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rrx 001  (MedChemExpress)


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    MedChemExpress rrx 001
    (A) Schematic of the pentose phosphate pathway, highlighting the oxidative branch and the non-oxidative branch. (B–C) Metabolic flux analysis using [U-¹³C] glucose tracing. The flux in the non-oxidative branch intermediate sedoheptulose-7-phosphate (M + 7) (B) and the oxidative branch intermediate 6-phosphogluconate (M + 6) (C) were presented. (D–E) Expression of the key PPP enzymes G6PD and TKT in N2a cells infected or mock-infected with JEV was detected using immunoblotting at 36 hpi, and the representative blots were presented (D) . The relative expression levels of these proteins were calculated (E) . (F–J) Effect of the oxidative PPP branch inhibitors on JEV replication. N2a cells were infected with JEV at an MOI of 5, followed by treatment of 250 <t>nM</t> <t>RRX-001</t> at 1.5 hpi. The relative viral RNA levels at indicated time points were measured (F) . Additionally, increasing concentrations of RRX-001 (G) or 6-AN (H) were used to treat the JEV-infected N2a cells, and the viral RNA levels were determined. (I–J) The regulatory role of G6PD in JEV replication in N2a cells. The G6pdx knockout (KO) N2a cell line and the control cells (NC) were infected with JEV at an MOI of 5. The expression of G6PD and JEV E proteins (I) and the viral RNA levels (J) were assessed at 24 hpi. (K–L) The regulatory role of TKT in JEV replication in N2a cells. Tkt -deficient (sg1 and sg2) and negative control (NC) N2a cells were infected with JEV at an MOI of 5. The expression of TKT and JEV E proteins (K) and the viral RNA levels were determined (L) . Data are presented as mean ± s.e.m. from 3 independent biological replicates (n = 3). Significance was determined by two-tailed unpaired Student’s t-test ( B-C, E, J and L ), one-way ANOVA (G-H) , or two-way ANOVA (F) (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001; ns, not significant).
    Rrx 001, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 24 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rrx+001/RRx-001/pmc13340812-256-8-17
    Average 95 stars, based on 24 article reviews
    rrx 001 - by Bioz Stars, 2026-10
    95/100 stars

    Images

    1) Product Images from "Japanese encephalitis virus hijacks the host purine biosynthetic network to promote viral replication in neurons"

    Article Title: Japanese encephalitis virus hijacks the host purine biosynthetic network to promote viral replication in neurons

