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gne 617  (MedChemExpress)


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    MedChemExpress gne 617
    Gne 617, 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/gne 617/product/MedChemExpress
    Average 94 stars, based on 6 article reviews
    gne 617 - by Bioz Stars, 2026-02
    94/100 stars

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    Selleck Chemicals fk866
    NAPRT loss confers sensitivity to NAMPTis in FH-deficient RCC models. A, Schematic of NAD + biosynthesis pathways, Triple arrow in the de novo synthesis pathway represents five additional enzymatic conversion steps in the pathway. B, YUNK1 cells treated with increasing concentrations of <t>FK866</t> with or without the addition of 10-μmol/L of NA. C, Total NAD + levels in YUNK1 and YUNK1 shFH cells at baseline and upon treatment with 25-nmol/L FK866 for 24 hours alone or with 10-μmol/L NA. D–F, FH-deficient and NAPRT-silenced NCCFH1 ( D ), UOK262 ( E ), and UOK268 ( F ) cell lines treated with increasing concentrations of FK866 after 8 ( D ), 6 ( E ), or 8 ( F ) days with or without 10-μmol/L NA. G–I, Total NAD + quantification in NCCFH1 ( G ), UOK262 ( H ), and UOK268 ( I ) after 24-hour treatment with 25-nmol/L FK866 alone or with 10-μmol/L NA. Two-way ANOVA, *, P = 0.0151; ****, P ≤ 0.0001. Trp, tryptophan; QA, quinolinic acid; QPRT, Quinolinate phosphoribosyl transferase; NAMN, nicotinic acid mononucleotide; NAPRT, nicotinate phosphoribosyltransferase; NA, nicotinic acid; NMNAT, Nicotinamide mononucleotide adenylyl transferase; NAAD, nicotinic acid adenine dinucleotide; NADS, NAD + synthetase; PARPs, poly(ADP-ribose) polymerases, NAM, nicotinamide; NAMPT, nicotinamide phosphoribosyltransferase; NMN, nicotinamide mononucleotide; NMNAT, nicotinamide mononucleotide adenylyl transferase.
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    MedChemExpress gne
    NAPRT loss confers sensitivity to NAMPTis in FH-deficient RCC models. A, Schematic of NAD + biosynthesis pathways, Triple arrow in the de novo synthesis pathway represents five additional enzymatic conversion steps in the pathway. B, YUNK1 cells treated with increasing concentrations of <t>FK866</t> with or without the addition of 10-μmol/L of NA. C, Total NAD + levels in YUNK1 and YUNK1 shFH cells at baseline and upon treatment with 25-nmol/L FK866 for 24 hours alone or with 10-μmol/L NA. D–F, FH-deficient and NAPRT-silenced NCCFH1 ( D ), UOK262 ( E ), and UOK268 ( F ) cell lines treated with increasing concentrations of FK866 after 8 ( D ), 6 ( E ), or 8 ( F ) days with or without 10-μmol/L NA. G–I, Total NAD + quantification in NCCFH1 ( G ), UOK262 ( H ), and UOK268 ( I ) after 24-hour treatment with 25-nmol/L FK866 alone or with 10-μmol/L NA. Two-way ANOVA, *, P = 0.0151; ****, P ≤ 0.0001. Trp, tryptophan; QA, quinolinic acid; QPRT, Quinolinate phosphoribosyl transferase; NAMN, nicotinic acid mononucleotide; NAPRT, nicotinate phosphoribosyltransferase; NA, nicotinic acid; NMNAT, Nicotinamide mononucleotide adenylyl transferase; NAAD, nicotinic acid adenine dinucleotide; NADS, NAD + synthetase; PARPs, poly(ADP-ribose) polymerases, NAM, nicotinamide; NAMPT, nicotinamide phosphoribosyltransferase; NMN, nicotinamide mononucleotide; NMNAT, nicotinamide mononucleotide adenylyl transferase.
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    NAPRT loss confers sensitivity to NAMPTis in FH-deficient RCC models. A, Schematic of NAD + biosynthesis pathways, Triple arrow in the de novo synthesis pathway represents five additional enzymatic conversion steps in the pathway. B, YUNK1 cells treated with increasing concentrations of FK866 with or without the addition of 10-μmol/L of NA. C, Total NAD + levels in YUNK1 and YUNK1 shFH cells at baseline and upon treatment with 25-nmol/L FK866 for 24 hours alone or with 10-μmol/L NA. D–F, FH-deficient and NAPRT-silenced NCCFH1 ( D ), UOK262 ( E ), and UOK268 ( F ) cell lines treated with increasing concentrations of FK866 after 8 ( D ), 6 ( E ), or 8 ( F ) days with or without 10-μmol/L NA. G–I, Total NAD + quantification in NCCFH1 ( G ), UOK262 ( H ), and UOK268 ( I ) after 24-hour treatment with 25-nmol/L FK866 alone or with 10-μmol/L NA. Two-way ANOVA, *, P = 0.0151; ****, P ≤ 0.0001. Trp, tryptophan; QA, quinolinic acid; QPRT, Quinolinate phosphoribosyl transferase; NAMN, nicotinic acid mononucleotide; NAPRT, nicotinate phosphoribosyltransferase; NA, nicotinic acid; NMNAT, Nicotinamide mononucleotide adenylyl transferase; NAAD, nicotinic acid adenine dinucleotide; NADS, NAD + synthetase; PARPs, poly(ADP-ribose) polymerases, NAM, nicotinamide; NAMPT, nicotinamide phosphoribosyltransferase; NMN, nicotinamide mononucleotide; NMNAT, nicotinamide mononucleotide adenylyl transferase.

