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MedChemExpress hsf1 inhibitor nxp800

Cytotoxicity assessment of the <t>HSF1</t> inhibitor <t>NXP800</t> in human hepatocellular carcinoma (HCC) cell lines. ( A ) The levels of the HSF1 protein were assessed in Hep3B, HLE, HLF, Huh7, and SNU449 cell lines by Western blot analysis. GAPDH was used as a loading control. ( B ) Cell viability was measured via MTT assay. The cell viability in percentage to DMSO control, expressed as non-linear regression curve fit over log10 drug concentrations, is depicted. The mean ± SD (n = 3) of at least three independent experiments each performed in triplicate is shown. Horizontal dotted line: 50% viable cells. IC 50 values per cell line are shown in each plot.

Hsf1 Inhibitor Nxp800, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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hsf1 inhibitor nxp800 - by Bioz Stars, 2026-08

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Article Title: The Novel HSF1 Inhibitor NXP800 Exhibits Robust Antitumor Activity in Hepatocellular Carcinoma

Journal: International Journal of Molecular Sciences

doi: 10.3390/ijms27062781

Cytotoxicity assessment of the HSF1 inhibitor NXP800 in human hepatocellular carcinoma (HCC) cell lines. ( A ) The levels of the HSF1 protein were assessed in Hep3B, HLE, HLF, Huh7, and SNU449 cell lines by Western blot analysis. GAPDH was used as a loading control. ( B ) Cell viability was measured via MTT assay. The cell viability in percentage to DMSO control, expressed as non-linear regression curve fit over log10 drug concentrations, is depicted. The mean ± SD (n = 3) of at least three independent experiments each performed in triplicate is shown. Horizontal dotted line: 50% viable cells. IC 50 values per cell line are shown in each plot.

Figure Legend Snippet: Cytotoxicity assessment of the HSF1 inhibitor NXP800 in human hepatocellular carcinoma (HCC) cell lines. ( A ) The levels of the HSF1 protein were assessed in Hep3B, HLE, HLF, Huh7, and SNU449 cell lines by Western blot analysis. GAPDH was used as a loading control. ( B ) Cell viability was measured via MTT assay. The cell viability in percentage to DMSO control, expressed as non-linear regression curve fit over log10 drug concentrations, is depicted. The mean ± SD (n = 3) of at least three independent experiments each performed in triplicate is shown. Horizontal dotted line: 50% viable cells. IC 50 values per cell line are shown in each plot.

Techniques Used: Western Blot, Control, MTT Assay

Effects of NXP800 on the proliferation, apoptosis, and DNA damage of HLF and SNU449 human hepatocellular carcinoma cell lines. To evaluate cell proliferation, the BrdU incorporation assay was conducted on HLF ( A ) and SNU449 ( D ) cells treated with NXP800 at concentrations of 50 nM and 500 nM for 48 h. Apoptosis was assessed in HLF ( B ) and SNU449 ( E ) cell lines after treatment with NXP800 for 48 h, using the same concentrations mentioned above. Additionally, a DNA damage assay was performed to measure the formation of apurinic/apyrimidinic (AP) sites, which represent one of the most common types of DNA lesion and a surrogate marker for DNA damage. This assay was applied to both cell lines ( C , F ) for 24 h at the two NXP800 concentrations. In all assays, untreated cells and those treated with DMSO (solvent) were used as controls. The results are presented as the mean ± standard deviation (SD) from three independent experiments, each conducted in triplicate. For statistical analysis, Tukey’s multiple comparisons test was used, with significance defined as p < 0.001. The following comparisons were conducted: a vs. untreated cells; b vs. DMSO; c vs. 50 nM NXP800.

Figure Legend Snippet: Effects of NXP800 on the proliferation, apoptosis, and DNA damage of HLF and SNU449 human hepatocellular carcinoma cell lines. To evaluate cell proliferation, the BrdU incorporation assay was conducted on HLF ( A ) and SNU449 ( D ) cells treated with NXP800 at concentrations of 50 nM and 500 nM for 48 h. Apoptosis was assessed in HLF ( B ) and SNU449 ( E ) cell lines after treatment with NXP800 for 48 h, using the same concentrations mentioned above. Additionally, a DNA damage assay was performed to measure the formation of apurinic/apyrimidinic (AP) sites, which represent one of the most common types of DNA lesion and a surrogate marker for DNA damage. This assay was applied to both cell lines ( C , F ) for 24 h at the two NXP800 concentrations. In all assays, untreated cells and those treated with DMSO (solvent) were used as controls. The results are presented as the mean ± standard deviation (SD) from three independent experiments, each conducted in triplicate. For statistical analysis, Tukey’s multiple comparisons test was used, with significance defined as p < 0.001. The following comparisons were conducted: a vs. untreated cells; b vs. DMSO; c vs. 50 nM NXP800.

Techniques Used: BrdU Incorporation Assay, Marker, Solvent, Standard Deviation

Gene expression analysis in hepatocellular carcinoma cell lines treated with the HSF1 inhibitor NXP800. HLF and SNU449 cells were treated for 48 h with DMSO control (vehicle), or NXP800 (50 nM or 500 nM in HLF or SNU449 cells, respectively). Panels ( A – Q ) show the relative mRNA expression levels of the indicated genes, presented as fold change to the untreated control (Ctrl), calculated using the 2 −ΔΔCt method, with ACTB used as the housekeeping gene. Data represents the mean ± SD of three independent experiments, each measured in technical duplicates. Statistical analysis was performed using two-way ANOVA followed by Tukey’s multiple comparisons test (*** p < 0.001, **** p < 0.0001).