    Journal: PLOS Pathogens

    doi: 10.1371/journal.ppat.1014335

    (A) Schematic of the pentose phosphate pathway, highlighting the oxidative branch and the non-oxidative branch. (B–C) Metabolic flux analysis using [U-¹³C] glucose tracing. The flux in the non-oxidative branch intermediate sedoheptulose-7-phosphate (M + 7) (B) and the oxidative branch intermediate 6-phosphogluconate (M + 6) (C) were presented. (D–E) Expression of the key PPP enzymes G6PD and TKT in N2a cells infected or mock-infected with JEV was detected using immunoblotting at 36 hpi, and the representative blots were presented (D) . The relative expression levels of these proteins were calculated (E) . (F–J) Effect of the oxidative PPP branch inhibitors on JEV replication. N2a cells were infected with JEV at an MOI of 5, followed by treatment of 250 nM RRX-001 at 1.5 hpi. The relative viral RNA levels at indicated time points were measured (F) . Additionally, increasing concentrations of RRX-001 (G) or 6-AN (H) were used to treat the JEV-infected N2a cells, and the viral RNA levels were determined. (I–J) The regulatory role of G6PD in JEV replication in N2a cells. The G6pdx knockout (KO) N2a cell line and the control cells (NC) were infected with JEV at an MOI of 5. The expression of G6PD and JEV E proteins (I) and the viral RNA levels (J) were assessed at 24 hpi. (K–L) The regulatory role of TKT in JEV replication in N2a cells. Tkt -deficient (sg1 and sg2) and negative control (NC) N2a cells were infected with JEV at an MOI of 5. The expression of TKT and JEV E proteins (K) and the viral RNA levels were determined (L) . Data are presented as mean ± s.e.m. from 3 independent biological replicates (n = 3). Significance was determined by two-tailed unpaired Student’s t-test ( B-C, E, J and L ), one-way ANOVA (G-H) , or two-way ANOVA (F) (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001; ns, not significant).
    Figure Legend Snippet: (A) Schematic of the pentose phosphate pathway, highlighting the oxidative branch and the non-oxidative branch. (B–C) Metabolic flux analysis using [U-¹³C] glucose tracing. The flux in the non-oxidative branch intermediate sedoheptulose-7-phosphate (M + 7) (B) and the oxidative branch intermediate 6-phosphogluconate (M + 6) (C) were presented. (D–E) Expression of the key PPP enzymes G6PD and TKT in N2a cells infected or mock-infected with JEV was detected using immunoblotting at 36 hpi, and the representative blots were presented (D) . The relative expression levels of these proteins were calculated (E) . (F–J) Effect of the oxidative PPP branch inhibitors on JEV replication. N2a cells were infected with JEV at an MOI of 5, followed by treatment of 250 nM RRX-001 at 1.5 hpi. The relative viral RNA levels at indicated time points were measured (F) . Additionally, increasing concentrations of RRX-001 (G) or 6-AN (H) were used to treat the JEV-infected N2a cells, and the viral RNA levels were determined. (I–J) The regulatory role of G6PD in JEV replication in N2a cells. The G6pdx knockout (KO) N2a cell line and the control cells (NC) were infected with JEV at an MOI of 5. The expression of G6PD and JEV E proteins (I) and the viral RNA levels (J) were assessed at 24 hpi. (K–L) The regulatory role of TKT in JEV replication in N2a cells. Tkt -deficient (sg1 and sg2) and negative control (NC) N2a cells were infected with JEV at an MOI of 5. The expression of TKT and JEV E proteins (K) and the viral RNA levels were determined (L) . Data are presented as mean ± s.e.m. from 3 independent biological replicates (n = 3). Significance was determined by two-tailed unpaired Student’s t-test ( B-C, E, J and L ), one-way ANOVA (G-H) , or two-way ANOVA (F) (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001; ns, not significant).

    Techniques Used: Expressing, Infection, Western Blot, Knock-Out, Control, Negative Control, Two Tailed Test

    Related Articles

    Recombinant:

    Article Title: Targeting the CD47-HCK-LGALS9 axis disrupts proliferation-immunosuppression coupling in early-stage endometrial cancer.
    Article Snippet: .. HEC-1A and KLE cells were treated with the following agents: RRX-001 (#HY-16438, MCE, USA) at 5, 6.25, and 7.5 μM; recombinant LGALS9 (#11147-H01H, Sino Biological, China) at 50 ng/mL; GSK5182 (#SML3150, Germany) at 10, 20, and 30 μM; progesterone (#HY-N0437, MCE, USA); and estradiol (#HY-B0141, MCE, USA). ..

    Article Title: Targeting the CD47-HCK-LGALS9 axis disrupts proliferation-immunosuppression coupling in early-stage endometrial cancer
    Article Snippet: .. HEC-1 A and KLE cells were treated with the following agents: RRX-001 (#HY-16438, MCE, USA) at 5, 6.25, and 7.5 μM; recombinant LGALS9 (#11147-H01H, Sino Biological, China) at 50 ng/mL; GSK5182 (#SML3150, Germany) at 10, 20, and 30 μM; progesterone (#HY-N0437, MCE, USA); and estradiol (#HY-B0141, MCE, USA). ..