    Journal: Molecular Cancer Research

    Article Title: NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD + Depletion

    doi: 10.1158/1541-7786.MCR-23-1003

    Figure Lengend Snippet: NAPRT loss confers sensitivity to NAMPTis in FH-deficient RCC models. A, Schematic of NAD + biosynthesis pathways, Triple arrow in the de novo synthesis pathway represents five additional enzymatic conversion steps in the pathway. B, YUNK1 cells treated with increasing concentrations of FK866 with or without the addition of 10-μmol/L of NA. C, Total NAD + levels in YUNK1 and YUNK1 shFH cells at baseline and upon treatment with 25-nmol/L FK866 for 24 hours alone or with 10-μmol/L NA. D–F, FH-deficient and NAPRT-silenced NCCFH1 ( D ), UOK262 ( E ), and UOK268 ( F ) cell lines treated with increasing concentrations of FK866 after 8 ( D ), 6 ( E ), or 8 ( F ) days with or without 10-μmol/L NA. G–I, Total NAD + quantification in NCCFH1 ( G ), UOK262 ( H ), and UOK268 ( I ) after 24-hour treatment with 25-nmol/L FK866 alone or with 10-μmol/L NA. Two-way ANOVA, *, P = 0.0151; ****, P ≤ 0.0001. Trp, tryptophan; QA, quinolinic acid; QPRT, Quinolinate phosphoribosyl transferase; NAMN, nicotinic acid mononucleotide; NAPRT, nicotinate phosphoribosyltransferase; NA, nicotinic acid; NMNAT, Nicotinamide mononucleotide adenylyl transferase; NAAD, nicotinic acid adenine dinucleotide; NADS, NAD + synthetase; PARPs, poly(ADP-ribose) polymerases, NAM, nicotinamide; NAMPT, nicotinamide phosphoribosyltransferase; NMN, nicotinamide mononucleotide; NMNAT, nicotinamide mononucleotide adenylyl transferase.

    Article Snippet: FK866 (Selleckchem), GNE-617 (Selleckchem), GMX1778 (Selleckchem), olaparib (Selleckchem), and BMN673 (Selleckchem) were dissolved in DMSO and used as indicated.

    Techniques:

    NAMPTi and PARPi synergize in NAPRT-deficient RCC models. A, Mapped synergy plots of YUNK1 parental (left) and YUNK1 shFH (right) cell lines treated with combinations of increasing doses of FK866 and olaparib for 6 days. B–D, Mapped synergy plots of UOK262 ( B ), NCCFH1 ( C ), and UOK268 ( D ) cell lines treated with increasing doses of FK866 and olaparib for 6 days. All synergies performed with 10-μmol/L NA and all synergy scores calculated with the BLISS model.

    Journal: Molecular Cancer Research

    Article Title: NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD + Depletion

    doi: 10.1158/1541-7786.MCR-23-1003

    Figure Lengend Snippet: NAMPTi and PARPi synergize in NAPRT-deficient RCC models. A, Mapped synergy plots of YUNK1 parental (left) and YUNK1 shFH (right) cell lines treated with combinations of increasing doses of FK866 and olaparib for 6 days. B–D, Mapped synergy plots of UOK262 ( B ), NCCFH1 ( C ), and UOK268 ( D ) cell lines treated with increasing doses of FK866 and olaparib for 6 days. All synergies performed with 10-μmol/L NA and all synergy scores calculated with the BLISS model.