Figure Legend Snippet: Gene expression analysis in hepatocellular carcinoma cell lines treated with the HSF1 inhibitor NXP800. HLF and SNU449 cells were treated for 48 h with DMSO control (vehicle), or NXP800 (50 nM or 500 nM in HLF or SNU449 cells, respectively). Panels ( A – Q ) show the relative mRNA expression levels of the indicated genes, presented as fold change to the untreated control (Ctrl), calculated using the 2 −ΔΔCt method, with ACTB used as the housekeeping gene. Data represents the mean ± SD of three independent experiments, each measured in technical duplicates. Statistical analysis was performed using two-way ANOVA followed by Tukey’s multiple comparisons test (*** p < 0.001, **** p < 0.0001).

Techniques Used: Gene Expression, Control, Expressing

Figure Legend Snippet: The effect of NXP800 on glycolysis in hepatocellular carcinoma cell lines. HLF and SNU449 cells were treated with DMSO or 5 µM NXP800 for 24 h. Data are presented as mean ± SEM of triplicate samples from two independent experiments, normalized to cell number (#) as quantified by HOECHST 33342 nuclear staining. Values are multiplied by 1 × 10 5 for visualization purposes. Statistical significance compared to the DMSO control is indicated as * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 (two-way ANOVA). ( A ) The standard Glycolytic Rate Assay profile shows the basal and compensatory glycolysis over time. Cells were sequentially challenged with mitochondrial inhibitors rotenone and antimycin A (Rot/AA) to inhibit mitochondrial respiration, which helps reveal the glycolytic proton efflux rate (glycoPER). This was followed by the addition of 2-deoxy-D-glucose (2-DG) to block glycolysis and confirm the specificity of the assay. ( B , C ) The glycoPER results (left panel) and bar graphs (right panel) display key parameters such as basal glycolysis, compensatory glycolysis, basal proton efflux rate (PER), and post-2-DG acidification for ( B ) HLF and ( C ) SNU449 cells.

Techniques Used: Staining, Control, Blocking Assay

Figure Legend Snippet: The effect of NXP800 on mitochondrial respiration in hepatocellular carcinoma cell lines. HLF and SNU449 cells were treated with DMSO or 5 µM NXP800 for 24 h. Data are presented as mean ± SEM of triplicate samples from two independent experi-ments, normalized to cell number as quantified by HOECHST 33342 nuclear staining. Values are multi-plied by 1 × 10 5 for visualization purposes. Statistical significance compared to the DMSO control is indicated as * p < 0.05, *** p < 0.001, **** p < 0.0001 (two-way ANOVA). ( A ) The standard Cell Mitochondrial Stress Test profile shows the oxidative consumption rate (OCR) over time. Basal respiration was followed by sequential injections of oligomycin (which measures ATP-linked OCR), carbonyl cyanide-4-phenylhydrazone (FCCP; which assesses maximal respiration and spare capacity), and Rot/AA (to determine non-mitochondrial OCR). ( B , C ) The OCR profile (left panel) and bar graphs (right panel) illustrate basal respiration, maximal respiration, spare respiratory capacity, ATP production, and proton leak for ( B ) HLF and ( C ) SNU449 cells.

Techniques Used: Staining, Control

NXP800 causes mitophagy and cristae degradation in HLF cells. ( A ) Representative electron micrographs of ( A ( a )) an untreated (DMSO, black outline) and ( A ( b )) a 5 µM NXP800-treated (red outline) HLF cell. Mt, mitochondria; N, nucleus; V, electron-lucent vacuoles; v*, electron-dense vacuoles; magnification: 10,000×; scale bars: 2 µm. ( B ( a – d )) TEM images of two (1 and 2) representative mitochondria of normal ( ) or abnormal ( ) morphology ( B ( a ): DMSO; B ( b – d ): 5 µM NXP800). Ma, matrix; IMM, inner mitochondrial membrane; OMM, outer mitochondrial membrane; Black arrow, crista; , swollen cristae; Black arrowhead, mitophagosome; White arrowhead, ballooning of OMM; Magnification: 40,000×; Scale bars: 500 nm.

Figure Legend Snippet: NXP800 causes mitophagy and cristae degradation in HLF cells. ( A ) Representative electron micrographs of ( A ( a )) an untreated (DMSO, black outline) and ( A ( b )) a 5 µM NXP800-treated (red outline) HLF cell. Mt, mitochondria; N, nucleus; V, electron-lucent vacuoles; v*, electron-dense vacuoles; magnification: 10,000×; scale bars: 2 µm. ( B ( a – d )) TEM images of two (1 and 2) representative mitochondria of normal ( ) or abnormal ( ) morphology ( B ( a ): DMSO; B ( b – d ): 5 µM NXP800). Ma, matrix; IMM, inner mitochondrial membrane; OMM, outer mitochondrial membrane; Black arrow, crista; , swollen cristae; Black arrowhead, mitophagosome; White arrowhead, ballooning of OMM; Magnification: 40,000×; Scale bars: 500 nm.

