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glut1 inhibitor bay 876 (MedChemExpress)

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MedChemExpress glut1 inhibitor bay 876
F-actin and nuclei in HuCCT1 and RBE cells transfected with si-NC, si-CD109 or si-EFNB2 and treated with 5 <t>µM</t> <t>BAY-876</t> or 1 µM TCEP for 24 h. si, small interfering; NC, negative control; TCEP, Tris-(2-carboxyethyl)-phosphine hydrochloride.

F-actin and nuclei in HuCCT1 and RBE cells transfected with si-NC, si-CD109 or si-EFNB2 and treated with 5 <t>µM</t> <t>BAY-876</t> or 1 µM TCEP for 24 h. si, small interfering; NC, negative control; TCEP, Tris-(2-carboxyethyl)-phosphine hydrochloride.

Glut1 Inhibitor Bay 876, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 96/100, based on 81 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/glut1+inhibitor+bay+876/BAY-876/pmc12793829-179-6-14
Average 96 stars, based on 81 article reviews

glut1 inhibitor bay 876 - by Bioz Stars, 2026-10

96/100 stars

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1) Product Images from "Exploring the role of disulfidptosis-related signatures in immune microenvironment, prognosis and therapeutic strategies of cholangiocarcinoma"

Article Title: Exploring the role of disulfidptosis-related signatures in immune microenvironment, prognosis and therapeutic strategies of cholangiocarcinoma

Journal: Oncology Reports

doi: 10.3892/or.2026.9042

F-actin and nuclei in HuCCT1 and RBE cells transfected with si-NC, si-CD109 or si-EFNB2 and treated with 5 µM BAY-876 or 1 µM TCEP for 24 h. si, small interfering; NC, negative control; TCEP, Tris-(2-carboxyethyl)-phosphine hydrochloride.

Figure Legend Snippet: F-actin and nuclei in HuCCT1 and RBE cells transfected with si-NC, si-CD109 or si-EFNB2 and treated with 5 µM BAY-876 or 1 µM TCEP for 24 h. si, small interfering; NC, negative control; TCEP, Tris-(2-carboxyethyl)-phosphine hydrochloride.

Techniques Used: Transfection, Negative Control

Construct:

Article Title: FOSL2 activates TGF ‐β1‐mediated GLUT1 / mTOR signaling to promote diabetic kidney disease
Article Snippet: .. FOSL2‐oe or oe‐NC‐treated MCs were further treated with the mTOR inhibitor Rapamycin at 100 nM for 48 h or GLUT1 inhibitor BAY‐876 (99.67%, HY‐100017, MedChemExpress) at 50 nM for 24 h , which were used to construct the oe‐NC + DMSO, FOSL2‐oe + DMSO, oe‐NC + Rapamycin, oe‐NC + BAY‐876, FOSL2‐oe + Rapamycin, and FOSL2‐oe + BAY‐876 groups. ..

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Journal: Oncology Reports

Article Title: Exploring the role of disulfidptosis-related signatures in immune microenvironment, prognosis and therapeutic strategies of cholangiocarcinoma

doi: 10.3892/or.2026.9042

Figure Lengend Snippet: F-actin and nuclei in HuCCT1 and RBE cells transfected with si-NC, si-CD109 or si-EFNB2 and treated with 5 µM BAY-876 or 1 µM TCEP for 24 h. si, small interfering; NC, negative control; TCEP, Tris-(2-carboxyethyl)-phosphine hydrochloride.

Article Snippet: Cells were then treated with the GLUT1 inhibitor BAY-876 (10 μM; cat. no. HY-100017, MedChemExpress) and/or the reducing agent, Tris-(2-carboxyethyl)-phosphine hydrochloride (TCEP; 20 mM; cat. no. A600974; Sangon Biotech Co., Ltd.) for 6 h at 37°C.