    Article Snippet: FK866 (Selleckchem), GNE-617 (Selleckchem), GMX1778 (Selleckchem), olaparib (Selleckchem), and BMN673 (Selleckchem) were dissolved in DMSO and used as indicated.

    Techniques:

    Combination of NAMPTi and PARPi reduces NAD + and PAR chain formation. A, Total NAD + quantification in NCCFH1 cell line after 24-hour treatment with FK866 alone or with 0.6-μmol/L olaparib. B, PAR chains detected by western blot (left) in NCCFH1 cells treated for 24 hours at indicated concentrations of FK866 and olaparib and quantified (right, n = 3). All samples were also treated with 10-μmol/L NA. Arrow indicates the molecular weight for PARP1-associated PARylation. C, Total NAD + quantification in UOK262 cell line after 24-hour treatment with FK866 alone or in combination with 0.6-μmol/L olaparib. D, PAR chains detected by western blot (left) in UOK262 cells treated for 24 hours with the indicated combinations of 1.0-nmol/L FK866, 0.6-μmol/L olaparib, and 10-μmol/L NA and quantified (right, n = 3). E, Total NAD + quantification in UOK268 cell line after 24-hour treatment with FK866 alone or in combination with 0.6-μmol/L olaparib. F, PAR chains detected by western blot (left) in UOK268 cells treated for 24 hours with the indicated combinations of 1.0-nmol/L FK866, 0.6-μmol/L olaparib, and 10-μmol/L NA and quantified (right, n = 3). All NAD + assays performed in the presence of 10 μmol/L NA. HKP, house-keeping protein. Two-way ANOVA: *, P ≤ 0.05; **, P ≤ 0.01; ***, P ≤ 0.001; ****, P ≤ 0.0001.

    Journal: Molecular Cancer Research

    Article Title: NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD + Depletion

    doi: 10.1158/1541-7786.MCR-23-1003

    Figure Lengend Snippet: Combination of NAMPTi and PARPi reduces NAD + and PAR chain formation. A, Total NAD + quantification in NCCFH1 cell line after 24-hour treatment with FK866 alone or with 0.6-μmol/L olaparib. B, PAR chains detected by western blot (left) in NCCFH1 cells treated for 24 hours at indicated concentrations of FK866 and olaparib and quantified (right, n = 3). All samples were also treated with 10-μmol/L NA. Arrow indicates the molecular weight for PARP1-associated PARylation. C, Total NAD + quantification in UOK262 cell line after 24-hour treatment with FK866 alone or in combination with 0.6-μmol/L olaparib. D, PAR chains detected by western blot (left) in UOK262 cells treated for 24 hours with the indicated combinations of 1.0-nmol/L FK866, 0.6-μmol/L olaparib, and 10-μmol/L NA and quantified (right, n = 3). E, Total NAD + quantification in UOK268 cell line after 24-hour treatment with FK866 alone or in combination with 0.6-μmol/L olaparib. F, PAR chains detected by western blot (left) in UOK268 cells treated for 24 hours with the indicated combinations of 1.0-nmol/L FK866, 0.6-μmol/L olaparib, and 10-μmol/L NA and quantified (right, n = 3). All NAD + assays performed in the presence of 10 μmol/L NA. HKP, house-keeping protein. Two-way ANOVA: *, P ≤ 0.05; **, P ≤ 0.01; ***, P ≤ 0.001; ****, P ≤ 0.0001.

    Article Snippet: FK866 (Selleckchem), GNE-617 (Selleckchem), GMX1778 (Selleckchem), olaparib (Selleckchem), and BMN673 (Selleckchem) were dissolved in DMSO and used as indicated.

    Techniques: Western Blot, Molecular Weight

    NAMPTi and PARPi combination increases PARP retention at the chromatin. A, Subcellular fractionation of NCCFH1 cells after treatment with combinations of 25-nmol/L FK866, 10-μmol/L olaparib, 10-μmol/L BMN673, and 0.01% MMS. B, Quantification of nuclear soluble PARP1 signal relative to Sirt6 signal (top) and chromatin-bound PARP1 signal relative to H3 signal (bottom) in NCCFH1 cells. All lanes were normalized to DMSO within the same blot ( n = 3). C, Subcellular fractionation of UOK268 cells after treatment with combinations of 25-nmol/L FK866, 10-umol/L olaparib, 10-umol/L BMN673, and 0.01% MMS. D, Quantification of nuclear soluble PARP1 signal relative to Sirt6 signal (top) and chromatin-bound PARP1 signal relative to H3 signal (bottom) in UOK268 cells. All lanes were normalized to DMSO within the same blot ( n = 3). Cells were treated with FK866 and 10-μmol/L NA for 24 hours and then with PARPis and/or MMS for 30 minutes before harvesting. Sirt6 is a nuclear-localized protein. H3 is a histone protein localized to chromatin. One-way ANOVA, **, P = 0.009; ***, P ≤ 0.001. Statistics for significant comparisons are shown ( B and D ), others are nonsignificant.

