The Novel Deacetylase Inhibitor AR-42 Demonstrates Pre-Clinical Activity in B-Cell Malignancies In Vitro and In Vivo
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{"title"=>"The novel deacetylase inhibitor AR-42 demonstrates pre-clinical activity in B-Cell malignancies In Vitro and In Vivo", "type"=>"journal", "authors"=>[{"first_name"=>"David M.", "last_name"=>"Lucas", "scopus_author_id"=>"7202026135"}, {"first_name"=>"Lapo", "last_name"=>"Alinari", "scopus_author_id"=>"6602776725"}, {"first_name"=>"Derek A.", "last_name"=>"West", "scopus_author_id"=>"26642197500"}, {"first_name"=>"Melanie E.", "last_name"=>"Davis", "scopus_author_id"=>"7404850092"}, {"first_name"=>"Ryan B.", "last_name"=>"Edwards", "scopus_author_id"=>"14065877600"}, {"first_name"=>"Amy J.", "last_name"=>"Johnson", "scopus_author_id"=>"24769524900"}, {"first_name"=>"Kristie A.", "last_name"=>"Blum", "scopus_author_id"=>"7102058245"}, {"first_name"=>"Craig C.", "last_name"=>"Hofmeister", "scopus_author_id"=>"6602001402"}, {"first_name"=>"Michael A.", "last_name"=>"Freitas", "scopus_author_id"=>"7102366671"}, {"first_name"=>"Mark R.", "last_name"=>"Parthun", "scopus_author_id"=>"6603908670"}, {"first_name"=>"Dasheng", "last_name"=>"Wang", "scopus_author_id"=>"55639180300"}, {"first_name"=>"Amy", "last_name"=>"Lehman", "scopus_author_id"=>"35464910300"}, {"first_name"=>"Xiaoli", "last_name"=>"Zhang", "scopus_author_id"=>"7410266420"}, {"first_name"=>"David", "last_name"=>"Jarjoura", "scopus_author_id"=>"7004918700"}, {"first_name"=>"Samuel K.", "last_name"=>"Kulp", "scopus_author_id"=>"7004693573"}, {"first_name"=>"Carlo M.", "last_name"=>"Croce", "scopus_author_id"=>"7202975031"}, {"first_name"=>"Michael R.", "last_name"=>"Grever", "scopus_author_id"=>"7005254341"}, {"first_name"=>"Ching Shih", "last_name"=>"Chen", "scopus_author_id"=>"36825554800"}, {"first_name"=>"Robert A.", "last_name"=>"Baiocchi", "scopus_author_id"=>"7004083709"}, {"first_name"=>"John C.", "last_name"=>"Byrd", "scopus_author_id"=>"35377719400"}], "year"=>2010, "source"=>"PLoS ONE", "identifiers"=>{"scopus"=>"2-s2.0-77956194142", "sgr"=>"77956194142", "issn"=>"19326203", "doi"=>"10.1371/journal.pone.0010941", "pmid"=>"20532179", "isbn"=>"1932-6203 (Electronic)\\r1932-6203 (Linking)", "pui"=>"359289603"}, "id"=>"b739ee05-b5d0-30f2-afde-575590bd6885", "abstract"=>"While deacetylase (DAC) inhibitors show promise for the treatment of B-cell malignancies, those introduced to date are weak inhibitors of class I and II DACs or potent inhibitors of class I DAC only, and have shown suboptimal activity or unacceptable toxicities. We therefore investigated the novel DAC inhibitor AR-42 to determine its efficacy in B-cell malignancies.\\n\\nIn mantle cell lymphoma (JeKo-1), Burkitt's lymphoma (Raji), and acute lymphoblastic leukemia (697) cell lines, the 48-hr IC50 (50% growth inhibitory concentration) of AR-42 is 0.61 µM or less. In chronic lymphocytic leukemia (CLL) patient cells, the 48-hr LC50 (concentration lethal to 50%) of AR-42 is 0.76 µM. AR-42 produces dose- and time-dependent acetylation both of histones and tubulin, and induces caspase-dependent apoptosis that is not reduced in the presence of stromal cells. AR-42 also sensitizes CLL cells to TNF-Related Apoptosis Inducing Ligand (TRAIL), potentially through reduction of c-FLIP. AR-42 significantly reduced leukocyte counts and/or prolonged survival in three separate mouse models of B-cell malignancy without evidence of toxicity.\\n\\nTogether, these data demonstrate that AR-42 has in vitro and in vivo efficacy at tolerable doses. These results strongly support upcoming phase I testing of AR-42 in B-cell malignancies.", "link"=>"http://www.mendeley.com/research/novel-deacetylase-inhibitor-ar42-demonstrates-preclinical-activity-bcell-malignancies-vitro-vivo", "reader_count"=>26, "reader_count_by_academic_status"=>{"Unspecified"=>2, "Professor > Associate Professor"=>3, "Student > Doctoral Student"=>1, "Researcher"=>8, "Student > Ph. D. Student"=>7, "Student > Postgraduate"=>1, "Student > Master"=>1, "Student > Bachelor"=>3}, "reader_count_by_user_role"=>{"Unspecified"=>2, "Professor > Associate Professor"=>3, "Student > Doctoral Student"=>1, "Researcher"=>8, "Student > Ph. D. Student"=>7, "Student > Postgraduate"=>1, "Student > Master"=>1, "Student > Bachelor"=>3}, "reader_count_by_subject_area"=>{"Unspecified"=>4, "Biochemistry, Genetics and Molecular Biology"=>7, "Agricultural and Biological Sciences"=>11, "Medicine and Dentistry"=>3, "Chemistry"=>1}, "reader_count_by_subdiscipline"=>{"Medicine and Dentistry"=>{"Medicine and Dentistry"=>3}, "Chemistry"=>{"Chemistry"=>1}, "Agricultural and Biological Sciences"=>{"Agricultural and Biological Sciences"=>11}, "Biochemistry, Genetics and Molecular Biology"=>{"Biochemistry, Genetics and Molecular Biology"=>7}, "Unspecified"=>{"Unspecified"=>4}}, "reader_count_by_country"=>{"United States"=>1}, "group_count"=>0}

Scopus | Further Information

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Figshare

  • {"files"=>["https://ndownloader.figshare.com/files/846790"], "description"=>"<p>(<b>A</b>) CLL patient samples (n = 6) were incubated with or without AR-42 (0.90 µM) and TRAIL (100 ng/mL). Romidepsin (0.04 µM) and F-ara A (2.0 µM) were included as positive and negative controls, respectively. Cells were assessed by flow cytometry at 48 hr, and percent live (annexin and PI negative) cells were calculated relative to the time-matched untreated samples. Co-incubation with AR-42 and TRAIL produced a significant reduction in cell viability (p<0.0001) compared to TRAIL or AR-42 alone. (<b>B</b>) CLL cells were incubated 24 hr with or without AR-42, and lysates were analyzed for expression of c-FLIP. Romidepsin and F-ara A were included as positive and negative controls, respectively. Example is representative of seven CLL samples.</p>", "links"=>[], "tags"=>["sensitizes", "cll", "cells", "mediates"], "article_id"=>517221, "categories"=>["Cell Biology"], "users"=>["David M. Lucas", "Lapo Alinari", "Derek A. West", "Melanie E. Davis", "Ryan B. Edwards", "Amy J. Johnson", "Kristie A. Blum", "Craig C. Hofmeister", "Michael A. Freitas", "Mark R. Parthun", "Dasheng Wang", "Amy Lehman", "Xiaoli Zhang", "David Jarjoura", "Samuel K. Kulp", "Carlo M. Croce", "Michael R. Grever", "Ching-Shih Chen", "Robert A. Baiocchi", "John C. Byrd"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0010941.g004", "stats"=>{"downloads"=>1, "page_views"=>11, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_AR_42_sensitizes_CLL_cells_to_TRAIL_and_mediates_reduction_of_c_FLIP_/517221", "title"=>"AR-42 sensitizes CLL cells to TRAIL and mediates reduction of c-FLIP.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2013-02-21 01:08:55"}
  • {"files"=>["https://ndownloader.figshare.com/files/846894"], "description"=>"<p>(<b>A</b>) SCID mice were engrafted with two million Raji cells via tail vein injection. Starting 3 days post-inoculation, mice were treated by oral gavage with vehicle only daily (n = 11), vorinostat at the maximum tolerated dose of 50 mg/kg daily (n = 5), and AR-42 at 75 mg/kg (n = 6) Monday, Wednesday and Friday. The median survival advantage in the AR-42 group relative to the vehicle control group was significant (p = 0.001). (<b>B</b>) SCID mice were engrafted with forty million JeKo-1 cells via tail vein injection. Starting on day 15 post-inoculation, mice were treated intraperitoneally with vehicle alone or 20 mg/kg AR-42 every three days (n = 5 per group). The improvement in median survival relative to control was significant (p = 0.003). (<b>C</b>) SCID mice were engrafted with one million Eμ-Tcl1 leukemia cells via tail vein injection. When the circulating leukocyte count averaged 20,000 cells/µL across the group (dashed horizontal line; 69 days post-inoculation), mice were randomized to two cohorts and treated Monday, Wednesday and Friday for two weeks with vehicle only (light bars) or with AR-42 at 75 mg/kg via oral gavage (dark bars) (n = 5, both groups). *The decrease in circulating leukocytes in AR-42 treated mice vs. controls at week 12 relative to week 10 was significant (p = 0.0007). (<b>D</b>) Animals in (<b>C</b>) were followed for survival (n = 5 per group). The increase in median survival in the AR-42 group relative to control was significant (p = 0.025).