    ATP Assay:

    Article Title: RRx-001 inhibits G6PD to deplete NADPH and trigger disulfidptosis coupled with DAMP-mediated immunogenic cell death in hepatocellular carcinoma.
    Article Snippet: Ferroptosis inhibitor, Ferrostatin-1. (MCE) Enzyme inhibitors, G6PDi-1 (MCE) and Deferoxaminemesylate AR TI CL E IN P RE SS (MCE). .. Other specific target inhibitors include DS18561882(AmBeed), NADS (MCE), AG16780(AmBeed), Etomoxir(AmBeed), TCEP (MCE) and RRx-001 (MCE).The following assay kits were acquired from Beyotime Biotechnology: ATP Assay Kit, Glucose-6-Phosphate Dehydrogenase (G6PDH) Activity Assay Kit, Reactive Oxygen Species (ROS) Detection Kit, Glucose Assay Kit, NADP+/NADPH Assay Kit, Reduced/Oxidized Glutathione (GSH/GSSG) Assay Kit, and Nitric Oxide (NO) Detection Kit. .. Phalloidin was sourced from Solarbio.

    Activity Assay:

    Article Title: RRx-001 inhibits G6PD to deplete NADPH and trigger disulfidptosis coupled with DAMP-mediated immunogenic cell death in hepatocellular carcinoma.
    Article Snippet: Ferroptosis inhibitor, Ferrostatin-1. (MCE) Enzyme inhibitors, G6PDi-1 (MCE) and Deferoxaminemesylate AR TI CL E IN P RE SS (MCE). .. Other specific target inhibitors include DS18561882(AmBeed), NADS (MCE), AG16780(AmBeed), Etomoxir(AmBeed), TCEP (MCE) and RRx-001 (MCE).The following assay kits were acquired from Beyotime Biotechnology: ATP Assay Kit, Glucose-6-Phosphate Dehydrogenase (G6PDH) Activity Assay Kit, Reactive Oxygen Species (ROS) Detection Kit, Glucose Assay Kit, NADP+/NADPH Assay Kit, Reduced/Oxidized Glutathione (GSH/GSSG) Assay Kit, and Nitric Oxide (NO) Detection Kit. .. Phalloidin was sourced from Solarbio.

    Glucose Assay:

    Article Title: RRx-001 inhibits G6PD to deplete NADPH and trigger disulfidptosis coupled with DAMP-mediated immunogenic cell death in hepatocellular carcinoma.
    Article Snippet: Ferroptosis inhibitor, Ferrostatin-1. (MCE) Enzyme inhibitors, G6PDi-1 (MCE) and Deferoxaminemesylate AR TI CL E IN P RE SS (MCE). .. Other specific target inhibitors include DS18561882(AmBeed), NADS (MCE), AG16780(AmBeed), Etomoxir(AmBeed), TCEP (MCE) and RRx-001 (MCE).The following assay kits were acquired from Beyotime Biotechnology: ATP Assay Kit, Glucose-6-Phosphate Dehydrogenase (G6PDH) Activity Assay Kit, Reactive Oxygen Species (ROS) Detection Kit, Glucose Assay Kit, NADP+/NADPH Assay Kit, Reduced/Oxidized Glutathione (GSH/GSSG) Assay Kit, and Nitric Oxide (NO) Detection Kit. .. Phalloidin was sourced from Solarbio.

    other:

    Article Title: Japanese encephalitis virus hijacks the host purine biosynthetic network to promote viral replication in neurons
    Article Snippet: Mycophenolic acid (MPA, HY-108325), Ag2037 (HY-14530), DS18561882 (HY-130251), RRx-001 (HY-16438) and 6-Aminonicotinamide (6-AN, HY-101966) were purchased from MedChem Express.