Techniques: Transfection, Negative Control

Fig. 4 GLUT1 drives Tp-induced cytokine production and increased glycolysis. A THP-1 cells were treated with PBS, DTp, and Tp (MOI of 2:1) for 24 h. Gene expression of different glucose transporters was measured by qRT-PCR, normalized to β-actin. B The mRNA levels of SLC2 A1 after THP-1 cells were treated with PBS, DTp, and Tp (MOI of 1:1, 2:1) for 24 h. C The expression of GLUT1 protein after THP-1 cells were treated with different concentrations of Tp (MOI of 1:1, 2:1, 4:1) for 24 h was measured by Western blot. Expression of GLUT1 protein after THP-1 cells were treated with Tp (MOI of 2:1) for different times was measured by Western blot. D GLUT1 membrane localization in THP-1 cells treated with PBS or Tp was assessed by immunofluorescence microscopy. Yellow arrows indicate the enlargement of some cells. The imaging is representative of three experiments. F-I THP-1 cells were pretreated with the GLUT1-specific inhibitor BAY876 (25, 50 nM) for 2 h and then cocultured with Tp (MOI of 2:1) for 24 h. The mRNA levels of (F) SLC2 A1, (G) HK1, (H) HK2, and (I) LDHA were detected by qRT-PCR. E Glucose uptake by THP-1 cells was measured by flow cytometry. J The time course of real-time changes in extracellular acidification after the glycolysis assay. K IL-6, (L) IL-8, and (M) CCL2 concentrations in the cell culture supernatants of THP-1 cells were quantified by ELISA. The data are shown as the mean ± SD. Statistical significance tested by one-way ANOVA test. *P < 0.05, **P < 0.01, ***P < 0.001, ns: no significant, n = 3

Journal: Cell communication and signaling : CCS

Article Title: HIF-1α regulated GLUT1-mediated glycolysis enhances Treponema pallidum-induced cytokine responses.

doi: 10.1186/s12964-025-02211-1

Figure Lengend Snippet: Fig. 4 GLUT1 drives Tp-induced cytokine production and increased glycolysis. A THP-1 cells were treated with PBS, DTp, and Tp (MOI of 2:1) for 24 h. Gene expression of different glucose transporters was measured by qRT-PCR, normalized to β-actin. B The mRNA levels of SLC2 A1 after THP-1 cells were treated with PBS, DTp, and Tp (MOI of 1:1, 2:1) for 24 h. C The expression of GLUT1 protein after THP-1 cells were treated with different concentrations of Tp (MOI of 1:1, 2:1, 4:1) for 24 h was measured by Western blot. Expression of GLUT1 protein after THP-1 cells were treated with Tp (MOI of 2:1) for different times was measured by Western blot. D GLUT1 membrane localization in THP-1 cells treated with PBS or Tp was assessed by immunofluorescence microscopy. Yellow arrows indicate the enlargement of some cells. The imaging is representative of three experiments. F-I THP-1 cells were pretreated with the GLUT1-specific inhibitor BAY876 (25, 50 nM) for 2 h and then cocultured with Tp (MOI of 2:1) for 24 h. The mRNA levels of (F) SLC2 A1, (G) HK1, (H) HK2, and (I) LDHA were detected by qRT-PCR. E Glucose uptake by THP-1 cells was measured by flow cytometry. J The time course of real-time changes in extracellular acidification after the glycolysis assay. K IL-6, (L) IL-8, and (M) CCL2 concentrations in the cell culture supernatants of THP-1 cells were quantified by ELISA. The data are shown as the mean ± SD. Statistical significance tested by one-way ANOVA test. *P < 0.05, **P < 0.01, ***P < 0.001, ns: no significant, n = 3

Article Snippet: For inhibition assays, THP-1 cells were treated with various chemicals, including glycolysis pathway inhibitor 2-deoxy-D-glucose (2-DG; HY-13966, Med Chem Express) and GLUT1 inhibitor BAY876 (HY-100017, Med Chem Express) for 2 h before Tp stimulation.

Techniques: Gene Expression, Quantitative RT-PCR, Expressing, Western Blot, Membrane, Immunofluorescence, Microscopy, Imaging, Flow Cytometry, Cell Culture, Enzyme-linked Immunosorbent Assay

Fig. 5 HIF-1α is involved in the regulation of GLUT1-mediated glycolysis and cytokine secretion after Tp treatment of monocytes. A The mRNA levels of HIF-1α after THP-1 cells were treated with different concentrations of Tp (MOI of 1:1, 2:1, and 4:1) for 24 h. B The expression of HIF-1α protein after THP-1 cells were treated with different concentrations of Tp (MOI of 1:1, 2:1, and 4:1) for 24 h was measured by Western blot. Expression of the HIF-1α protein after THP-1 cells were treated with Tp (MOI of 2:1) for different times was measured by Western blot. C Representative images from immunofluorescence analysis of HIF-1α protein accumulation and nuclear localization in THP-1 cells treated by PBS or Tp. Nuclei were stained with DAPI. Immunofluorescence was observed and photographed by a fluorescence microscope. D Nuclear and cytoplasmic extraction reagents were used to extract the nuclear and cytoplasmic proteins from the cells. Western blot analysis was performed after THP-1 cells were treated with different concentrations of Tp (MOI of 1:1, 2:1, and 4:1) for 24 h. β-actin was used as a loading control of cytoplasmic protein (abbreviated as ‘Cyto’ in the figure), and HDAC1 was used as a loading control of nuclear protein (abbreviated as ‘Nuc’ in the figure). E-N THP-1 cells were transfected with Si-NC or Si-HIF-1α for 24 h, and then the transfected THP-1 cells were treated with Tp (MOI of 2:1) for 24 h. The mRNA levels of (E) HIF-1α, (F) SLC2 A1, (G) HK1, (H) HK2, and (I) LDHA were detected by qRT-PCR. J The glucose uptake capacity of THP-1 cells was analyzed by flow cytometry. K The time course of real-time changes in extracellular acidification after the glycolysis assay. L IL-6, (M) IL-8, and (N) CCL2 concentrations in the cell culture supernatants of THP-1 cells were quantified by ELISA. The data are presented as the mean ± SD of three independent experiments. Statistical significance tested by one-way ANOVA test. *P < 0.05, **P < 0.01, ***P < 0.001, ns: no significant

Journal: Cell communication and signaling : CCS

Article Title: HIF-1α regulated GLUT1-mediated glycolysis enhances Treponema pallidum-induced cytokine responses.

doi: 10.1186/s12964-025-02211-1

Figure Lengend Snippet: Fig. 5 HIF-1α is involved in the regulation of GLUT1-mediated glycolysis and cytokine secretion after Tp treatment of monocytes. A The mRNA levels of HIF-1α after THP-1 cells were treated with different concentrations of Tp (MOI of 1:1, 2:1, and 4:1) for 24 h. B The expression of HIF-1α protein after THP-1 cells were treated with different concentrations of Tp (MOI of 1:1, 2:1, and 4:1) for 24 h was measured by Western blot. Expression of the HIF-1α protein after THP-1 cells were treated with Tp (MOI of 2:1) for different times was measured by Western blot. C Representative images from immunofluorescence analysis of HIF-1α protein accumulation and nuclear localization in THP-1 cells treated by PBS or Tp. Nuclei were stained with DAPI. Immunofluorescence was observed and photographed by a fluorescence microscope. D Nuclear and cytoplasmic extraction reagents were used to extract the nuclear and cytoplasmic proteins from the cells. Western blot analysis was performed after THP-1 cells were treated with different concentrations of Tp (MOI of 1:1, 2:1, and 4:1) for 24 h. β-actin was used as a loading control of cytoplasmic protein (abbreviated as ‘Cyto’ in the figure), and HDAC1 was used as a loading control of nuclear protein (abbreviated as ‘Nuc’ in the figure). E-N THP-1 cells were transfected with Si-NC or Si-HIF-1α for 24 h, and then the transfected THP-1 cells were treated with Tp (MOI of 2:1) for 24 h. The mRNA levels of (E) HIF-1α, (F) SLC2 A1, (G) HK1, (H) HK2, and (I) LDHA were detected by qRT-PCR. J The glucose uptake capacity of THP-1 cells was analyzed by flow cytometry. K The time course of real-time changes in extracellular acidification after the glycolysis assay. L IL-6, (M) IL-8, and (N) CCL2 concentrations in the cell culture supernatants of THP-1 cells were quantified by ELISA. The data are presented as the mean ± SD of three independent experiments. Statistical significance tested by one-way ANOVA test. *P < 0.05, **P < 0.01, ***P < 0.001, ns: no significant

