumor growth and brain metastases by Stat3 inhibition
Article Snippet: STA-21 were obtained from Biomol (Plymouth Meeting, PA).

Article Title: Signal transducer and activator of transcription 3 is a proviral host factor for hepatitis C virus.
Article Snippet: Host factors play an important role in all facets of the hepatitis C virus (HCV) life cycle and one such host factor is signal transducer and activator of transcription 3 (STAT3).. The HCV core protein has been shown to directly interact with and activate STAT3, while oxidative stress generated during HCV replication in a replicon-based model also induced STAT3 activation.. However, despite these findings the precise role of STAT3 in the HCV life cycle remains unknown.

Article Title: Interleukin-10-Induced Neutrophil Gelatinase-Associated Lipocalin Production in Macrophages with Consequences for Tumor Growth
Article Snippet: STA-21 was delivered by Biomol (Hamburg, Germany).

Activity Assay:

Article Title: STAT3 is required for proliferation and maintenance of multipotency in glioblastoma stem cells
Article Snippet: Inhibitor experiments were performed using 100 μM S3I-201 (NCI) or 30 μM STA-21 (BioMol International, NCI) unless otherwise indicated.

Article Title: Inhibition of glycogen synthase kinase-3 increases NKG2D ligand MICA expression and sensitivity to NK cell-mediated cytotoxicity in multiple myeloma cells: role of STAT3.
Article Snippet: STA-21, a selective inhibitor of STAT3, was purchased from BIOMOL/Enzo Life Sciences (Farmingdale, NY).

Article Title: Caveolin-1 upregulation mediates suppression of primary breast tumor growth and brain metastases by Stat3 inhibition
Article Snippet: STA-21 were obtained from Biomol (Plymouth Meeting, PA).

Article Title: Signal transducer and activator of transcription 3 is a proviral host factor for hepatitis C virus.
Article Snippet: Host factors play an important role in all facets of the hepatitis C virus (HCV) life cycle and one such host factor is signal transducer and activator of transcription 3 (STAT3).. The HCV core protein has been shown to directly interact with and activate STAT3, while oxidative stress generated during HCV replication in a replicon-based model also induced STAT3 activation.. However, despite these findings the precise role of STAT3 in the HCV life cycle remains unknown.

Article Title: Interleukin-10-Induced Neutrophil Gelatinase-Associated Lipocalin Production in Macrophages with Consequences for Tumor Growth
Article Snippet: STA-21 was delivered by Biomol (Hamburg, Germany).



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Figure 5 |LPS-activated microglia promote astrocyte proliferation in vitro. (A) EdU staining and cellular localization with astrocytes cocultured under different conditions. (B) Western blotting analysis of <t>STAT3,</t> pSTAT3 and GFAP in the mixed cells after 24 hours of incubation. (C, D) The quantification of pSTAT3 (C, n = 3) and GFAP (D, n = 3) was normalized to β-actin. (E) LPS-activated microglia significantly increases the proportion of EdU+/GFAP+ astrocytes, which was reversed by <t>STA21</t> (an inhibitor of STAT3) pretreatment (n = 6). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 (one-way analysis of variance with Tukey’s post hoc test). Data are expressed as the mean ± SD. Western blot experiments were repeated three times. Immunofluorescence staining was repeated six times. DAPI: 4′,6-Diamidino-2-phenylindole; EdU: 5-ethynyl-2-deoxyuridine; GFAP: glial fibrillary acidic protein; LPS: lipopolysaccharide; pSTAT3: phosphorylated STAT3; SCI: spinal cord injury; STAT3: signal transducers and activators of transcription 3.
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Figure 5 |LPS-activated microglia promote astrocyte proliferation in vitro. (A) EdU staining and cellular localization with astrocytes cocultured under different conditions. (B) Western blotting analysis of <t>STAT3,</t> pSTAT3 and GFAP in the mixed cells after 24 hours of incubation. (C, D) The quantification of pSTAT3 (C, n = 3) and GFAP (D, n = 3) was normalized to β-actin. (E) LPS-activated microglia significantly increases the proportion of EdU+/GFAP+ astrocytes, which was reversed by <t>STA21</t> (an inhibitor of STAT3) pretreatment (n = 6). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 (one-way analysis of variance with Tukey’s post hoc test). Data are expressed as the mean ± SD. Western blot experiments were repeated three times. Immunofluorescence staining was repeated six times. DAPI: 4′,6-Diamidino-2-phenylindole; EdU: 5-ethynyl-2-deoxyuridine; GFAP: glial fibrillary acidic protein; LPS: lipopolysaccharide; pSTAT3: phosphorylated STAT3; SCI: spinal cord injury; STAT3: signal transducers and activators of transcription 3.
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Figure 5 |LPS-activated microglia promote astrocyte proliferation in vitro. (A) EdU staining and cellular localization with astrocytes cocultured under different conditions. (B) Western blotting analysis of <t>STAT3,</t> pSTAT3 and GFAP in the mixed cells after 24 hours of incubation. (C, D) The quantification of pSTAT3 (C, n = 3) and GFAP (D, n = 3) was normalized to β-actin. (E) LPS-activated microglia significantly increases the proportion of EdU+/GFAP+ astrocytes, which was reversed by <t>STA21</t> (an inhibitor of STAT3) pretreatment (n = 6). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 (one-way analysis of variance with Tukey’s post hoc test). Data are expressed as the mean ± SD. Western blot experiments were repeated three times. Immunofluorescence staining was repeated six times. DAPI: 4′,6-Diamidino-2-phenylindole; EdU: 5-ethynyl-2-deoxyuridine; GFAP: glial fibrillary acidic protein; LPS: lipopolysaccharide; pSTAT3: phosphorylated STAT3; SCI: spinal cord injury; STAT3: signal transducers and activators of transcription 3.
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Image Search Results