Techniques Used: Membrane

NXP800 causes mitophagy and cristae degradation in HLF cells. ( A ) Quantification of mitochondrial parameters including ( A ( a )) mitochondrial number per cell (n = 5 cells; p = 0.0873), ( A ( b )) size (µm 2 ; **** p < 0.0001), ( A ( c )) perimeter (µm; **** p < 0.0001), ( A ( d )) aspect ratio (* p = 0.0249), and ( A ( e ) circularity index ( p = 0.6589), and ( A ( f )) density (mitochondrial area in µm/cytoplasmic area in µm, %; **** p < 0.0001). The boxplots show min. to max. excluding outliers with median; Mitochondria, n (DMSO) = 93, n (NXP800) = 122. ( B ) Quantification of cristae parameters including ( B ( a )) cristae number per mitochondrion (*** p = 0.0004), ( B ( b )) size (µm 2 ; * p = 0.0111), ( B ( c )) density (cristae area/mitochondria area, %; p = 0.6503), ( B ( d )) perimeter (µm; p = 0.1833), ( B ( e )) aspect ratio ( *** p = 0.0002), and ( B ( f )) cristae class score (class I, >4 cristae per mitochondrion; class II, 2–3 cristae; class III, ≤1 crista). The boxplots show min. to max. excluding outliers with median; Cristae, n (DMSO) = 312, n (NXP800) = 222. Statistical significance is indicated by asterisks (* p ≤ 0.05, *** p ≤ 0.001, and **** p ≤ 0.0001; Mann–Whitney test).

Figure Legend Snippet: NXP800 causes mitophagy and cristae degradation in HLF cells. ( A ) Quantification of mitochondrial parameters including ( A ( a )) mitochondrial number per cell (n = 5 cells; p = 0.0873), ( A ( b )) size (µm 2 ; **** p < 0.0001), ( A ( c )) perimeter (µm; **** p < 0.0001), ( A ( d )) aspect ratio (* p = 0.0249), and ( A ( e ) circularity index ( p = 0.6589), and ( A ( f )) density (mitochondrial area in µm/cytoplasmic area in µm, %; **** p < 0.0001). The boxplots show min. to max. excluding outliers with median; Mitochondria, n (DMSO) = 93, n (NXP800) = 122. ( B ) Quantification of cristae parameters including ( B ( a )) cristae number per mitochondrion (*** p = 0.0004), ( B ( b )) size (µm 2 ; * p = 0.0111), ( B ( c )) density (cristae area/mitochondria area, %; p = 0.6503), ( B ( d )) perimeter (µm; p = 0.1833), ( B ( e )) aspect ratio ( *** p = 0.0002), and ( B ( f )) cristae class score (class I, >4 cristae per mitochondrion; class II, 2–3 cristae; class III, ≤1 crista). The boxplots show min. to max. excluding outliers with median; Cristae, n (DMSO) = 312, n (NXP800) = 222. Statistical significance is indicated by asterisks (* p ≤ 0.05, *** p ≤ 0.001, and **** p ≤ 0.0001; Mann–Whitney test).

Techniques Used: MANN-WHITNEY

Characterization of patient-derived hepatocellular carcinoma organoids and effect of NXP800 on in vitro growth. ( A ) Characterization of P558 and P151 patient-derived organoids (PDOs). The two organoids exhibited positive immunoreactivity for AFP and HAS hepatocellular markers and were negative for the cholangiocellular marker CK7. Scale bar: 50 µm. Abbreviation: H&E, hematoxylin and eosin staining. ( B ) HCC PDOs were treated for 48 h, and cell viability was evaluated via CellTiter-Glo ® 3D Luminescent Cell Viability Assay (Promega, Madison, WI, USA) according to the manufacturer’s instructions. Cell viability results were normalized on a 0.1% DMSO control, and IC 50 was obtained on GraphPad Prism 10.0 as a non-linear regression of normalized response.

Figure Legend Snippet: Characterization of patient-derived hepatocellular carcinoma organoids and effect of NXP800 on in vitro growth. ( A ) Characterization of P558 and P151 patient-derived organoids (PDOs). The two organoids exhibited positive immunoreactivity for AFP and HAS hepatocellular markers and were negative for the cholangiocellular marker CK7. Scale bar: 50 µm. Abbreviation: H&E, hematoxylin and eosin staining. ( B ) HCC PDOs were treated for 48 h, and cell viability was evaluated via CellTiter-Glo ® 3D Luminescent Cell Viability Assay (Promega, Madison, WI, USA) according to the manufacturer’s instructions. Cell viability results were normalized on a 0.1% DMSO control, and IC 50 was obtained on GraphPad Prism 10.0 as a non-linear regression of normalized response.

Techniques Used: Derivative Assay, In Vitro, Marker, Staining, Cell Viability Assay, Control

NXP800 treatment induces rarefaction of patient-derived hepatocellular carcinoma organoids, downregulation of the proliferation marker Ki67, and upregulation of apoptosis and DNA damage. The P151 ( A ) and P558 ( B ) patient-derived organoids (PDOs) were treated with 500 Nm NXP800 for 48 h, and levels of the proliferation marker Ki67, the apoptosis marker cleaved caspase 3, and the DNA damage marker phosphorylated/activated (p)histone H2A.X were evaluated immunohistochemically. The two PDOs showed positive immunoreactivity for Ki67 in most of the DMSO-treated PDOs, whereas only a few nuclei were positive for Ki67 immunolabeling in NXP800-treated PDOs. In striking contrast, higher immunoreactivity for cleaved caspase 3 (indicated by arrows) and phosphorylated/activated histone H2A.X characterized the NXP800-treated organoids. Scale bar: 50 µm. Abbreviations: Cl., cleaved; H&E, hematoxylin and eosin staining.