</p>", "links"=>[], "tags"=>["shows", "efficacy", "models", "B-cell"], "article_id"=>517315, "categories"=>["Cell Biology"], "users"=>["David M. Lucas", "Lapo Alinari", "Derek A. West", "Melanie E. Davis", "Ryan B. Edwards", "Amy J. Johnson", "Kristie A. Blum", "Craig C. Hofmeister", "Michael A. Freitas", "Mark R. Parthun", "Dasheng Wang", "Amy Lehman", "Xiaoli Zhang", "David Jarjoura", "Samuel K. Kulp", "Carlo M. Croce", "Michael R. Grever", "Ching-Shih Chen", "Robert A. Baiocchi", "John C. Byrd"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0010941.g005", "stats"=>{"downloads"=>1, "page_views"=>9, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_AR_42_shows_in_vivo_efficacy_in_multiple_models_of_B_cell_malignancy_/517315", "title"=>"AR-42 shows <i>in vivo</i> efficacy in multiple models of B-cell malignancy.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2013-02-21 01:09:27"}
  • {"files"=>["https://ndownloader.figshare.com/files/846673"], "description"=>"<p>(<b>A</b>) CLL cells were incubated with or without AR-42 (0.90 µM) for the times noted. Lysates from 697 cells incubated 16 hr without or with 0.04 µM romidepsin were included as controls. Extracts were analyzed by immunoblot for acetylated tubulin and histone H3, plus GAPDH as a loading control. Data are representative of six patient samples. (<b>B</b>) CLL tumor cells were incubated with or without DAC inhibitors romidepsin (0.04 µM), AR-42 (0.90 µM), or vorinostat (5.0 µM) as indicated. 697 cells incubated 24 hr with or without 5.0 µM vorinostat were included as a control (left). Extracts were analyzed by immunoblot for acetylated tubulin and histone H3, plus GAPDH as loading control. Data are representative of seven CLL samples. (<b>C</b>) CLL patient cells (n = 4) were incubated without or with tubacin as indicated for 72 hr, and viability was analyzed by MTT assay. Data are shown relative to the time-matched untreated control. There were no significant changes in viability across doses (p = 0.265).</p>", "links"=>[], "tags"=>["exhibits", "ii", "dac", "inhibitory"], "article_id"=>517114, "categories"=>["Cell Biology"], "users"=>["David M. Lucas", "Lapo Alinari", "Derek A. West", "Melanie E. Davis", "Ryan B. Edwards", "Amy J. Johnson", "Kristie A. Blum", "Craig C. Hofmeister", "Michael A. Freitas", "Mark R. Parthun", "Dasheng Wang", "Amy Lehman", "Xiaoli Zhang", "David Jarjoura", "Samuel K. Kulp", "Carlo M. Croce", "Michael R. Grever", "Ching-Shih Chen", "Robert A. Baiocchi", "John C. Byrd"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0010941.g003", "stats"=>{"downloads"=>2, "page_views"=>18, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_AR_42_exhibits_class_I_and_II_DAC_inhibitory_activity_/517114", "title"=>"AR-42 exhibits class I and II DAC inhibitory activity.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2013-02-21 01:08:16"}
  • {"files"=>["https://ndownloader.figshare.com/files/846386"], "description"=>"<p>(<b>A</b>) Raji, 697 and JeKo-1 B-cell lines (n = 3 each) or CLL patient cells (n = 11) were incubated 48 hr with or without AR-42. Growth inhibition (for cell lines) or viability (for non-proliferating CLL patient cells) was assessed by MTT assay and calculated relative to time-matched untreated cells. Bars represent +/− standard deviation. (<b>B</b>) CLL cells were incubated with or without AR-42 (0.90 µM). At 4 hr or 16 hr, cells were replated in fresh media with or without drug. At 48 hr, viability was assessed by MTT assay and is shown relative to time-matched, untreated controls (n = 5 for 4 and 16 hr exposures; n = 11 for 48 hr exposure and untreated controls). Bars represent +/− standard deviation. There was no significant difference in viability between untreated samples and samples with 4 hr AR-42 exposure. The difference in viability between untreated samples or those with 16 hr exposures was significant (p<0.0001). (<b>C</b>) 697 cells were incubated 24 hr (solid bars) or 48 hr (striped bars) with or without AR-42, using RPMI 1640 supplemented either with 10% FBS (white bars) or 10% human serum (grey bars) (n = 3). Viability was assessed by MTT assay and calculated relative to the untreated samples. Bars represent +/− standard deviation. AR-42 cytotoxicity in media with human serum or FBS was similar (0.45 µM: p = 0.20 and p = 1.0 at 24 and 48 hr respectively; 1.35 µM: p = 0.21 and p = 0.24 at 24 and 48 hr, respectively).</p>", "links"=>[], "tags"=>["exhibits", "potent", "cytotoxicity"], "article_id"=>516802, "categories"=>["Cell Biology"], "users"=>["David M. Lucas", "Lapo Alinari", "Derek A. West", "Melanie E. Davis", "Ryan B. Edwards", "Amy J. Johnson", "Kristie A. Blum", "Craig C. Hofmeister", "Michael A. Freitas", "Mark R. Parthun", "Dasheng Wang", "Amy Lehman", "Xiaoli Zhang", "David Jarjoura", "Samuel K. Kulp", "Carlo M. Croce", "Michael R. Grever", "Ching-Shih Chen", "Robert A. Baiocchi", "John C. Byrd"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0010941.g001", "stats"=>{"downloads"=>1, "page_views"=>6, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_AR_42_exhibits_potent_cytotoxicity_in_B_leukemia_lymphoma_cells_/516802", "title"=>"AR-42 exhibits potent cytotoxicity in B-leukemia/lymphoma cells.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2013-02-21 01:06:32"}
  • {"files"=>["https://ndownloader.figshare.com/files/846518"], "description"=>"<p>(<b>A</b>) CLL patient cells (n = 8) were incubated 16 hr with or without AR-42 (0.90 µM), then washed and cultured in the absence or presence of HS-5 stromal cells for a total of 48 hr. CLL cells were collected and analyzed by flow cytometry. Data for each patient are shown individually (light dotted lines) as absolute percent annexin-positive cells. Averages for each group are shown as a dark bar, connected by a solid line. The difference in HS-5 protection of CLL cells between untreated and AR-42 treated was significant (p = 0.016). (<b>B</b>) JeKo-1 cells (n = 3) were incubated 24 hr with or without AR-42 (0.90 µM), romidepsin (rom; 0.04 µM), F-ara A (5.0 µM) and Z-VAD-fmk (100 µM). Cells were analyzed by annexin/PI flow cytometry (top) or by immunoblot for PARP (bottom). Results with 697 cells were similar. (<b>C</b>) CLL cells (n = 5) were incubated with or without AR-42 (0.90 µM) and Z-VAD-fmk (100 µM). Cells were analyzed by flow cytometry at 48 hr and percent live cells (annexin and PI negative) were calculated relative to time-matched untreated samples. Bars represent +/− standard deviation. In AR-42 treated cells, increase in live cells with Z-VAD-fmk was significant (p = 0.0002). (<b>D</b>) Extracts from CLL cells incubated 24 hr with or without AR-42 and Z-VAD-fmk were immunoblotted for PARP. Result is representative of seven CLL samples.</p>", "links"=>[], "tags"=>["efficacy", "stromal", "factors", "involves", "caspase"], "article_id"=>516943, "categories"=>["Cell Biology"], "users"=>["David M. Lucas", "Lapo Alinari", "Derek A. West", "Melanie E. Davis", "Ryan B. Edwards", "Amy J. Johnson", "Kristie A. Blum", "Craig C. Hofmeister", "Michael A. Freitas", "Mark R. Parthun", "Dasheng Wang", "Amy Lehman", "Xiaoli Zhang", "David Jarjoura", "Samuel K. Kulp", "Carlo M. Croce", "Michael R. Grever", "Ching-Shih Chen", "Robert A. Baiocchi", "John C. Byrd"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0010941.g002", "stats"=>{"downloads"=>1, "page_views"=>12, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_AR_42_efficacy_is_independent_of_stromal_survival_factors_but_involves_caspase_activation_/516943", "title"=>"AR-42 efficacy is independent of stromal survival factors but involves caspase activation.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2013-02-21 01:07:19"}

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