    Journal: Molecular Cancer Research

    Article Title: NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD + Depletion

    doi: 10.1158/1541-7786.MCR-23-1003

    Figure Lengend Snippet: NAMPTi and PARPi combination increases PARP retention at the chromatin. A, Subcellular fractionation of NCCFH1 cells after treatment with combinations of 25-nmol/L FK866, 10-μmol/L olaparib, 10-μmol/L BMN673, and 0.01% MMS. B, Quantification of nuclear soluble PARP1 signal relative to Sirt6 signal (top) and chromatin-bound PARP1 signal relative to H3 signal (bottom) in NCCFH1 cells. All lanes were normalized to DMSO within the same blot ( n = 3). C, Subcellular fractionation of UOK268 cells after treatment with combinations of 25-nmol/L FK866, 10-umol/L olaparib, 10-umol/L BMN673, and 0.01% MMS. D, Quantification of nuclear soluble PARP1 signal relative to Sirt6 signal (top) and chromatin-bound PARP1 signal relative to H3 signal (bottom) in UOK268 cells. All lanes were normalized to DMSO within the same blot ( n = 3). Cells were treated with FK866 and 10-μmol/L NA for 24 hours and then with PARPis and/or MMS for 30 minutes before harvesting. Sirt6 is a nuclear-localized protein. H3 is a histone protein localized to chromatin. One-way ANOVA, **, P = 0.009; ***, P ≤ 0.001. Statistics for significant comparisons are shown ( B and D ), others are nonsignificant.

    Article Snippet: FK866 (Selleckchem), GNE-617 (Selleckchem), GMX1778 (Selleckchem), olaparib (Selleckchem), and BMN673 (Selleckchem) were dissolved in DMSO and used as indicated.

    Techniques: Fractionation

    Combination of PARPi and NAMPTi increases DNA damage in NAPRT-silenced models. A, Representative images of NCCFH1 (top), UOK262 (middle), and UOK268 (bottom) with indicated 25-nmol/L FK866 and/or 5-μmol/L olaparib treatment for 24 hours. All cells were treated with 10-μmol/L NA. Scale bar, 50 μm. B–D. Quantification of the proportion of γH2AX foci positive cells in NCCFH1 ( B ), UOK262 ( C ), and UOK268 ( D ) cells. Thresholds for counting foci positive cells were set by the number of γH2AX foci in DMSO-treated cells. One-way ANOVA, **, P ≤ 0.01; ***, P ≤ 0.001; ****, P ≤ 0.0001. E, Schematic describing current understanding of NAPRT silencing in 75% of FH-deficient cell lines and 90% of patient samples and associated drug sensitivity in FH-deficient cancers.

    Journal: Molecular Cancer Research

    Article Title: NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD + Depletion

    doi: 10.1158/1541-7786.MCR-23-1003

    Figure Lengend Snippet: Combination of PARPi and NAMPTi increases DNA damage in NAPRT-silenced models. A, Representative images of NCCFH1 (top), UOK262 (middle), and UOK268 (bottom) with indicated 25-nmol/L FK866 and/or 5-μmol/L olaparib treatment for 24 hours. All cells were treated with 10-μmol/L NA. Scale bar, 50 μm. B–D. Quantification of the proportion of γH2AX foci positive cells in NCCFH1 ( B ), UOK262 ( C ), and UOK268 ( D ) cells. Thresholds for counting foci positive cells were set by the number of γH2AX foci in DMSO-treated cells. One-way ANOVA, **, P ≤ 0.01; ***, P ≤ 0.001; ****, P ≤ 0.0001. E, Schematic describing current understanding of NAPRT silencing in 75% of FH-deficient cell lines and 90% of patient samples and associated drug sensitivity in FH-deficient cancers.

    Article Snippet: FK866 (Selleckchem), GNE-617 (Selleckchem), GMX1778 (Selleckchem), olaparib (Selleckchem), and BMN673 (Selleckchem) were dissolved in DMSO and used as indicated.

    Techniques: