mocetinostat sellechem lmk 235 lmk 235 sellechem acy 1215  (MedChemExpress)


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    MedChemExpress mocetinostat sellechem lmk 235 lmk 235 sellechem acy 1215
    Pharmacological inhibition of HDACs 1, 2, and 6 enhances the effects of gemcitabine on PDAC cells in vitro and in vivo. ( A.i ) The indicated cells were treated with vehicle, 40 nM gemcitabine (Gem), 8 nM Romidepsin (Rom), and/or 1 µM <t>ACY-1215</t> (ACY) for 48 h, and the expression of PARP, cleaved caspase 3, and GAPDH was determined by Western blotting. Vertical lines indicate rearrangement of lanes from a single membrane for clarity. Data are representative of three independent experiments. ( A.ii ) PDAC cells treated as in ( i ) were analyzed for apoptosis based on cell surface phosphatidylserine using Annexin V-FITC. Data are means ± s.e. * Significantly different from Gemcitabine and Rom/ACY, p
    Mocetinostat Sellechem Lmk 235 Lmk 235 Sellechem Acy 1215, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mocetinostat sellechem lmk 235 lmk 235 sellechem acy 1215/product/MedChemExpress
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    mocetinostat sellechem lmk 235 lmk 235 sellechem acy 1215 - by Bioz Stars, 2022-05
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    1) Product Images from "Selective Inhibition of Histone Deacetylases 1/2/6 in Combination with Gemcitabine: A Promising Combination for Pancreatic Cancer Therapy"

    Article Title: Selective Inhibition of Histone Deacetylases 1/2/6 in Combination with Gemcitabine: A Promising Combination for Pancreatic Cancer Therapy

    Journal: Cancers

    doi: 10.3390/cancers11091327

    Pharmacological inhibition of HDACs 1, 2, and 6 enhances the effects of gemcitabine on PDAC cells in vitro and in vivo. ( A.i ) The indicated cells were treated with vehicle, 40 nM gemcitabine (Gem), 8 nM Romidepsin (Rom), and/or 1 µM ACY-1215 (ACY) for 48 h, and the expression of PARP, cleaved caspase 3, and GAPDH was determined by Western blotting. Vertical lines indicate rearrangement of lanes from a single membrane for clarity. Data are representative of three independent experiments. ( A.ii ) PDAC cells treated as in ( i ) were analyzed for apoptosis based on cell surface phosphatidylserine using Annexin V-FITC. Data are means ± s.e. * Significantly different from Gemcitabine and Rom/ACY, p
    Figure Legend Snippet: Pharmacological inhibition of HDACs 1, 2, and 6 enhances the effects of gemcitabine on PDAC cells in vitro and in vivo. ( A.i ) The indicated cells were treated with vehicle, 40 nM gemcitabine (Gem), 8 nM Romidepsin (Rom), and/or 1 µM ACY-1215 (ACY) for 48 h, and the expression of PARP, cleaved caspase 3, and GAPDH was determined by Western blotting. Vertical lines indicate rearrangement of lanes from a single membrane for clarity. Data are representative of three independent experiments. ( A.ii ) PDAC cells treated as in ( i ) were analyzed for apoptosis based on cell surface phosphatidylserine using Annexin V-FITC. Data are means ± s.e. * Significantly different from Gemcitabine and Rom/ACY, p

    Techniques Used: Inhibition, In Vitro, In Vivo, Expressing, Western Blot

    Synergistic interactions of Mocetinostat, LMK-235, and gemcitabine in pancreatic ductal adenocarcinoma (PDAC) cells. ( A ) MiaPaCa-2 cells treated with 100 nM Panobinostat, 10 µM Droxinostat, 10 µM Mocetinostat, or 10 µM LMK-235 for the indicated times and analyzed for poly (ADP-ribose) polymerase (PARP), caspase 7, and GAPDH expression by Western blotting. Arrow indicates the migration of cleaved proteins. ( B.i ) ED 50 values for Mocetinostat and LMK-235 in pancreatic cancer cell lines. ( B.ii ) The indicated cell lines were treated with LMK-235, Mocetinostat, or a combination of LMK-235 and Mocetinostat at a constant ratio. After 72 h, 3-(4,5 Dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide (MTT) assays were performed, and the combination index (CI) value for the combination treatment is presented. Dotted line indicates CI value of one, which divides synergistic interaction (CI
    Figure Legend Snippet: Synergistic interactions of Mocetinostat, LMK-235, and gemcitabine in pancreatic ductal adenocarcinoma (PDAC) cells. ( A ) MiaPaCa-2 cells treated with 100 nM Panobinostat, 10 µM Droxinostat, 10 µM Mocetinostat, or 10 µM LMK-235 for the indicated times and analyzed for poly (ADP-ribose) polymerase (PARP), caspase 7, and GAPDH expression by Western blotting. Arrow indicates the migration of cleaved proteins. ( B.i ) ED 50 values for Mocetinostat and LMK-235 in pancreatic cancer cell lines. ( B.ii ) The indicated cell lines were treated with LMK-235, Mocetinostat, or a combination of LMK-235 and Mocetinostat at a constant ratio. After 72 h, 3-(4,5 Dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide (MTT) assays were performed, and the combination index (CI) value for the combination treatment is presented. Dotted line indicates CI value of one, which divides synergistic interaction (CI

    Techniques Used: Expressing, Western Blot, Migration, MTT Assay

    Inhibition of HDACs 1, 2, and 6 cooperates with gemcitabine. ( A.i,ii ) Capan-1 cells were transfected with non-targeting siRNA (N.T.) or ONTARGET plus SMARTPool siRNAs targeting HDACs 1, 2, and 6 and treated with gemcitabine as indicated for 72 h. ( B.i ) Capan-1 and MiaPaCa-2 cells were treated with the vehicle or the indicated concentrations of ACY-1215 for 24 h, and expression of acetyl-α-Tubulin (ac-α-Tubulin), acetyl-Histone 3 (ac-Histone 3), and GAPDH was assessed by Western blotting. ( ii ) The indicated cells were treated with 1 µM ACY-1215, and the number of viable cells was determined after 72 h. ( C ) The indicated cell lines were treated with Romidepsin, gemcitabine, or a combination of Romidepsin and gemcitabine at a constant ratio in the presence or the absence of 1 µM ACY-1215. After 72 h, CI values for the combination treatment were calculated as in Figure 1 . * Significantly different from Romedepsin + Gemcitabine, p
    Figure Legend Snippet: Inhibition of HDACs 1, 2, and 6 cooperates with gemcitabine. ( A.i,ii ) Capan-1 cells were transfected with non-targeting siRNA (N.T.) or ONTARGET plus SMARTPool siRNAs targeting HDACs 1, 2, and 6 and treated with gemcitabine as indicated for 72 h. ( B.i ) Capan-1 and MiaPaCa-2 cells were treated with the vehicle or the indicated concentrations of ACY-1215 for 24 h, and expression of acetyl-α-Tubulin (ac-α-Tubulin), acetyl-Histone 3 (ac-Histone 3), and GAPDH was assessed by Western blotting. ( ii ) The indicated cells were treated with 1 µM ACY-1215, and the number of viable cells was determined after 72 h. ( C ) The indicated cell lines were treated with Romidepsin, gemcitabine, or a combination of Romidepsin and gemcitabine at a constant ratio in the presence or the absence of 1 µM ACY-1215. After 72 h, CI values for the combination treatment were calculated as in Figure 1 . * Significantly different from Romedepsin + Gemcitabine, p

    Techniques Used: Inhibition, Transfection, Expressing, Western Blot

    HDACs 1, 2, and 6 account for the synergism between Mocetinostat and LMK-235 in PDAC cells. HDACs 1, 2, and 3 ( A , B ) or HDACs 4, 5, and 6 ( C ) were knocked down (KD) in MiaPaCa-2 and/or Capan-1 cells by transfection with ONTARGET plus SMARTPool siRNAs targeting specific HDACs either individually or in combination, as indicated. Control cells were treated with non-targeting (N.T.) siRNA and, 24 h after transfection, cells were treated with various concentrations of LMK-235 ( A , B ) or Mocetinostat ( C ) and subjected to MTT assay after 72 h of drug treatment. ( i ) Representative graph of the effect of various concentrations of LMK-235 or Mocetinostat on the relative number of viable cells (absorption at 570 nm) following knockdown of the indicated HDACs (mean ± s.d. of six technical replicates for each condition). ( ii ) ED 50 values for LMK-235 ( A , B ) or Mocetinostat ( C ) in cells transfected with the indicated siRNAs (mean ± s.d. for three biological replicates).
    Figure Legend Snippet: HDACs 1, 2, and 6 account for the synergism between Mocetinostat and LMK-235 in PDAC cells. HDACs 1, 2, and 3 ( A , B ) or HDACs 4, 5, and 6 ( C ) were knocked down (KD) in MiaPaCa-2 and/or Capan-1 cells by transfection with ONTARGET plus SMARTPool siRNAs targeting specific HDACs either individually or in combination, as indicated. Control cells were treated with non-targeting (N.T.) siRNA and, 24 h after transfection, cells were treated with various concentrations of LMK-235 ( A , B ) or Mocetinostat ( C ) and subjected to MTT assay after 72 h of drug treatment. ( i ) Representative graph of the effect of various concentrations of LMK-235 or Mocetinostat on the relative number of viable cells (absorption at 570 nm) following knockdown of the indicated HDACs (mean ± s.d. of six technical replicates for each condition). ( ii ) ED 50 values for LMK-235 ( A , B ) or Mocetinostat ( C ) in cells transfected with the indicated siRNAs (mean ± s.d. for three biological replicates).

    Techniques Used: Transfection, MTT Assay

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    MedChemExpress mocetinostat sellechem lmk 235 lmk 235 sellechem acy 1215
    Pharmacological inhibition of HDACs 1, 2, and 6 enhances the effects of gemcitabine on PDAC cells in vitro and in vivo. ( A.i ) The indicated cells were treated with vehicle, 40 nM gemcitabine (Gem), 8 nM Romidepsin (Rom), and/or 1 µM <t>ACY-1215</t> (ACY) for 48 h, and the expression of PARP, cleaved caspase 3, and GAPDH was determined by Western blotting. Vertical lines indicate rearrangement of lanes from a single membrane for clarity. Data are representative of three independent experiments. ( A.ii ) PDAC cells treated as in ( i ) were analyzed for apoptosis based on cell surface phosphatidylserine using Annexin V-FITC. Data are means ± s.e. * Significantly different from Gemcitabine and Rom/ACY, p
    Mocetinostat Sellechem Lmk 235 Lmk 235 Sellechem Acy 1215, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mocetinostat sellechem lmk 235 lmk 235 sellechem acy 1215/product/MedChemExpress
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    mocetinostat sellechem lmk 235 lmk 235 sellechem acy 1215 - by Bioz Stars, 2022-05
    94/100 stars
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    Pharmacological inhibition of HDACs 1, 2, and 6 enhances the effects of gemcitabine on PDAC cells in vitro and in vivo. ( A.i ) The indicated cells were treated with vehicle, 40 nM gemcitabine (Gem), 8 nM Romidepsin (Rom), and/or 1 µM ACY-1215 (ACY) for 48 h, and the expression of PARP, cleaved caspase 3, and GAPDH was determined by Western blotting. Vertical lines indicate rearrangement of lanes from a single membrane for clarity. Data are representative of three independent experiments. ( A.ii ) PDAC cells treated as in ( i ) were analyzed for apoptosis based on cell surface phosphatidylserine using Annexin V-FITC. Data are means ± s.e. * Significantly different from Gemcitabine and Rom/ACY, p

    Journal: Cancers

    Article Title: Selective Inhibition of Histone Deacetylases 1/2/6 in Combination with Gemcitabine: A Promising Combination for Pancreatic Cancer Therapy

    doi: 10.3390/cancers11091327

    Figure Lengend Snippet: Pharmacological inhibition of HDACs 1, 2, and 6 enhances the effects of gemcitabine on PDAC cells in vitro and in vivo. ( A.i ) The indicated cells were treated with vehicle, 40 nM gemcitabine (Gem), 8 nM Romidepsin (Rom), and/or 1 µM ACY-1215 (ACY) for 48 h, and the expression of PARP, cleaved caspase 3, and GAPDH was determined by Western blotting. Vertical lines indicate rearrangement of lanes from a single membrane for clarity. Data are representative of three independent experiments. ( A.ii ) PDAC cells treated as in ( i ) were analyzed for apoptosis based on cell surface phosphatidylserine using Annexin V-FITC. Data are means ± s.e. * Significantly different from Gemcitabine and Rom/ACY, p

    Article Snippet: Where indicated, cells were treated with Panobinostat (Sellechem, Houston, TX, USA), Mocetinostat (Sellechem), LMK-235 (Sellechem), ACY-1215 (MedChem Express, Monmouth Junction, NJ, USA), Romidepsin (MedChem Express), and/or gemcitabine (Sagent Pharmaceuticals, Schaumburg, IL, USA) in DMSO (except gemcitabine, which was in sterile water).

    Techniques: Inhibition, In Vitro, In Vivo, Expressing, Western Blot

    Synergistic interactions of Mocetinostat, LMK-235, and gemcitabine in pancreatic ductal adenocarcinoma (PDAC) cells. ( A ) MiaPaCa-2 cells treated with 100 nM Panobinostat, 10 µM Droxinostat, 10 µM Mocetinostat, or 10 µM LMK-235 for the indicated times and analyzed for poly (ADP-ribose) polymerase (PARP), caspase 7, and GAPDH expression by Western blotting. Arrow indicates the migration of cleaved proteins. ( B.i ) ED 50 values for Mocetinostat and LMK-235 in pancreatic cancer cell lines. ( B.ii ) The indicated cell lines were treated with LMK-235, Mocetinostat, or a combination of LMK-235 and Mocetinostat at a constant ratio. After 72 h, 3-(4,5 Dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide (MTT) assays were performed, and the combination index (CI) value for the combination treatment is presented. Dotted line indicates CI value of one, which divides synergistic interaction (CI

    Journal: Cancers

    Article Title: Selective Inhibition of Histone Deacetylases 1/2/6 in Combination with Gemcitabine: A Promising Combination for Pancreatic Cancer Therapy

    doi: 10.3390/cancers11091327

    Figure Lengend Snippet: Synergistic interactions of Mocetinostat, LMK-235, and gemcitabine in pancreatic ductal adenocarcinoma (PDAC) cells. ( A ) MiaPaCa-2 cells treated with 100 nM Panobinostat, 10 µM Droxinostat, 10 µM Mocetinostat, or 10 µM LMK-235 for the indicated times and analyzed for poly (ADP-ribose) polymerase (PARP), caspase 7, and GAPDH expression by Western blotting. Arrow indicates the migration of cleaved proteins. ( B.i ) ED 50 values for Mocetinostat and LMK-235 in pancreatic cancer cell lines. ( B.ii ) The indicated cell lines were treated with LMK-235, Mocetinostat, or a combination of LMK-235 and Mocetinostat at a constant ratio. After 72 h, 3-(4,5 Dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide (MTT) assays were performed, and the combination index (CI) value for the combination treatment is presented. Dotted line indicates CI value of one, which divides synergistic interaction (CI

    Article Snippet: Where indicated, cells were treated with Panobinostat (Sellechem, Houston, TX, USA), Mocetinostat (Sellechem), LMK-235 (Sellechem), ACY-1215 (MedChem Express, Monmouth Junction, NJ, USA), Romidepsin (MedChem Express), and/or gemcitabine (Sagent Pharmaceuticals, Schaumburg, IL, USA) in DMSO (except gemcitabine, which was in sterile water).

    Techniques: Expressing, Western Blot, Migration, MTT Assay

    Inhibition of HDACs 1, 2, and 6 cooperates with gemcitabine. ( A.i,ii ) Capan-1 cells were transfected with non-targeting siRNA (N.T.) or ONTARGET plus SMARTPool siRNAs targeting HDACs 1, 2, and 6 and treated with gemcitabine as indicated for 72 h. ( B.i ) Capan-1 and MiaPaCa-2 cells were treated with the vehicle or the indicated concentrations of ACY-1215 for 24 h, and expression of acetyl-α-Tubulin (ac-α-Tubulin), acetyl-Histone 3 (ac-Histone 3), and GAPDH was assessed by Western blotting. ( ii ) The indicated cells were treated with 1 µM ACY-1215, and the number of viable cells was determined after 72 h. ( C ) The indicated cell lines were treated with Romidepsin, gemcitabine, or a combination of Romidepsin and gemcitabine at a constant ratio in the presence or the absence of 1 µM ACY-1215. After 72 h, CI values for the combination treatment were calculated as in Figure 1 . * Significantly different from Romedepsin + Gemcitabine, p

