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           Search results for: HDAC Inhibitor Drug Screening Kit   

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#26223923   2015/07/30 Save this To Up

Synergistic suppressive effect of PARP-1 inhibitor PJ34 and HDAC inhibitor SAHA on proliferation of liver cancer cells.

Poly (ADP-ribose) polymerase-1 (PARP-1) inhibitors and histone deacetylase (HDAC) inhibitors have recently emerged as promising anticancer drugs. The aim of this study was to investigate the effect of combination treatment with the PARP inhibitor PJ34 and HDAC inhibitor SAHA on the proliferation of liver cancer cells. Cell proliferation and apoptosis were assessed in three human liver cancer cell lines (HepG2, Hep3B and HCC-LM3) treated with PJ34 (8 μmol/L) and SAHA (1 μmol/L), alone or combined, by Cell Counting Kit-8 assay and flow cytometry, respectively. The nude mice bearing subcutaneous HepG2 tumors were administered different groups of drugs (10 mg/kg PJ34, 25 mg/kg SAHA, 10 mg/kg PJ34+25 mg/kg SAHA), and the inhibition rates of tumor growth were compared between groups. The results showed that combined use of PJ34 and SAHA could synergistically inhibit the proliferation of liver cancer cell lines HepG2, Hep3B and HCC-LM3. The apoptosis rate of HepG2 cells treated with PJ34+SAHA was significantly higher than that of HepG2 cells treated with PJ34 or SAHA alone (P<0.05). In vivo, the tumor inhibition rates were 53.5%, 61.4% and 82.6% in PJ34, SAHA and PJ34+SAHA groups, respectively. The combined use of PJ34 and SAHA could significantly inhibit the xenograft tumor growth when compared with use of PJ34 or SAHA alone (P<0.05). It was led to conclude that PJ34 and SAHA can synergistically suppress the proliferation of liver cancer cells.

1066 related Products with: Synergistic suppressive effect of PARP-1 inhibitor PJ34 and HDAC inhibitor SAHA on proliferation of liver cancer cells.

AZD-2281 (Olaparib) Mecha HDAC Inhibitor Drug Scree HDAC-3 Inhibitor Screenin Caspase-3 Inhibitor Z-DEV Caspase-3 Inhibitor Z-DEV Caspase 3 Inhibitor Z DEV Caspase 3 Inhibitor Z DEV Caspase-Family Inhibitor Caspase-Family Inhibitor Caspase Family Inhibitor Caspase Family Inhibitor Caspase-6 Inhibitor Z-VEI

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#26187774   2015/08/12 Save this To Up

Emerging Agents for the Treatment of Advanced, Imatinib-Resistant Gastrointestinal Stromal Tumors: Current Status and Future Directions.

Imatinib is strongly positioned as the recommended first-line agent for most patients with advanced gastrointestinal stromal tumor (GIST) due to its good efficacy and tolerability. Imatinib-resistant advanced GIST continues to pose a therapeutic challenge, likely due to the frequent presence of multiple mutations that confer drug resistance. Sunitinib and regorafenib are approved as second- and third-line agents, respectively, for patients whose GIST does not respond to imatinib or who do not tolerate imatinib, and their use is supported by large randomized trials. ATP-mimetic tyrosine kinase inhibitors provide clinical benefit even in heavily pretreated GIST suggesting that oncogenic dependency on KIT frequently persists. Several potentially useful tyrosine kinase inhibitors with distinct inhibitory profiles against both KIT ATP-binding domain and activation loop mutations have not yet been fully evaluated. Agents that have been found promising in preclinical models and early clinical trials include small molecule KIT and PDGFRA mutation-specific inhibitors, heat shock protein inhibitors, histone deacetylase inhibitors, allosteric KIT inhibitors, KIT and PDGFRA signaling pathway inhibitors, and immunological approaches including antibody-drug conjugates. Concomitant or sequential administration of tyrosine kinase inhibitors with KIT signaling pathway inhibitors require further evaluation, as well as rotation of tyrosine kinase inhibitors as a means to suppress drug-resistant cell clones.

1721 related Products with: Emerging Agents for the Treatment of Advanced, Imatinib-Resistant Gastrointestinal Stromal Tumors: Current Status and Future Directions.

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#25884486   2015/07/16 Save this To Up

Inhibition of breast cancer progression by a novel histone deacetylase inhibitor, LW479, by down-regulating EGFR expression.

Compounds targeting epigenetic events of tumours are likely to be an important addition to anticancer therapy. Histone deacetylase inhibitors (HDACI) have emerged as a promising novel class for therapeutic interventions associated with cancer, and many of them are currently in clinical investigation. Here, we assessed a novel hydroxamate-based HDACI, LW479, in breast cancer progression and explored its underlying mechanism(s).

1979 related Products with: Inhibition of breast cancer progression by a novel histone deacetylase inhibitor, LW479, by down-regulating EGFR expression.

BYL-719 Mechanisms: PI3K- Breast cancer mid density Breast disease spectrum ( Breast cancer membrane pr BIBW-2992 (Afatinib) Mech Adrenal gland disease spe Rectum disease spectrum ( Kidney disease spectrum ( Breast cancer (multiple t Breast cancer tissue arra Breast cancer (IDC) tissu Breast cancer and adjacen

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#25188886   2014/09/24 Save this To Up

PP242 synergizes with suberoylanilide hydroxamic acid to inhibit growth of ovarian cancer cells.

Overexpression of histone deacetylases and activation of the phosphatidylinositol 3-kinase/mammalian target of rapamycin pathway are common aberrations in ovarian cancer. For this reason, simultaneous inhibition of such targets is a rational therapeutic strategy to treat patients with ovarian cancer. This study aimed to investigate the biological effect of the histone deacetylase inhibitor, suberoylanilide hydroxamic acid (SAHA), in combination with the dual mTOR complex 1 and mTOR complex 2 inhibitor, PP242, against ovarian cancer cells.

1776 related Products with: PP242 synergizes with suberoylanilide hydroxamic acid to inhibit growth of ovarian cancer cells.

CA125, Ovarian Cancer An CA125, Ovarian Cancer An CA125, Ovarian Cancer An Epidermal Growth Factor ( Epidermal Growth Factor ( Fibroblast Growth Factor Fibroblast Growth Factor Human Fibroblast Growth F GST Inhibitor 2 (Ethacryn Mouse Fibroblast Growth F Rat ovarian cancer marker (2S)-2-Amino-benzenebutan

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#22760542   2012/10/01 Save this To Up

Valproic acid confers functional pluripotency to human amniotic fluid stem cells in a transgene-free approach.

Induced pluripotent stem cells (iPSCs) with potential for therapeutic applications can be derived from somatic cells via ectopic expression of a set of limited and defined transcription factors. However, due to risks of random integration of the reprogramming transgenes into the host genome, the low efficiency of the process, and the potential risk of virally induced tumorigenicity, alternative methods have been developed to generate pluripotent cells using nonintegrating systems, albeit with limited success. Here, we show that c-KIT+ human first-trimester amniotic fluid stem cells (AFSCs) can be fully reprogrammed to pluripotency without ectopic factors, by culture on Matrigel in human embryonic stem cell (hESC) medium supplemented with the histone deacetylase inhibitor (HDACi) valproic acid (VPA). The cells share 82% transcriptome identity with hESCs and are capable of forming embryoid bodies (EBs) in vitro and teratomas in vivo. After long-term expansion, they maintain genetic stability, protein level expression of key pluripotency factors, high cell-division kinetics, telomerase activity, repression of X-inactivation, and capacity to differentiate into lineages of the three germ layers, such as definitive endoderm, hepatocytes, bone, fat, cartilage, neurons, and oligodendrocytes. We conclude that AFSC can be utilized for cell banking of patient-specific pluripotent cells for potential applications in allogeneic cellular replacement therapies, pharmaceutical screening, and disease modeling.

1976 related Products with: Valproic acid confers functional pluripotency to human amniotic fluid stem cells in a transgene-free approach.

Macrophage Colony Stimula Macrophage Colony Stimula Recombinant Human Interfe Human Internal Mammary Ar GFP Expressing Human Inte Goat Anti-Human TOM1L1 SR Total Human tPA Functiona MarkerGeneTM Live Dead As Rabbit Anti-Human Toll In Human Dnak (HSP70) His ta Fatty acid free heat sho Fatty acid free heat sho

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#21632108   2011/08/15 Save this To Up

Heat shock protein 90 inhibition results in altered downstream signaling of mutant KIT and exerts synergistic effects on Kasumi-1 cells when combining with histone deacetylase inhibitor.

KIT mutations may be associated with a poor prognosis in t(8;21) AML. Heat shock protein 90 (Hsp90) is a molecular chaperone frequently used by cancer cells to stabilize mutant oncoproteins. Inhibition of Hsp90 by 17-allylamino-17-demethoxygeldanamycin (17-AAG) disrupted downstream signaling pathways of mutant KIT in Kasumi-1 cells. AML1-ETO fusion gene and mutated KIT act as "two-hit" factors in Kasumi-1 cells. Histone deacetylation (HDAC) inhibitors sodium phenylbutyrate (PB) and valproic acid (VPA) block AML1-ETO. Co-treatment with 17-AAG and PB or 17-AAG and VPA resulted in a synergistic effect in Kasumi-1 cells. Our results confirmed that Hsp90 and mutated KIT were valid molecular targets in the therapy of AML.

1974 related Products with: Heat shock protein 90 inhibition results in altered downstream signaling of mutant KIT and exerts synergistic effects on Kasumi-1 cells when combining with histone deacetylase inhibitor.

Rabbit heat shock protein Rabbit heat shock protein MMP-13 inhibitor assay ki Proteinase Inhibitor 9 (P Proteinase Inhibitor 9 (P Proteinase Inhibitor 9 (P Proteinase Inhibitor 9 (P Proteinase Inhibitor 9 (P Proteinase Inhibitor 6 (P Heat Shock Protein 20, hu Heat Shock Protein 22, hu Heat Shock Protein 27, hu

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#20613486   2010/07/30 Save this To Up

Chimeric tyrosine kinase-HDAC inhibitors as antiproliferative agents.