Figure Legend Snippet: NXP800 treatment induces rarefaction of patient-derived hepatocellular carcinoma organoids, downregulation of the proliferation marker Ki67, and upregulation of apoptosis and DNA damage. The P151 ( A ) and P558 ( B ) patient-derived organoids (PDOs) were treated with 500 Nm NXP800 for 48 h, and levels of the proliferation marker Ki67, the apoptosis marker cleaved caspase 3, and the DNA damage marker phosphorylated/activated (p)histone H2A.X were evaluated immunohistochemically. The two PDOs showed positive immunoreactivity for Ki67 in most of the DMSO-treated PDOs, whereas only a few nuclei were positive for Ki67 immunolabeling in NXP800-treated PDOs. In striking contrast, higher immunoreactivity for cleaved caspase 3 (indicated by arrows) and phosphorylated/activated histone H2A.X characterized the NXP800-treated organoids. Scale bar: 50 µm. Abbreviations: Cl., cleaved; H&E, hematoxylin and eosin staining.

Techniques Used: Derivative Assay, Marker, Immunolabeling, Staining

Effect of treatment with NXP800 either alone or associated with doxorubicin administration on cell proliferation, apoptosis, and DNA of HCC cell lines. To evaluate cell proliferation, the BrdU incorporation assay was conducted on HLF ( A ) and SNU449 ( D ) cells treated with NXP800 at a 50 nM concentration, either alone or in association with 50 μM doxorubicin. Apoptosis was assessed in HLF ( B ) and SNU449 ( E ) cell lines after treatment with NXP800 and doxorubicin for 24 h, using the same concentrations mentioned above. Additionally, a DNA damage assay was performed to measure the formation of apurinic/apyrimidinic (AP) sites, which represent one of the most common types of DNA lesion. This assay was applied to both cell lines ( C , F ) for 24 h at with NXP800 at a 50 nM concentration, either alone or associated with 50 μM doxorubicin. In all assays, untreated cells and those treated with DMSO (solvent) were used as controls. Treatments were limited to 24 h because massive cell death was observed at 48 h in the HCC cells subjected to the combinatorial treatment. The results are presented as the mean ± standard deviation (SD) from three independent experiments, each conducted in triplicate. For statistical analysis, Tukey’s multiple comparisons test was used, with significance defined as p < 0.001. The following comparisons were conducted: a vs. untreated cells; b vs. DMSO; c vs. 50 nM NXP800; d vs. doxorubicin.

Figure Legend Snippet: Effect of treatment with NXP800 either alone or associated with doxorubicin administration on cell proliferation, apoptosis, and DNA of HCC cell lines. To evaluate cell proliferation, the BrdU incorporation assay was conducted on HLF ( A ) and SNU449 ( D ) cells treated with NXP800 at a 50 nM concentration, either alone or in association with 50 μM doxorubicin. Apoptosis was assessed in HLF ( B ) and SNU449 ( E ) cell lines after treatment with NXP800 and doxorubicin for 24 h, using the same concentrations mentioned above. Additionally, a DNA damage assay was performed to measure the formation of apurinic/apyrimidinic (AP) sites, which represent one of the most common types of DNA lesion. This assay was applied to both cell lines ( C , F ) for 24 h at with NXP800 at a 50 nM concentration, either alone or associated with 50 μM doxorubicin. In all assays, untreated cells and those treated with DMSO (solvent) were used as controls. Treatments were limited to 24 h because massive cell death was observed at 48 h in the HCC cells subjected to the combinatorial treatment. The results are presented as the mean ± standard deviation (SD) from three independent experiments, each conducted in triplicate. For statistical analysis, Tukey’s multiple comparisons test was used, with significance defined as p < 0.001. The following comparisons were conducted: a vs. untreated cells; b vs. DMSO; c vs. 50 nM NXP800; d vs. doxorubicin.

Techniques Used: BrdU Incorporation Assay, Concentration Assay, Solvent, Standard Deviation

Synergy analysis of NXP800 and doxorubicin in HLF and SNU449 cells. HLF and SNU449 cells were treated with increasing concentrations of NXP800 and doxorubicin as single agents and in combination in a dose–response matrix. Cell viability was assessed by MTT assay after 48 h of treatment, and drug interaction analysis was performed using the ZIP model implemented in SynergyFinder 3. ( A , E ) MTT viability assay showing the dose-dependent effect of doxorubicin monotherapy in HLF ( A ) and SNU449 ( E ) cells. ( B , F ) Dose–response curves of NXP800 and doxorubicin monotherapies generated using SynergyFinder 3. ( C , G ) Inhibition matrices displaying percent growth inhibition as a heatmap (red indicates stronger inhibition). ( D , H ) Two-dimensional ZIP synergy score maps for all tested drug combinations. Scores > 5 indicate synergistic interactions.

Figure Legend Snippet: Synergy analysis of NXP800 and doxorubicin in HLF and SNU449 cells. HLF and SNU449 cells were treated with increasing concentrations of NXP800 and doxorubicin as single agents and in combination in a dose–response matrix. Cell viability was assessed by MTT assay after 48 h of treatment, and drug interaction analysis was performed using the ZIP model implemented in SynergyFinder 3. ( A , E ) MTT viability assay showing the dose-dependent effect of doxorubicin monotherapy in HLF ( A ) and SNU449 ( E ) cells. ( B , F ) Dose–response curves of NXP800 and doxorubicin monotherapies generated using SynergyFinder 3. ( C , G ) Inhibition matrices displaying percent growth inhibition as a heatmap (red indicates stronger inhibition). ( D , H ) Two-dimensional ZIP synergy score maps for all tested drug combinations. Scores > 5 indicate synergistic interactions.

Techniques Used: MTT Assay, MTT Viability Assay, Generated, Inhibition

Effect of treatment with NXP800 either alone or associated with the PARP inhibitor olaparib (OLA) on cell proliferation, apoptosis, and DNA of HCC cell lines. To evaluate cell proliferation, the BrdU incorporation assay was conducted on HLF ( A ) and SNU449 ( D ) cells treated with NXP800 at 50 nM concentration, either alone or in association with 5 OLA. Apoptosis was assessed in HLF ( B ) and SNU449 ( E ) cell lines after treatment with NXP800 and OLA, using the same concentrations mentioned above. Additionally, a DNA damage assay was performed to measure the formation of apurinic/apyrimidinic (AP) sites. This assay was applied to both cell lines ( C , F ) for 48 h with NXP800 at 50 nM concentration, either alone or associated with 5 μM OLA. Untreated cells and those treated with DMSO (solvent) were used as controls. The results are presented as the mean ± standard deviation (SD) from three independent experiments, each conducted in triplicate. For statistical analysis, Tukey’s multiple comparisons test was used, with significance defined as p < 0.001. The following comparisons were performed: a vs. untreated cells; b vs. DMSO; c vs. 50 nM NXP800; d vs. OLA.

Figure Legend Snippet: Effect of treatment with NXP800 either alone or associated with the PARP inhibitor olaparib (OLA) on cell proliferation, apoptosis, and DNA of HCC cell lines. To evaluate cell proliferation, the BrdU incorporation assay was conducted on HLF ( A ) and SNU449 ( D ) cells treated with NXP800 at 50 nM concentration, either alone or in association with 5 OLA. Apoptosis was assessed in HLF ( B ) and SNU449 ( E ) cell lines after treatment with NXP800 and OLA, using the same concentrations mentioned above. Additionally, a DNA damage assay was performed to measure the formation of apurinic/apyrimidinic (AP) sites. This assay was applied to both cell lines ( C , F ) for 48 h with NXP800 at 50 nM concentration, either alone or associated with 5 μM OLA. Untreated cells and those treated with DMSO (solvent) were used as controls. The results are presented as the mean ± standard deviation (SD) from three independent experiments, each conducted in triplicate. For statistical analysis, Tukey’s multiple comparisons test was used, with significance defined as p < 0.001. The following comparisons were performed: a vs. untreated cells; b vs. DMSO; c vs. 50 nM NXP800; d vs. OLA.

Techniques Used: BrdU Incorporation Assay, Concentration Assay, Solvent, Standard Deviation

Image Search Results

Journal: International Journal of Molecular Sciences

Article Title: The Novel HSF1 Inhibitor NXP800 Exhibits Robust Antitumor Activity in Hepatocellular Carcinoma

doi: 10.3390/ijms27062781

Figure Lengend Snippet: Cytotoxicity assessment of the HSF1 inhibitor NXP800 in human hepatocellular carcinoma (HCC) cell lines. ( A ) The levels of the HSF1 protein were assessed in Hep3B, HLE, HLF, Huh7, and SNU449 cell lines by Western blot analysis. GAPDH was used as a loading control. ( B ) Cell viability was measured via MTT assay. The cell viability in percentage to DMSO control, expressed as non-linear regression curve fit over log10 drug concentrations, is depicted. The mean ± SD (n = 3) of at least three independent experiments each performed in triplicate is shown. Horizontal dotted line: 50% viable cells. IC 50 values per cell line are shown in each plot.

Article Snippet: The HSF1 inhibitor NXP800 (#HY-145927) and the PARP-1 inhibitor olaparib (HY-10162) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Western Blot, Control, MTT Assay

Journal: International Journal of Molecular Sciences

Article Title: The Novel HSF1 Inhibitor NXP800 Exhibits Robust Antitumor Activity in Hepatocellular Carcinoma

doi: 10.3390/ijms27062781

Figure Lengend Snippet: Effects of NXP800 on the proliferation, apoptosis, and DNA damage of HLF and SNU449 human hepatocellular carcinoma cell lines. To evaluate cell proliferation, the BrdU incorporation assay was conducted on HLF ( A ) and SNU449 ( D ) cells treated with NXP800 at concentrations of 50 nM and 500 nM for 48 h. Apoptosis was assessed in HLF ( B ) and SNU449 ( E ) cell lines after treatment with NXP800 for 48 h, using the same concentrations mentioned above. Additionally, a DNA damage assay was performed to measure the formation of apurinic/apyrimidinic (AP) sites, which represent one of the most common types of DNA lesion and a surrogate marker for DNA damage. This assay was applied to both cell lines ( C , F ) for 24 h at the two NXP800 concentrations. In all assays, untreated cells and those treated with DMSO (solvent) were used as controls. The results are presented as the mean ± standard deviation (SD) from three independent experiments, each conducted in triplicate. For statistical analysis, Tukey’s multiple comparisons test was used, with significance defined as p < 0.001. The following comparisons were conducted: a vs. untreated cells; b vs. DMSO; c vs. 50 nM NXP800.

Article Snippet: The HSF1 inhibitor NXP800 (#HY-145927) and the PARP-1 inhibitor olaparib (HY-10162) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: BrdU Incorporation Assay, Marker, Solvent, Standard Deviation

Journal: International Journal of Molecular Sciences

Article Title: The Novel HSF1 Inhibitor NXP800 Exhibits Robust Antitumor Activity in Hepatocellular Carcinoma

doi: 10.3390/ijms27062781

Figure Lengend Snippet: Gene expression analysis in hepatocellular carcinoma cell lines treated with the HSF1 inhibitor NXP800. HLF and SNU449 cells were treated for 48 h with DMSO control (vehicle), or NXP800 (50 nM or 500 nM in HLF or SNU449 cells, respectively). Panels ( A – Q ) show the relative mRNA expression levels of the indicated genes, presented as fold change to the untreated control (Ctrl), calculated using the 2 −ΔΔCt method, with ACTB used as the housekeeping gene. Data represents the mean ± SD of three independent experiments, each measured in technical duplicates. Statistical analysis was performed using two-way ANOVA followed by Tukey’s multiple comparisons test (*** p < 0.001, **** p < 0.0001).

Article Snippet: The HSF1 inhibitor NXP800 (#HY-145927) and the PARP-1 inhibitor olaparib (HY-10162) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Gene Expression, Control, Expressing

Journal: International Journal of Molecular Sciences

Article Title: The Novel HSF1 Inhibitor NXP800 Exhibits Robust Antitumor Activity in Hepatocellular Carcinoma

doi: 10.3390/ijms27062781

Figure Lengend Snippet: The effect of NXP800 on glycolysis in hepatocellular carcinoma cell lines. HLF and SNU449 cells were treated with DMSO or 5 µM NXP800 for 24 h. Data are presented as mean ± SEM of triplicate samples from two independent experiments, normalized to cell number (#) as quantified by HOECHST 33342 nuclear staining. Values are multiplied by 1 × 10 5 for visualization purposes. Statistical significance compared to the DMSO control is indicated as * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 (two-way ANOVA). ( A ) The standard Glycolytic Rate Assay profile shows the basal and compensatory glycolysis over time. Cells were sequentially challenged with mitochondrial inhibitors rotenone and antimycin A (Rot/AA) to inhibit mitochondrial respiration, which helps reveal the glycolytic proton efflux rate (glycoPER). This was followed by the addition of 2-deoxy-D-glucose (2-DG) to block glycolysis and confirm the specificity of the assay. ( B , C ) The glycoPER results (left panel) and bar graphs (right panel) display key parameters such as basal glycolysis, compensatory glycolysis, basal proton efflux rate (PER), and post-2-DG acidification for ( B ) HLF and ( C ) SNU449 cells.

Article Snippet: The HSF1 inhibitor NXP800 (#HY-145927) and the PARP-1 inhibitor olaparib (HY-10162) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Staining, Control, Blocking Assay

Journal: International Journal of Molecular Sciences

Article Title: The Novel HSF1 Inhibitor NXP800 Exhibits Robust Antitumor Activity in Hepatocellular Carcinoma

doi: 10.3390/ijms27062781

Figure Lengend Snippet: The effect of NXP800 on mitochondrial respiration in hepatocellular carcinoma cell lines. HLF and SNU449 cells were treated with DMSO or 5 µM NXP800 for 24 h. Data are presented as mean ± SEM of triplicate samples from two independent experi-ments, normalized to cell number as quantified by HOECHST 33342 nuclear staining. Values are multi-plied by 1 × 10 5 for visualization purposes. Statistical significance compared to the DMSO control is indicated as * p < 0.05, *** p < 0.001, **** p < 0.0001 (two-way ANOVA). ( A ) The standard Cell Mitochondrial Stress Test profile shows the oxidative consumption rate (OCR) over time. Basal respiration was followed by sequential injections of oligomycin (which measures ATP-linked OCR), carbonyl cyanide-4-phenylhydrazone (FCCP; which assesses maximal respiration and spare capacity), and Rot/AA (to determine non-mitochondrial OCR). ( B , C ) The OCR profile (left panel) and bar graphs (right panel) illustrate basal respiration, maximal respiration, spare respiratory capacity, ATP production, and proton leak for ( B ) HLF and ( C ) SNU449 cells.

Article Snippet: The HSF1 inhibitor NXP800 (#HY-145927) and the PARP-1 inhibitor olaparib (HY-10162) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Staining, Control

Journal: International Journal of Molecular Sciences

Article Title: The Novel HSF1 Inhibitor NXP800 Exhibits Robust Antitumor Activity in Hepatocellular Carcinoma

doi: 10.3390/ijms27062781

Figure Lengend Snippet: NXP800 causes mitophagy and cristae degradation in HLF cells. ( A ) Representative electron micrographs of ( A ( a )) an untreated (DMSO, black outline) and ( A ( b )) a 5 µM NXP800-treated (red outline) HLF cell. Mt, mitochondria; N, nucleus; V, electron-lucent vacuoles; v*, electron-dense vacuoles; magnification: 10,000×; scale bars: 2 µm. ( B ( a – d )) TEM images of two (1 and 2) representative mitochondria of normal ( ) or abnormal ( ) morphology ( B ( a ): DMSO; B ( b – d ): 5 µM NXP800). Ma, matrix; IMM, inner mitochondrial membrane; OMM, outer mitochondrial membrane; Black arrow, crista; , swollen cristae; Black arrowhead, mitophagosome; White arrowhead, ballooning of OMM; Magnification: 40,000×; Scale bars: 500 nm.

Article Snippet: The HSF1 inhibitor NXP800 (#HY-145927) and the PARP-1 inhibitor olaparib (HY-10162) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Membrane

Journal: International Journal of Molecular Sciences

Article Title: The Novel HSF1 Inhibitor NXP800 Exhibits Robust Antitumor Activity in Hepatocellular Carcinoma

doi: 10.3390/ijms27062781

Figure Lengend Snippet: NXP800 causes mitophagy and cristae degradation in HLF cells. ( A ) Quantification of mitochondrial parameters including ( A ( a )) mitochondrial number per cell (n = 5 cells; p = 0.0873), ( A ( b )) size (µm 2 ; **** p < 0.0001), ( A ( c )) perimeter (µm; **** p < 0.0001), ( A ( d )) aspect ratio (* p = 0.0249), and ( A ( e ) circularity index ( p = 0.6589), and ( A ( f )) density (mitochondrial area in µm/cytoplasmic area in µm, %; **** p < 0.0001). The boxplots show min. to max. excluding outliers with median; Mitochondria, n (DMSO) = 93, n (NXP800) = 122. ( B ) Quantification of cristae parameters including ( B ( a )) cristae number per mitochondrion (*** p = 0.0004), ( B ( b )) size (µm 2 ; * p = 0.0111), ( B ( c )) density (cristae area/mitochondria area, %; p = 0.6503), ( B ( d )) perimeter (µm; p = 0.1833), ( B ( e )) aspect ratio ( *** p = 0.0002), and ( B ( f )) cristae class score (class I, >4 cristae per mitochondrion; class II, 2–3 cristae; class III, ≤1 crista). The boxplots show min. to max. excluding outliers with median; Cristae, n (DMSO) = 312, n (NXP800) = 222. Statistical significance is indicated by asterisks (* p ≤ 0.05, *** p ≤ 0.001, and **** p ≤ 0.0001; Mann–Whitney test).

Article Snippet: The HSF1 inhibitor NXP800 (#HY-145927) and the PARP-1 inhibitor olaparib (HY-10162) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: MANN-WHITNEY

Journal: International Journal of Molecular Sciences

Article Title: The Novel HSF1 Inhibitor NXP800 Exhibits Robust Antitumor Activity in Hepatocellular Carcinoma

doi: 10.3390/ijms27062781

Figure Lengend Snippet: Characterization of patient-derived hepatocellular carcinoma organoids and effect of NXP800 on in vitro growth. ( A ) Characterization of P558 and P151 patient-derived organoids (PDOs). The two organoids exhibited positive immunoreactivity for AFP and HAS hepatocellular markers and were negative for the cholangiocellular marker CK7. Scale bar: 50 µm. Abbreviation: H&E, hematoxylin and eosin staining. ( B ) HCC PDOs were treated for 48 h, and cell viability was evaluated via CellTiter-Glo ® 3D Luminescent Cell Viability Assay (Promega, Madison, WI, USA) according to the manufacturer’s instructions. Cell viability results were normalized on a 0.1% DMSO control, and IC 50 was obtained on GraphPad Prism 10.0 as a non-linear regression of normalized response.

Article Snippet: The HSF1 inhibitor NXP800 (#HY-145927) and the PARP-1 inhibitor olaparib (HY-10162) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Derivative Assay, In Vitro, Marker, Staining, Cell Viability Assay, Control

Journal: International Journal of Molecular Sciences

Article Title: The Novel HSF1 Inhibitor NXP800 Exhibits Robust Antitumor Activity in Hepatocellular Carcinoma

doi: 10.3390/ijms27062781

Figure Lengend Snippet: NXP800 treatment induces rarefaction of patient-derived hepatocellular carcinoma organoids, downregulation of the proliferation marker Ki67, and upregulation of apoptosis and DNA damage. The P151 ( A ) and P558 ( B ) patient-derived organoids (PDOs) were treated with 500 Nm NXP800 for 48 h, and levels of the proliferation marker Ki67, the apoptosis marker cleaved caspase 3, and the DNA damage marker phosphorylated/activated (p)histone H2A.X were evaluated immunohistochemically. The two PDOs showed positive immunoreactivity for Ki67 in most of the DMSO-treated PDOs, whereas only a few nuclei were positive for Ki67 immunolabeling in NXP800-treated PDOs. In striking contrast, higher immunoreactivity for cleaved caspase 3 (indicated by arrows) and phosphorylated/activated histone H2A.X characterized the NXP800-treated organoids. Scale bar: 50 µm. Abbreviations: Cl., cleaved; H&E, hematoxylin and eosin staining.

Article Snippet: The HSF1 inhibitor NXP800 (#HY-145927) and the PARP-1 inhibitor olaparib (HY-10162) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Derivative Assay, Marker, Immunolabeling, Staining

Journal: International Journal of Molecular Sciences

Article Title: The Novel HSF1 Inhibitor NXP800 Exhibits Robust Antitumor Activity in Hepatocellular Carcinoma

doi: 10.3390/ijms27062781

Figure Lengend Snippet: Effect of treatment with NXP800 either alone or associated with doxorubicin administration on cell proliferation, apoptosis, and DNA of HCC cell lines. To evaluate cell proliferation, the BrdU incorporation assay was conducted on HLF ( A ) and SNU449 ( D ) cells treated with NXP800 at a 50 nM concentration, either alone or in association with 50 μM doxorubicin. Apoptosis was assessed in HLF ( B ) and SNU449 ( E ) cell lines after treatment with NXP800 and doxorubicin for 24 h, using the same concentrations mentioned above. Additionally, a DNA damage assay was performed to measure the formation of apurinic/apyrimidinic (AP) sites, which represent one of the most common types of DNA lesion. This assay was applied to both cell lines ( C , F ) for 24 h at with NXP800 at a 50 nM concentration, either alone or associated with 50 μM doxorubicin. In all assays, untreated cells and those treated with DMSO (solvent) were used as controls. Treatments were limited to 24 h because massive cell death was observed at 48 h in the HCC cells subjected to the combinatorial treatment. The results are presented as the mean ± standard deviation (SD) from three independent experiments, each conducted in triplicate. For statistical analysis, Tukey’s multiple comparisons test was used, with significance defined as p < 0.001. The following comparisons were conducted: a vs. untreated cells; b vs. DMSO; c vs. 50 nM NXP800; d vs. doxorubicin.

Article Snippet: The HSF1 inhibitor NXP800 (#HY-145927) and the PARP-1 inhibitor olaparib (HY-10162) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: BrdU Incorporation Assay, Concentration Assay, Solvent, Standard Deviation

Journal: International Journal of Molecular Sciences

Article Title: The Novel HSF1 Inhibitor NXP800 Exhibits Robust Antitumor Activity in Hepatocellular Carcinoma

doi: 10.3390/ijms27062781

Figure Lengend Snippet: Synergy analysis of NXP800 and doxorubicin in HLF and SNU449 cells. HLF and SNU449 cells were treated with increasing concentrations of NXP800 and doxorubicin as single agents and in combination in a dose–response matrix. Cell viability was assessed by MTT assay after 48 h of treatment, and drug interaction analysis was performed using the ZIP model implemented in SynergyFinder 3. ( A , E ) MTT viability assay showing the dose-dependent effect of doxorubicin monotherapy in HLF ( A ) and SNU449 ( E ) cells. ( B , F ) Dose–response curves of NXP800 and doxorubicin monotherapies generated using SynergyFinder 3. ( C , G ) Inhibition matrices displaying percent growth inhibition as a heatmap (red indicates stronger inhibition). ( D , H ) Two-dimensional ZIP synergy score maps for all tested drug combinations. Scores > 5 indicate synergistic interactions.

Article Snippet: The HSF1 inhibitor NXP800 (#HY-145927) and the PARP-1 inhibitor olaparib (HY-10162) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: MTT Assay, MTT Viability Assay, Generated, Inhibition

Journal: International Journal of Molecular Sciences

Article Title: The Novel HSF1 Inhibitor NXP800 Exhibits Robust Antitumor Activity in Hepatocellular Carcinoma

doi: 10.3390/ijms27062781

Figure Lengend Snippet: Effect of treatment with NXP800 either alone or associated with the PARP inhibitor olaparib (OLA) on cell proliferation, apoptosis, and DNA of HCC cell lines. To evaluate cell proliferation, the BrdU incorporation assay was conducted on HLF ( A ) and SNU449 ( D ) cells treated with NXP800 at 50 nM concentration, either alone or in association with 5 OLA. Apoptosis was assessed in HLF ( B ) and SNU449 ( E ) cell lines after treatment with NXP800 and OLA, using the same concentrations mentioned above. Additionally, a DNA damage assay was performed to measure the formation of apurinic/apyrimidinic (AP) sites. This assay was applied to both cell lines ( C , F ) for 48 h with NXP800 at 50 nM concentration, either alone or associated with 5 μM OLA. Untreated cells and those treated with DMSO (solvent) were used as controls. The results are presented as the mean ± standard deviation (SD) from three independent experiments, each conducted in triplicate. For statistical analysis, Tukey’s multiple comparisons test was used, with significance defined as p < 0.001. The following comparisons were performed: a vs. untreated cells; b vs. DMSO; c vs. 50 nM NXP800; d vs. OLA.

Article Snippet: The HSF1 inhibitor NXP800 (#HY-145927) and the PARP-1 inhibitor olaparib (HY-10162) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: BrdU Incorporation Assay, Concentration Assay, Solvent, Standard Deviation

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