Techniques: Expressing, Western Blot, Immunofluorescence, Staining, Fluorescence, Microscopy, Extraction, Control, Transfection, Quantitative RT-PCR, Flow Cytometry, Cell Culture, Enzyme-linked Immunosorbent Assay

Fig. 7 HIF1-α regulates GLUT1-mediated glycolysis, leading to increased monocyte cytokine production following Treponema pallidum infection. Under normal physiological conditions, monocytes uptake glucose through various glucose transporters and metabolize it via glycolysis and mitochondrial respiration to maintain cellular homeostasis. Following Tp infection, there is an induction of HIF-1α expression in the nucleus of monocytes, leading to the upregulation of GLUT1, LDHA, and other glycolytic enzyme genes, thereby enhancing monocyte glycolysis and subsequently promoting monocyte cytokine secretion

Journal: Cell communication and signaling : CCS

Article Title: HIF-1α regulated GLUT1-mediated glycolysis enhances Treponema pallidum-induced cytokine responses.

doi: 10.1186/s12964-025-02211-1

Figure Lengend Snippet: Fig. 7 HIF1-α regulates GLUT1-mediated glycolysis, leading to increased monocyte cytokine production following Treponema pallidum infection. Under normal physiological conditions, monocytes uptake glucose through various glucose transporters and metabolize it via glycolysis and mitochondrial respiration to maintain cellular homeostasis. Following Tp infection, there is an induction of HIF-1α expression in the nucleus of monocytes, leading to the upregulation of GLUT1, LDHA, and other glycolytic enzyme genes, thereby enhancing monocyte glycolysis and subsequently promoting monocyte cytokine secretion

Techniques: Infection, Expressing

Figure 4. GLUT1 is a target of miR-22 in HCC and regulates cell metabolism. (A) WB analysis of GLUT1 expression in the miR-22-silenced (MZIP-22) HepG2 cells and miR-22-overexpressing (pMXs-22) Huh-7 cells and related controls (shRNA). GAPDH was used as a housekeeping gene; WB analysis was performed in two independent experiments. GLUT1 molecular weight (MW) is from 45 to 60 kDa, and all the bands in this MW range have been considered for the analysis. (B) Dual-luciferase activity assay of wild-type (WT) and mutant (MUT) GLUT1-3′UTR vectors co-transfected with miR-22 in HepG2 and Huh-7 cells. NC: negative control precursor miRNA.

Journal: International journal of molecular sciences

Article Title: MiR-22/GLUT1 Axis Induces Metabolic Reprogramming and Sorafenib Resistance in Hepatocellular Carcinoma.

doi: 10.3390/ijms26083808

Figure Lengend Snippet: Figure 4. GLUT1 is a target of miR-22 in HCC and regulates cell metabolism. (A) WB analysis of GLUT1 expression in the miR-22-silenced (MZIP-22) HepG2 cells and miR-22-overexpressing (pMXs-22) Huh-7 cells and related controls (shRNA). GAPDH was used as a housekeeping gene; WB analysis was performed in two independent experiments. GLUT1 molecular weight (MW) is from 45 to 60 kDa, and all the bands in this MW range have been considered for the analysis. (B) Dual-luciferase activity assay of wild-type (WT) and mutant (MUT) GLUT1-3′UTR vectors co-transfected with miR-22 in HepG2 and Huh-7 cells. NC: negative control precursor miRNA.

Article Snippet: The cells were treated with 2.5–5.0 μM sorafenib tosylate (Bayer, Leverkusen, Germany) or 2.5–5.0 μM GLUT1 inhibitor BAY-876 or 100 μM CoCl2 (Selleck Chemicals, Houston, TX, USA).

Techniques: Expressing, shRNA, Molecular Weight, Luciferase, Activity Assay, Mutagenesis, Transfection, Negative Control