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    (A) Schematic of the pentose phosphate pathway, highlighting the oxidative branch and the non-oxidative branch. (B–C) Metabolic flux analysis using [U-¹³C] glucose tracing. The flux in the non-oxidative branch intermediate sedoheptulose-7-phosphate (M + 7) (B) and the oxidative branch intermediate 6-phosphogluconate (M + 6) (C) were presented. (D–E) Expression of the key PPP enzymes G6PD and TKT in N2a cells infected or mock-infected with JEV was detected using immunoblotting at 36 hpi, and the representative blots were presented (D) . The relative expression levels of these proteins were calculated (E) . (F–J) Effect of the oxidative PPP branch inhibitors on JEV replication. N2a cells were infected with JEV at an MOI of 5, followed by treatment of 250 <t>nM</t> <t>RRX-001</t> at 1.5 hpi. The relative viral RNA levels at indicated time points were measured (F) . Additionally, increasing concentrations of RRX-001 (G) or 6-AN (H) were used to treat the JEV-infected N2a cells, and the viral RNA levels were determined. (I–J) The regulatory role of G6PD in JEV replication in N2a cells. The G6pdx knockout (KO) N2a cell line and the control cells (NC) were infected with JEV at an MOI of 5. The expression of G6PD and JEV E proteins (I) and the viral RNA levels (J) were assessed at 24 hpi. (K–L) The regulatory role of TKT in JEV replication in N2a cells. Tkt -deficient (sg1 and sg2) and negative control (NC) N2a cells were infected with JEV at an MOI of 5. The expression of TKT and JEV E proteins (K) and the viral RNA levels were determined (L) . Data are presented as mean ± s.e.m. from 3 independent biological replicates (n = 3). Significance was determined by two-tailed unpaired Student’s t-test ( B-C, E, J and L ), one-way ANOVA (G-H) , or two-way ANOVA (F) (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001; ns, not significant).
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    (A) Schematic of the pentose phosphate pathway, highlighting the oxidative branch and the non-oxidative branch. (B–C) Metabolic flux analysis using [U-¹³C] glucose tracing. The flux in the non-oxidative branch intermediate sedoheptulose-7-phosphate (M + 7) (B) and the oxidative branch intermediate 6-phosphogluconate (M + 6) (C) were presented. (D–E) Expression of the key PPP enzymes G6PD and TKT in N2a cells infected or mock-infected with JEV was detected using immunoblotting at 36 hpi, and the representative blots were presented (D) . The relative expression levels of these proteins were calculated (E) . (F–J) Effect of the oxidative PPP branch inhibitors on JEV replication. N2a cells were infected with JEV at an MOI of 5, followed by treatment of 250 <t>nM</t> <t>RRX-001</t> at 1.5 hpi. The relative viral RNA levels at indicated time points were measured (F) . Additionally, increasing concentrations of RRX-001 (G) or 6-AN (H) were used to treat the JEV-infected N2a cells, and the viral RNA levels were determined. (I–J) The regulatory role of G6PD in JEV replication in N2a cells. The G6pdx knockout (KO) N2a cell line and the control cells (NC) were infected with JEV at an MOI of 5. The expression of G6PD and JEV E proteins (I) and the viral RNA levels (J) were assessed at 24 hpi. (K–L) The regulatory role of TKT in JEV replication in N2a cells. Tkt -deficient (sg1 and sg2) and negative control (NC) N2a cells were infected with JEV at an MOI of 5. The expression of TKT and JEV E proteins (K) and the viral RNA levels were determined (L) . Data are presented as mean ± s.e.m. from 3 independent biological replicates (n = 3). Significance was determined by two-tailed unpaired Student’s t-test ( B-C, E, J and L ), one-way ANOVA (G-H) , or two-way ANOVA (F) (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001; ns, not significant).
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    Image Search Results