    Journal: Cancers

    Article Title: Selective Inhibition of Histone Deacetylases 1/2/6 in Combination with Gemcitabine: A Promising Combination for Pancreatic Cancer Therapy

    doi: 10.3390/cancers11091327

    Figure Lengend Snippet: Inhibition of HDACs 1, 2, and 6 cooperates with gemcitabine. ( A.i,ii ) Capan-1 cells were transfected with non-targeting siRNA (N.T.) or ONTARGET plus SMARTPool siRNAs targeting HDACs 1, 2, and 6 and treated with gemcitabine as indicated for 72 h. ( B.i ) Capan-1 and MiaPaCa-2 cells were treated with the vehicle or the indicated concentrations of ACY-1215 for 24 h, and expression of acetyl-α-Tubulin (ac-α-Tubulin), acetyl-Histone 3 (ac-Histone 3), and GAPDH was assessed by Western blotting. ( ii ) The indicated cells were treated with 1 µM ACY-1215, and the number of viable cells was determined after 72 h. ( C ) The indicated cell lines were treated with Romidepsin, gemcitabine, or a combination of Romidepsin and gemcitabine at a constant ratio in the presence or the absence of 1 µM ACY-1215. After 72 h, CI values for the combination treatment were calculated as in Figure 1 . * Significantly different from Romedepsin + Gemcitabine, p

    Article Snippet: Where indicated, cells were treated with Panobinostat (Sellechem, Houston, TX, USA), Mocetinostat (Sellechem), LMK-235 (Sellechem), ACY-1215 (MedChem Express, Monmouth Junction, NJ, USA), Romidepsin (MedChem Express), and/or gemcitabine (Sagent Pharmaceuticals, Schaumburg, IL, USA) in DMSO (except gemcitabine, which was in sterile water).

    Techniques: Inhibition, Transfection, Expressing, Western Blot

    HDACs 1, 2, and 6 account for the synergism between Mocetinostat and LMK-235 in PDAC cells. HDACs 1, 2, and 3 ( A , B ) or HDACs 4, 5, and 6 ( C ) were knocked down (KD) in MiaPaCa-2 and/or Capan-1 cells by transfection with ONTARGET plus SMARTPool siRNAs targeting specific HDACs either individually or in combination, as indicated. Control cells were treated with non-targeting (N.T.) siRNA and, 24 h after transfection, cells were treated with various concentrations of LMK-235 ( A , B ) or Mocetinostat ( C ) and subjected to MTT assay after 72 h of drug treatment. ( i ) Representative graph of the effect of various concentrations of LMK-235 or Mocetinostat on the relative number of viable cells (absorption at 570 nm) following knockdown of the indicated HDACs (mean ± s.d. of six technical replicates for each condition). ( ii ) ED 50 values for LMK-235 ( A , B ) or Mocetinostat ( C ) in cells transfected with the indicated siRNAs (mean ± s.d. for three biological replicates).

    Journal: Cancers

    Article Title: Selective Inhibition of Histone Deacetylases 1/2/6 in Combination with Gemcitabine: A Promising Combination for Pancreatic Cancer Therapy

    doi: 10.3390/cancers11091327

    Figure Lengend Snippet: HDACs 1, 2, and 6 account for the synergism between Mocetinostat and LMK-235 in PDAC cells. HDACs 1, 2, and 3 ( A , B ) or HDACs 4, 5, and 6 ( C ) were knocked down (KD) in MiaPaCa-2 and/or Capan-1 cells by transfection with ONTARGET plus SMARTPool siRNAs targeting specific HDACs either individually or in combination, as indicated. Control cells were treated with non-targeting (N.T.) siRNA and, 24 h after transfection, cells were treated with various concentrations of LMK-235 ( A , B ) or Mocetinostat ( C ) and subjected to MTT assay after 72 h of drug treatment. ( i ) Representative graph of the effect of various concentrations of LMK-235 or Mocetinostat on the relative number of viable cells (absorption at 570 nm) following knockdown of the indicated HDACs (mean ± s.d. of six technical replicates for each condition). ( ii ) ED 50 values for LMK-235 ( A , B ) or Mocetinostat ( C ) in cells transfected with the indicated siRNAs (mean ± s.d. for three biological replicates).

    Article Snippet: Where indicated, cells were treated with Panobinostat (Sellechem, Houston, TX, USA), Mocetinostat (Sellechem), LMK-235 (Sellechem), ACY-1215 (MedChem Express, Monmouth Junction, NJ, USA), Romidepsin (MedChem Express), and/or gemcitabine (Sagent Pharmaceuticals, Schaumburg, IL, USA) in DMSO (except gemcitabine, which was in sterile water).

    Techniques: Transfection, MTT Assay