Figure 5. miR-22 downregulation is associated with sorafenib resistance in HCC. (A) Growth curves of the miR-22-silenced (MZIP-22) HepG2 cells and miR-22-overexpressing (pMXs-22) Huh-7 cells and re- lated controls (shRNA) under sorafenib treatment. Rescue experiment in the miR-22-silenced (MZIP-22) HepG2 cells treated with the GLUT1-inhibitor BAY-876 or vehicle (DMSO) and sorafenib. The growth curves were normalized to T0. Mean ± SD values are reported. Two independent experiments were performed in quadruplicate. WB analysis of GLUT1 expression in the same setting. WB was performed in two independent experiments, and GAPDH was used as a housekeeping gene. (B,C) Box plot graph of the miR-22 (B) and GLUT1 (C) levels in responder (N = 8) and non-responder (N = 7) HCC nodules from sorafenib-treated rats. The Y-axis reports the 2−∆∆Ct values corresponding to the miR-22 or GLUT1 levels. Correlation graph between miR-22 (B) or GLUT1 (C) expression and tumor volume of sorafenib-treated DEN-HCC rats. The axes report the 2−∆∆Ct values corresponding to mRNA levels and tumor size (mm3) of HCC nodules transformed in a log2 form. Beta-actin or U6RNA were used as housekeeping genes. Real-Time PCR analysis was run in triplicate. (D) Correlation graphs between the

Journal: International journal of molecular sciences

Article Title: MiR-22/GLUT1 Axis Induces Metabolic Reprogramming and Sorafenib Resistance in Hepatocellular Carcinoma.

doi: 10.3390/ijms26083808

Figure Lengend Snippet: Figure 5. miR-22 downregulation is associated with sorafenib resistance in HCC. (A) Growth curves of the miR-22-silenced (MZIP-22) HepG2 cells and miR-22-overexpressing (pMXs-22) Huh-7 cells and re- lated controls (shRNA) under sorafenib treatment. Rescue experiment in the miR-22-silenced (MZIP-22) HepG2 cells treated with the GLUT1-inhibitor BAY-876 or vehicle (DMSO) and sorafenib. The growth curves were normalized to T0. Mean ± SD values are reported. Two independent experiments were performed in quadruplicate. WB analysis of GLUT1 expression in the same setting. WB was performed in two independent experiments, and GAPDH was used as a housekeeping gene. (B,C) Box plot graph of the miR-22 (B) and GLUT1 (C) levels in responder (N = 8) and non-responder (N = 7) HCC nodules from sorafenib-treated rats. The Y-axis reports the 2−∆∆Ct values corresponding to the miR-22 or GLUT1 levels. Correlation graph between miR-22 (B) or GLUT1 (C) expression and tumor volume of sorafenib-treated DEN-HCC rats. The axes report the 2−∆∆Ct values corresponding to mRNA levels and tumor size (mm3) of HCC nodules transformed in a log2 form. Beta-actin or U6RNA were used as housekeeping genes. Real-Time PCR analysis was run in triplicate. (D) Correlation graphs between the

Techniques: shRNA, Expressing, Transformation Assay, Real-time Polymerase Chain Reaction

Figure 6. miR-22 circulating levels predict sorafenib resistance in human and rat HCCs. (A) Box plot graph of GLUT1 expression in early HCCs from the Bologna cohort divided based on serum miR-22 levels (high, N = 11; low, N = 10). The Y-axis reports the 2−∆∆Ct values. Mean ± SD values are displayed. GAPDH was used as a housekeeping gene. (B) Correlation graph between the tissue and serum miR-22 expression levels in early HCCs from the Bologna cohort. The axes report the 2−∆∆Ct values corresponding to the

Journal: International journal of molecular sciences

Article Title: MiR-22/GLUT1 Axis Induces Metabolic Reprogramming and Sorafenib Resistance in Hepatocellular Carcinoma.

doi: 10.3390/ijms26083808

Figure Lengend Snippet: Figure 6. miR-22 circulating levels predict sorafenib resistance in human and rat HCCs. (A) Box plot graph of GLUT1 expression in early HCCs from the Bologna cohort divided based on serum miR-22 levels (high, N = 11; low, N = 10). The Y-axis reports the 2−∆∆Ct values. Mean ± SD values are displayed. GAPDH was used as a housekeeping gene. (B) Correlation graph between the tissue and serum miR-22 expression levels in early HCCs from the Bologna cohort. The axes report the 2−∆∆Ct values corresponding to the

Techniques: Expressing

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glut1 inhibitor bay 876 (MedChemExpress)

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1) Product Images from "Exploring the role of disulfidptosis-related signatures in immune microenvironment, prognosis and therapeutic strategies of cholangiocarcinoma"

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