    (A) Schematic of the pentose phosphate pathway, highlighting the oxidative branch and the non-oxidative branch. (B–C) Metabolic flux analysis using [U-¹³C] glucose tracing. The flux in the non-oxidative branch intermediate sedoheptulose-7-phosphate (M + 7) (B) and the oxidative branch intermediate 6-phosphogluconate (M + 6) (C) were presented. (D–E) Expression of the key PPP enzymes G6PD and TKT in N2a cells infected or mock-infected with JEV was detected using immunoblotting at 36 hpi, and the representative blots were presented (D) . The relative expression levels of these proteins were calculated (E) . (F–J) Effect of the oxidative PPP branch inhibitors on JEV replication. N2a cells were infected with JEV at an MOI of 5, followed by treatment of 250 nM RRX-001 at 1.5 hpi. The relative viral RNA levels at indicated time points were measured (F) . Additionally, increasing concentrations of RRX-001 (G) or 6-AN (H) were used to treat the JEV-infected N2a cells, and the viral RNA levels were determined. (I–J) The regulatory role of G6PD in JEV replication in N2a cells. The G6pdx knockout (KO) N2a cell line and the control cells (NC) were infected with JEV at an MOI of 5. The expression of G6PD and JEV E proteins (I) and the viral RNA levels (J) were assessed at 24 hpi. (K–L) The regulatory role of TKT in JEV replication in N2a cells. Tkt -deficient (sg1 and sg2) and negative control (NC) N2a cells were infected with JEV at an MOI of 5. The expression of TKT and JEV E proteins (K) and the viral RNA levels were determined (L) . Data are presented as mean ± s.e.m. from 3 independent biological replicates (n = 3). Significance was determined by two-tailed unpaired Student’s t-test ( B-C, E, J and L ), one-way ANOVA (G-H) , or two-way ANOVA (F) (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001; ns, not significant).

    Journal: PLOS Pathogens

    Article Title: Japanese encephalitis virus hijacks the host purine biosynthetic network to promote viral replication in neurons

    doi: 10.1371/journal.ppat.1014335

    Figure Lengend Snippet: (A) Schematic of the pentose phosphate pathway, highlighting the oxidative branch and the non-oxidative branch. (B–C) Metabolic flux analysis using [U-¹³C] glucose tracing. The flux in the non-oxidative branch intermediate sedoheptulose-7-phosphate (M + 7) (B) and the oxidative branch intermediate 6-phosphogluconate (M + 6) (C) were presented. (D–E) Expression of the key PPP enzymes G6PD and TKT in N2a cells infected or mock-infected with JEV was detected using immunoblotting at 36 hpi, and the representative blots were presented (D) . The relative expression levels of these proteins were calculated (E) . (F–J) Effect of the oxidative PPP branch inhibitors on JEV replication. N2a cells were infected with JEV at an MOI of 5, followed by treatment of 250 nM RRX-001 at 1.5 hpi. The relative viral RNA levels at indicated time points were measured (F) . Additionally, increasing concentrations of RRX-001 (G) or 6-AN (H) were used to treat the JEV-infected N2a cells, and the viral RNA levels were determined. (I–J) The regulatory role of G6PD in JEV replication in N2a cells. The G6pdx knockout (KO) N2a cell line and the control cells (NC) were infected with JEV at an MOI of 5. The expression of G6PD and JEV E proteins (I) and the viral RNA levels (J) were assessed at 24 hpi. (K–L) The regulatory role of TKT in JEV replication in N2a cells. Tkt -deficient (sg1 and sg2) and negative control (NC) N2a cells were infected with JEV at an MOI of 5. The expression of TKT and JEV E proteins (K) and the viral RNA levels were determined (L) . Data are presented as mean ± s.e.m. from 3 independent biological replicates (n = 3). Significance was determined by two-tailed unpaired Student’s t-test ( B-C, E, J and L ), one-way ANOVA (G-H) , or two-way ANOVA (F) (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001; ns, not significant).

    Article Snippet: Mycophenolic acid (MPA, HY-108325), Ag2037 (HY-14530), DS18561882 (HY-130251), RRx-001 (HY-16438) and 6-Aminonicotinamide (6-AN, HY-101966) were purchased from MedChem Express.

