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背景介绍 PCI-24781 is a pan-HDAC inhibitor that shows antitumor activity in vitro and in vivo preclinically and is under evaluation in phase I clinical trials for cancer, particularly B-cell lymphoma. PCI-24781 induces caspase and reactive oxygen species-dependent apoptosis through NF-?B mechanisms in Hodgkin lymphoma and non-Hodgkin lymphoma cell lines. 产品介绍 PCI-24781 (also known as CRA-024781) is a novel, broad spectrum inhibitor of HDACs that shows antitumor activity in vitro. PCI-24781 primarily targets HDAC1 (Ki = 7 nM). It also exhibits modest potenty toward HDACs 2, 3, 6, and 10 and greater than 40-fold selectivity against HDAC8.
询价背景介绍 PCI-24781 is a pan-HDAC inhibitor that shows antitumor activity in vitro and in vivo preclinically and is under evaluation in phase I clinical trials for cancer, particularly B-cell lymphoma. PCI-24781 induces caspase and reactive oxygen species-dependent apoptosis through NF-?B mechanisms in Hodgkin lymphoma and non-Hodgkin lymphoma cell lines. 产品介绍 PCI-24781 (also known as CRA-024781) is a novel, broad spectrum inhibitor of HDACs that shows antitumor activity in vitro. PCI-24781 primarily targets HDAC1 (Ki = 7 nM). It also exhibits modest potenty toward HDACs 2, 3, 6, and 10 and greater than 40-fold selectivity against HDAC8.
询价背景介绍 Parthenolide is a sesquiterpene lactone and the active principle of feverfew (Chrysanthemum parthenium) 产品介绍 Parthenolide specifically inhibits HDAC1 without affecting other class I/II HDACs.
询价背景介绍 Parthenolide is a sesquiterpene lactone, a class of naturally occurring plant terpenoids, and the active principle of feverfew (Chrysanthemum parthenium). Parthenolide has demonstrated anti-inflammatory, antisecretory and spasmolytic activity. Parthenolide has been shown to inhibit the release of various chemical mediators such as Cox-2, TNF-α and IL-1 in LPS-stimulated macrophages and activation of MAP kinase and NFκβ. Recent findings indicate that parthenolide binds to and directly inhibits Iκβ kinase. The compound has also been shown to block the production of thromboxane B2 and leukotriene B4. 产品介绍 Parthenolide specifically inhibits HDAC1 without affecting other class I/II HDACs.
询价背景介绍 USP7, known as herpes-associated-ubiquitin-specificprotease (HAUSP), is a deubiquitylating enzyme that regulates the levels of the oncoprotein HDM2 and its substrate, the tumor suppressor p53. P005091 accelerated the degradation of HDM2, while analogs of the compound induced dose- and time-dependent increases in the protein levels of p53 and p21. P005091 induced apoptosis in numerous cancer cell lines, including both p53+/+ and p53-mutant cancer cell lines. P005091 also downregulated claspin and phosphorylation of the DNA checkpoint kinase Chk1. 产品介绍 P005091 is a selective, potent inhibitor of USP7 deubiquitylating activity.
询价背景介绍 USP7, known as herpes-associated-ubiquitin-specificprotease (HAUSP), is a deubiquitylating enzyme that regulates the levels of the oncoprotein HDM2 and its substrate, the tumor suppressor p53. P005091 accelerated the degradation of HDM2, while analogs of the compound induced dose- and time-dependent increases in the protein levels of p53 and p21. P005091 induced apoptosis in numerous cancer cell lines, including both p53+/+ and p53-mutant cancer cell lines. P005091 also downregulated claspin and phosphorylation of the DNA checkpoint kinase Chk1. 产品介绍 P005091 is a selective, potent inhibitor of USP7 deubiquitylating activity.
询价背景介绍 NVP-BEP800 binds to the N-terminal ATP-binding pocket of Hsp90. Hsp90 is a ubiquitously expressed molecular chaperone with ATPase activity involved in the conformational maturation and stability of key signaling molecules involved in cell proliferation, survival, and transformation. In BT-474 cells and A375 cells, NVP-BEP800 causes the Hsp90-p23 dissociation and client protein degradation (ErbB2) as well as the reduction of client protein phosphorylation (phospho-Akt). Degradation of these oncogenic client proteins results in tumor cell growth arrest and death. 产品介绍 NVP-BEP800 is a novel, fully synthetic, orally bioavailable inhibitor that binds to the NH(2)-terminal ATP-binding pocket of Hsp90. NVP-BEP800 (also known as VER-82576) is a novel ATP-competitive HSP90β inhibitor that binds to the NH(2)-terminal ATP-binding pocket of Heat shock protein 90 (Hsp90). NVP-BEP800 induced robust antitumor responses in tumor xenograft models, including regression in the BT-474 breast cancer model. NVP-BEP800 can radiosensitise tumour cell lines of different entities through destabilisation and depletion of several Hsp90 client proteins, thus causing the depletion of S phase and G2/M arrest, increased DNA damage and repair protraction and, to some extent, apoptosis.
询价背景介绍 NVP-BEP800 binds to the N-terminal ATP-binding pocket of Hsp90. Hsp90 is a ubiquitously expressed molecular chaperone with ATPase activity involved in the conformational maturation and stability of key signaling molecules involved in cell proliferation, survival, and transformation. In BT-474 cells and A375 cells, NVP-BEP800 causes the Hsp90-p23 dissociation and client protein degradation (ErbB2) as well as the reduction of client protein phosphorylation (phospho-Akt). Degradation of these oncogenic client proteins results in tumor cell growth arrest and death. 产品介绍 NVP-BEP800 is a novel, fully synthetic, orally bioavailable inhibitor that binds to the NH(2)-terminal ATP-binding pocket of Hsp90. NVP-BEP800 (also known as VER-82576) is a novel ATP-competitive HSP90β inhibitor that binds to the NH(2)-terminal ATP-binding pocket of Heat shock protein 90 (Hsp90). NVP-BEP800 induced robust antitumor responses in tumor xenograft models, including regression in the BT-474 breast cancer model. NVP-BEP800 can radiosensitise tumour cell lines of different entities through destabilisation and depletion of several Hsp90 client proteins, thus causing the depletion of S phase and G2/M arrest, increased DNA damage and repair protraction and, to some extent, apoptosis.
询价背景介绍 NVP-BEP800 binds to the N-terminal ATP-binding pocket of Hsp90. Hsp90 is a ubiquitously expressed molecular chaperone with ATPase activity involved in the conformational maturation and stability of key signaling molecules involved in cell proliferation, survival, and transformation. In BT-474 cells and A375 cells, NVP-BEP800 causes the Hsp90-p23 dissociation and client protein degradation (ErbB2) as well as the reduction of client protein phosphorylation (phospho-Akt). Degradation of these oncogenic client proteins results in tumor cell growth arrest and death. 产品介绍 NVP-BEP800 is a novel, fully synthetic, orally bioavailable inhibitor that binds to the NH(2)-terminal ATP-binding pocket of Hsp90. NVP-BEP800 (also known as VER-82576) is a novel ATP-competitive HSP90β inhibitor that binds to the NH(2)-terminal ATP-binding pocket of Heat shock protein 90 (Hsp90). NVP-BEP800 induced robust antitumor responses in tumor xenograft models, including regression in the BT-474 breast cancer model. NVP-BEP800 can radiosensitise tumour cell lines of different entities through destabilisation and depletion of several Hsp90 client proteins, thus causing the depletion of S phase and G2/M arrest, increased DNA damage and repair protraction and, to some extent, apoptosis.
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