Combined treatment with tyrosine kinase inhibitors (TKi) and additional drugs is emerging as a promising strategy for cancer therapy. TKi and histone-deacetylase inhibitors (HDI) are two classes of anti-tumor agents with distant mechanisms of action. We have designed and synthesized chimeric compounds, which comprise structural elements of the TKi imatinib, and of prototypical HDI compounds. These compounds retain TKi activity similar to imatinib, exemplified by the inhibition of the platelet-derived growth factor receptor, and c-Kit kinase in intact cells. In addition, the chimeric compounds have in vitro and cellular HDI activity, and potently inhibit growth of cancer cell lines, including that of imatinib-resistant cell lines. Chimeric molecules with combined TKi and HDI activity may simplify combination treatment and be applicable to overcome clinical resistance to TKi single-agent therapy.

1585 related Products with: Chimeric tyrosine kinase-HDAC inhibitors as antiproliferative agents.

EnzyChrom™ Kinase Assay DiscoveryPak™ EGFR Tyro DiscoveryPak™ Receptor Amplite™ Fluorimetric H Amplite™ Universal Fluo HDAC assay buffer HDAC Fluorogenic Assay Ki Fluorogenic HDAC class 2a Tyrosine Kinase Adaptors Mouse ALK tyrosine kinase Human Lemur Tyrosine Kina EnzyChrom™ Creatine Kin

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#19509176   2009/06/16 Save this To Up

High efficacy of panobinostat towards human gastrointestinal stromal tumors in a xenograft mouse model.

Histone deacetylase inhibitors have emerged as potent anticancer compounds. Using a nude-mouse xenograft model, for the first time we evaluated the response of human gastrointestinal stromal tumors (GIST) carrying different oncogenic KIT mutations to panobinostat (LBH589), administered single or in combination with imatinib.

2340 related Products with: High efficacy of panobinostat towards human gastrointestinal stromal tumors in a xenograft mouse model.

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#15892618   2005/05/16 Save this To Up

Molecularly targeted therapy for gastrointestinal cancer.

Receptor and non-receptor tyrosine kinases (TKs) have emerged as clinically useful drug target molecules for treating gastrointestinal cancer. Imatinib mesilate (STI-571, Gleevec(TM)), an inhibitior of bcr-abl TK, which was primarily designed to treat chronic myeloid leukemia is also an inhibitor of c-kit receptor TK, and is currently the drug of choice for the therapy of metastatic gastrointestinal stromal tumors (GISTs), which frequently express constitutively activated forms of the c-kit-receptor. The epidermal growth factor receptor (EGFR), which is involved in cell proliferation, metastasis and angiogenesis, is another important target. The two main classes of EGFR inhibitors are the TK inhibitors and monoclonal antibodies. Gefitinib (ZD1839, Iressa(TM)) has been on trial for esophageal and colorectal cancer (CRC) and erlotinib (OSI-774, Tarceva(TM)) on trial for esophageal, colorectal, hepatocellular, and biliary carcinoma. In addition, erlotinib has been evaluated in a Phase III study for the treatment of pancreatic cancer. Cetuximab (IMC-C225, Erbitux(TM)), a monoclonal EGFR antibody, has been FDA approved for the therapy of irinotecan resistant colorectal cancer and has been tested for pancreatic cancer. Vascular endothelial growth factor (VEGF) and its receptor (VEGFR) are critical regulators of tumor angiogenesis. Bevacizumab (Avastin(TM)), a monoclonal antibody against VEGF, was efficient in two randomized clinical trials investigating the treatment of metastatic colorectal cancer. It is also currently investigated for the therapy of pancreatic cancer in combination with gemcitabine. Other promising new drugs currently under preclinical and clinical evaluation, are VEGFR2 inhibitor PTK787/ZK 222584, thalidomide, farnesyl transferase inhibitor R115777 (tipifarnib, Zarnestra(TM)), matrix metalloproteinase inhibitors, proteasome inhibitor bortezomib (Velcade(TM)), mammalian target of rapamycin (mTOR) inhibitors, cyclooxygenase-2 (COX-2) inhibitors, platelet derived growth factor receptor (PDGF-R) inhibitors, protein kinase C (PKC) inhibitors, mitogen-activated protein kinase kinase (MEK) 1/2 inhibitors, Rous sarcoma virus transforming oncogene (SRC) kinase inhibitors, histondeacetylase (HDAC) inhibitors, small hypoxia-inducible factor (HIF) inhibitors, aurora kinase inhibitors, hedgehog inhibitors, and TGF-beta signalling inhibitors.

2983 related Products with: Molecularly targeted therapy for gastrointestinal cancer.

Mouse Anti-Human CA19-9 ( Multiple organ gastrointe Human Gastrointestinal Ca Cellufine Formyl , 50 ml Cellufine Formyl Media Cellufine Formyl , 500 ml Cellufine Formyl Media Cellufine Formyl Media CA125, Ovarian Cancer An CA125, Ovarian Cancer An CA125, Ovarian Cancer An Formalin Solution (20%)

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