Figure 5 |LPS-activated microglia promote astrocyte proliferation in vitro. (A) EdU staining and cellular localization with astrocytes cocultured under different conditions. (B) Western blotting analysis of STAT3, pSTAT3 and GFAP in the mixed cells after 24 hours of incubation. (C, D) The quantification of pSTAT3 (C, n = 3) and GFAP (D, n = 3) was normalized to β-actin. (E) LPS-activated microglia significantly increases the proportion of EdU+/GFAP+ astrocytes, which was reversed by STA21 (an inhibitor of STAT3) pretreatment (n = 6). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 (one-way analysis of variance with Tukey’s post hoc test). Data are expressed as the mean ± SD. Western blot experiments were repeated three times. Immunofluorescence staining was repeated six times. DAPI: 4′,6-Diamidino-2-phenylindole; EdU: 5-ethynyl-2-deoxyuridine; GFAP: glial fibrillary acidic protein; LPS: lipopolysaccharide; pSTAT3: phosphorylated STAT3; SCI: spinal cord injury; STAT3: signal transducers and activators of transcription 3.

Journal: Neural regeneration research

Article Title: Microglial depletion impairs glial scar formation and aggravates inflammation partly by inhibiting STAT3 phosphorylation in astrocytes after spinal cord injury.

doi: 10.4103/1673-5374.357912

Figure Lengend Snippet: Figure 5 |LPS-activated microglia promote astrocyte proliferation in vitro. (A) EdU staining and cellular localization with astrocytes cocultured under different conditions. (B) Western blotting analysis of STAT3, pSTAT3 and GFAP in the mixed cells after 24 hours of incubation. (C, D) The quantification of pSTAT3 (C, n = 3) and GFAP (D, n = 3) was normalized to β-actin. (E) LPS-activated microglia significantly increases the proportion of EdU+/GFAP+ astrocytes, which was reversed by STA21 (an inhibitor of STAT3) pretreatment (n = 6). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 (one-way analysis of variance with Tukey’s post hoc test). Data are expressed as the mean ± SD. Western blot experiments were repeated three times. Immunofluorescence staining was repeated six times. DAPI: 4′,6-Diamidino-2-phenylindole; EdU: 5-ethynyl-2-deoxyuridine; GFAP: glial fibrillary acidic protein; LPS: lipopolysaccharide; pSTAT3: phosphorylated STAT3; SCI: spinal cord injury; STAT3: signal transducers and activators of transcription 3.

Article Snippet: To assess the role of STAT3 signaling, astrocytes were pretreated with 10 μM STA21 (an inhibitor of STAT3, Selleck, Shanghai, China, Cat# S7951) for 72 hours before coculture.

Techniques: In Vitro, Staining, Western Blot, Incubation, Immunofluorescence