    Techniques: Expressing, Infection, Western Blot, Knock-Out, Control, Negative Control, Two Tailed Test

    Variations in G6PD Expression Across Pan-Cancer Types. A Expression levels of G6PD mRNA in normal tissues and pan-cancer tissues were determined using the TCGA and GTEx datasets. B G6PD protein expression levels provided by the HPA database. C, D Relationships between G6PD expression and tumor clinical stage ( C ) and tumor histological grade ( D ). * p < 0.05, ** p < 0.01, *** p < 0.001

    Journal: Discover Oncology

    Article Title: Identification of the disulfidptosis-related gene G6PD as a potential biomarker and therapeutic target in pancreatic ductal adenocarcinoma by integrative bioinformatics analysis and experimental validation

    doi: 10.1007/s12672-026-04753-3

    Figure Lengend Snippet: Variations in G6PD Expression Across Pan-Cancer Types. A Expression levels of G6PD mRNA in normal tissues and pan-cancer tissues were determined using the TCGA and GTEx datasets. B G6PD protein expression levels provided by the HPA database. C, D Relationships between G6PD expression and tumor clinical stage ( C ) and tumor histological grade ( D ). * p < 0.05, ** p < 0.01, *** p < 0.001

    Article Snippet: The G6PD inhibitor RRx-001 was obtained from Med Chem Express (MCE) and dissolved in dimethyl sulfoxide (DMSO) to prepare a stock solution.

    Techniques: Expressing

    Expression of G6PD in PAAD. A Boxplot showing differential G6PD expression between PAAD tumor tissues and normal tissues. B-D G6PD expression levels in three GEO cohorts. E RT-qPCR detection of G6PD mRNA expression levels. F Immunohistochemical sections of G6PD from the HPA database. G Analysis of G6PD protein expression levels using the CPTAC database. H Western blot analysis of G6PD protein levels. I Quantification of the Western blot results. J Immunohistochemical staining of G6PD protein expression in pancreatic cancer tissues. K Quantification of the IHC staining data. L RT-qPCR assessment of G6PD mRNA levels in pancreatic cancer tissues. * p < 0.05, ** p < 0.01, *** p < 0.001

    Journal: Discover Oncology

    Article Title: Identification of the disulfidptosis-related gene G6PD as a potential biomarker and therapeutic target in pancreatic ductal adenocarcinoma by integrative bioinformatics analysis and experimental validation

    doi: 10.1007/s12672-026-04753-3

    Figure Lengend Snippet: Expression of G6PD in PAAD. A Boxplot showing differential G6PD expression between PAAD tumor tissues and normal tissues. B-D G6PD expression levels in three GEO cohorts. E RT-qPCR detection of G6PD mRNA expression levels. F Immunohistochemical sections of G6PD from the HPA database. G Analysis of G6PD protein expression levels using the CPTAC database. H Western blot analysis of G6PD protein levels. I Quantification of the Western blot results. J Immunohistochemical staining of G6PD protein expression in pancreatic cancer tissues. K Quantification of the IHC staining data. L RT-qPCR assessment of G6PD mRNA levels in pancreatic cancer tissues. * p < 0.05, ** p < 0.01, *** p < 0.001

    Article Snippet: The G6PD inhibitor RRx-001 was obtained from Med Chem Express (MCE) and dissolved in dimethyl sulfoxide (DMSO) to prepare a stock solution.

    Techniques: Expressing, Quantitative RT-PCR, Immunohistochemical staining, Western Blot, Staining, Immunohistochemistry

    Prognostic Value of G6PD Expression in PAAD. A Kaplan-Meier survival curves comparing DFS in patients with different G6PD expression levels. B ROC curve analysis of the diagnostic potential of G6PD in PAAD. ( C ) Time-dependent ROC analysis. D-J Graphical representation of the association between G6PD mRNA expression and various clinical variables in PAAD patients, including clinical stage ( D ), histological grade ( E ), T stage ( F ), N stage ( G ), M stage ( H ), age ( I ), and gender ( J ). * p < 0.05, ** p < 0.01, *** p < 0.001

    Journal: Discover Oncology

    Article Title: Identification of the disulfidptosis-related gene G6PD as a potential biomarker and therapeutic target in pancreatic ductal adenocarcinoma by integrative bioinformatics analysis and experimental validation

    doi: 10.1007/s12672-026-04753-3

    Figure Lengend Snippet: Prognostic Value of G6PD Expression in PAAD. A Kaplan-Meier survival curves comparing DFS in patients with different G6PD expression levels. B ROC curve analysis of the diagnostic potential of G6PD in PAAD. ( C ) Time-dependent ROC analysis. D-J Graphical representation of the association between G6PD mRNA expression and various clinical variables in PAAD patients, including clinical stage ( D ), histological grade ( E ), T stage ( F ), N stage ( G ), M stage ( H ), age ( I ), and gender ( J ). * p < 0.05, ** p < 0.01, *** p < 0.001

    Article Snippet: The G6PD inhibitor RRx-001 was obtained from Med Chem Express (MCE) and dissolved in dimethyl sulfoxide (DMSO) to prepare a stock solution.

    Techniques: Expressing, Diagnostic Assay

    Correlation Analysis of G6PD Expression with Immune Cell Infiltration in PAAD. A Lollipop plot showing the correlation between G6PD expression and infiltration of 24 immune cell types. B Scatter plot displaying the correlation between G6PD expression and various immune cells. C Dot plot of immune infiltration scores for high and low G6PD expression groups. D-F Scatter plots showing the correlation between G6PD and ImmuneScore ( D ), StromalScore ( E ), and ESTIMATEScore ( F ). * p < 0.05, ** p < 0.01, *** p < 0.001

    Journal: Discover Oncology

    Article Title: Identification of the disulfidptosis-related gene G6PD as a potential biomarker and therapeutic target in pancreatic ductal adenocarcinoma by integrative bioinformatics analysis and experimental validation

    doi: 10.1007/s12672-026-04753-3

    Figure Lengend Snippet: Correlation Analysis of G6PD Expression with Immune Cell Infiltration in PAAD. A Lollipop plot showing the correlation between G6PD expression and infiltration of 24 immune cell types. B Scatter plot displaying the correlation between G6PD expression and various immune cells. C Dot plot of immune infiltration scores for high and low G6PD expression groups. D-F Scatter plots showing the correlation between G6PD and ImmuneScore ( D ), StromalScore ( E ), and ESTIMATEScore ( F ). * p < 0.05, ** p < 0.01, *** p < 0.001

    Article Snippet: The G6PD inhibitor RRx-001 was obtained from Med Chem Express (MCE) and dissolved in dimethyl sulfoxide (DMSO) to prepare a stock solution.

    Techniques: Expressing

    Correlation of G6PD Expression with Immune Regulatory Genes. A-C Correlation of G6PD expression with three types of immune regulators (including immunosuppressive agents, immunostimulatory agents, and MHC-related molecules). D, E Correlation of G6PD expression with chemokines and their receptors. On the right side of each panel, the two cells/molecules with the highest positive or negative correlation with G6PD expression are shown. F, G The linked medications that target G6PD were predicted using the CTRP ( F ) and GDSC ( G ) databases. * p < 0.05, ** p < 0.01, *** p < 0.001

    Journal: Discover Oncology

    Article Title: Identification of the disulfidptosis-related gene G6PD as a potential biomarker and therapeutic target in pancreatic ductal adenocarcinoma by integrative bioinformatics analysis and experimental validation

    doi: 10.1007/s12672-026-04753-3

    Figure Lengend Snippet: Correlation of G6PD Expression with Immune Regulatory Genes. A-C Correlation of G6PD expression with three types of immune regulators (including immunosuppressive agents, immunostimulatory agents, and MHC-related molecules). D, E Correlation of G6PD expression with chemokines and their receptors. On the right side of each panel, the two cells/molecules with the highest positive or negative correlation with G6PD expression are shown. F, G The linked medications that target G6PD were predicted using the CTRP ( F ) and GDSC ( G ) databases. * p < 0.05, ** p < 0.01, *** p < 0.001

    Article Snippet: The G6PD inhibitor RRx-001 was obtained from Med Chem Express (MCE) and dissolved in dimethyl sulfoxide (DMSO) to prepare a stock solution.

    Techniques: Expressing, Medications

    Functional Enrichment Analysis of G6PD-Interacting and Co-Expressed Genes. A Co-expression heatmap of the top 20 genes most strongly correlated with G6PD. B-E GO and KEGG enrichment analysis of genes correlated with G6PD expression. F-G Gene Set Enrichment Analysis (GSEA) of PAAD patient cohorts stratified by G6PD expression levels. * p < 0.05, ** p < 0.01, *** p < 0.001

    Journal: Discover Oncology

    Article Title: Identification of the disulfidptosis-related gene G6PD as a potential biomarker and therapeutic target in pancreatic ductal adenocarcinoma by integrative bioinformatics analysis and experimental validation

    doi: 10.1007/s12672-026-04753-3

    Figure Lengend Snippet: Functional Enrichment Analysis of G6PD-Interacting and Co-Expressed Genes. A Co-expression heatmap of the top 20 genes most strongly correlated with G6PD. B-E GO and KEGG enrichment analysis of genes correlated with G6PD expression. F-G Gene Set Enrichment Analysis (GSEA) of PAAD patient cohorts stratified by G6PD expression levels. * p < 0.05, ** p < 0.01, *** p < 0.001

    Article Snippet: The G6PD inhibitor RRx-001 was obtained from Med Chem Express (MCE) and dissolved in dimethyl sulfoxide (DMSO) to prepare a stock solution.

    Techniques: Functional Assay, Expressing

    G6PD Inhibitor RRx-001 Activates Disulfide-Mediated Cell Death in SW1990 Cells. A Molecular docking and optimization of RRx-001 with G6PD. B CCK-8 assay to detect the proliferation capacity of SW1990 cells. C-E Flow cytometry analysis of SW1990 cell death rates. F WST-8 colorimetric assay to measure NADPH levels in SW1990 cells. G Fluorescence microplate assay to determine cystine uptake capacity in SW1990 cells. H Representative immunofluorescence images of F-actin (phalloidin staining) and nuclei (DAPI) in SW1990 cells treated with RRx-001 or vehicle control. I Quantification of immunofluorescence staining. * p < 0.05, ** p < 0.01, *** p < 0.001

    Journal: Discover Oncology

    Article Title: Identification of the disulfidptosis-related gene G6PD as a potential biomarker and therapeutic target in pancreatic ductal adenocarcinoma by integrative bioinformatics analysis and experimental validation

    doi: 10.1007/s12672-026-04753-3

    Figure Lengend Snippet: G6PD Inhibitor RRx-001 Activates Disulfide-Mediated Cell Death in SW1990 Cells. A Molecular docking and optimization of RRx-001 with G6PD. B CCK-8 assay to detect the proliferation capacity of SW1990 cells. C-E Flow cytometry analysis of SW1990 cell death rates. F WST-8 colorimetric assay to measure NADPH levels in SW1990 cells. G Fluorescence microplate assay to determine cystine uptake capacity in SW1990 cells. H Representative immunofluorescence images of F-actin (phalloidin staining) and nuclei (DAPI) in SW1990 cells treated with RRx-001 or vehicle control. I Quantification of immunofluorescence staining. * p < 0.05, ** p < 0.01, *** p < 0.001

    Article Snippet: The G6PD inhibitor RRx-001 was obtained from Med Chem Express (MCE) and dissolved in dimethyl sulfoxide (DMSO) to prepare a stock solution.

    Techniques: CCK-8 Assay, Flow Cytometry, Colorimetric Assay, Fluorescence, Immunofluorescence, Staining, Control