目录号 | 产品详情 | 靶点 | |
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T62041 | |||
XP5 是一种有效的、具有口服活性的HDAC6抑制剂(IC50= 31 nM)。XP5高效抑制各种癌细胞系(包括抗 HDACi 的 YCC3/7 胃癌细胞)的增殖 (IC50=0.16-2.31 μM)。 | |||
T61962 | |||
PARP-1/HDAC-IN-1 是有效的 PARP-1/HDAC6双重抑制剂,IC50分别为 68.90 nM 和 510 nM。PARP-1/HDAC-IN-1 具有抗癌、抗迁移和抗血管生成活性。 | |||
T61630 | |||
HDAC-IN-42 (compound 14f) is a highly potent and selective inhibitor of histone deacetylase (HDAC) enzymes, with IC50 values of 0.19 μM for HDAC1 and 4.98 μM for HDAC6. It exhibits remarkable anticancer properties and inhibits cell proliferation. Additionally, HDAC-IN-42 induces apoptosis and causes cell cycle arrest specifically at the G2/M phase [1]. | |||
T61429 | |||
HDAC-IN-33 is a highly potent HDAC inhibitor, effectively inhibiting HDAC1, HDAC2, and HDAC6 with IC50 values of 24, 46, and 47 nM, respectively. This compound demonstrates significant antiproliferation activity against tumor cells and exhibits remarkable in vivo antitumor efficacy. Additionally, HDAC-IN-33 initiates the activation of antitumor immunity [1]. | |||
T62649 | |||
HDAC-IN-34 (compound 27) 是一种 HDAC 的有效抑制剂,能够作用于 HDAC1 (IC50: 0.022 μM) 和 HDAC6 (IC50: 0.45 μM)。HDAC-IN-34 可以与 DNA 结合,造成 DNA 损伤。HDAC-IN-34 利用 p53 信号通路引起细胞凋亡。HDAC-IN-34 对 HCT-116 细胞表现出明显的抗增殖作用 (IC50: 1.41 μM)。 | |||
T62006 | |||
HDAC-IN-30 是多种HDAC 蛋白的抑制剂,包括HDAC1(IC50=13.4 nM),HDAC2(IC50=28.0 nM),HDAC3(IC50=9.18 nM),HDAC6(IC50=42.7 nM),HDAC8(IC50=131 nM)。HDAC-IN-30 显示除强大的抗肿瘤作用。 | |||
T61337 | |||
PTG-0861 is a highly specific inhibitor of histone deacetylase 6 (HDAC6), demonstrating an impressive IC50 value of 5.92 nm. This compound effectively triggers apoptosis and holds potential for research pertaining to acute myeloid leukemia, multiple myeloma, and other hematological cancers [1]. | |||
T72872 | HDAC | ||
HDAC/BET-IN-1表现出对HDAC1 (IC50= 0.163 μM) 和HDAC6 (IC50= 0.067 μM) 的亚微摩尔级别抑制作用,以及对BRD4 (Ki= 0.076 μM) 的抑制活性,同时也显示出显著的抗白血病活性。 | |||
T62708 | |||
HDAC-IN-37 是一种 HDAC 的有效抑制剂,作用于 HDAC1 (IC50: 0.0551 μM)、HDAC3 (IC50: 1.24 μM)、HDAC8 (IC50: 0.948 μM) 和 HDAC6 (IC50: 34.2 μM)。HDAC-IN-37 能够缓慢诱导组蛋白乙酰化。HDAC-IN-37 阻碍细胞由 G1 期向 S 期转变,诱导早期细胞凋亡。 | |||
T6637 | HDAC | ||
Resminostat (4SC-201) 是一种可口服的HDAC1、HDAC3和HDAC6抑制剂,IC50值分别为 42.5、50.1和71.8 nM,具有潜在抗肿瘤活性。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPH-01474 | HDAC6 Protein, Human, Recombinant (His) | Human | E. coli | ||
HDAC6 Protein, Human, Recombinant (His) is expressed in E. coli.
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TMPH-02631 | PRKN Protein, Mouse, Recombinant (GST) | Mouse | E. coli | ||
Functions within a multiprotein E3 ubiquitin ligase complex, catalyzing the covalent attachment of ubiquitin moieties onto substrate proteins. Substrates include SYT11 and VDAC1. Other substrates are BCL2, CCNE1, GPR37, RHOT1/MIRO1, MFN1, MFN2, STUB1, SNCAIP, SEPTIN5, TOMM20, USP30, ZNF746, MIRO1 and AIMP2. Mediates monoubiquitination as well as 'Lys-6', 'Lys-11', 'Lys-48'-linked and 'Lys-63'-linked polyubiquitination of substrates depending on the context. Participates in the removal and/or detoxification of abnormally folded or damaged protein by mediating 'Lys-63'-linked polyubiquitination of misfolded proteins such as PARK7: 'Lys-63'-linked polyubiquitinated misfolded proteins are then recognized by HDAC6, leading to their recruitment to aggresomes, followed by degradation. Mediates 'Lys-63'-linked polyubiquitination of a 22 kDa O-linked glycosylated isoform of SNCAIP, possibly playing a role in Lewy-body formation. Mediates monoubiquitination of BCL2, thereby acting as a positive regulator of autophagy. Protects against mitochondrial dysfunction during cellular stress, by acting downstream of PINK1 to coordinate mitochondrial quality control mechanisms that remove and replace dysfunctional mitochondrial components. Depending on the severity of mitochondrial damage and/or dysfunction, activity ranges from preventing apoptosis and stimulating mitochondrial biogenesis to regulating mitochondrial dynamics and eliminating severely damaged mitochondria via mitophagy. Activation and recruitment onto the outer membrane of damaged/dysfunctional mitochondria (OMM) requires PINK1-mediated phosphorylation of both PRKN and ubiquitin. After mitochondrial damage, functions with PINK1 to mediate the decision between mitophagy or preventing apoptosis by inducing either the poly- or monoubiquitination of VDAC1, respectively; polyubiquitination of VDAC1 promotes mitophagy, while monoubiquitination of VDAC1 decreases mitochondrial calcium influx which ultimately inhibits apoptosis. When cellular stress results in irreversible mitochondrial damage, promotes the autophagic degradation of dysfunctional depolarized mitochondria (mitophagy) by promoting the ubiquitination of mitochondrial proteins such as TOMM20, RHOT1/MIRO1, MFN1 and USP30. Preferentially assembles 'Lys-6'-, 'Lys-11'- and 'Lys-63'-linked polyubiquitin chains, leading to mitophagy. The PINK1-PRKN pathway also promotes fission of damaged mitochondria by PINK1-mediated phosphorylation which promotes the PRKN-dependent degradation of mitochondrial proteins involved in fission such as MFN2. This prevents the refusion of unhealthy mitochondria with the mitochondrial network or initiates mitochondrial fragmentation facilitating their later engulfment by autophagosomes. Regulates motility of damaged mitochondria via the ubiquitination and subsequent degradation of MIRO1 and MIRO2; in motor neurons, this likely inhibits mitochondrial intracellular anterograde transport along the axons which probably increases the chance of the mitochondria undergoing mitophagy in the soma. Involved in mitochondrial biogenesis via the 'Lys-48'-linked polyubiquitination of transcriptional repressor ZNF746/PARIS which leads to its subsequent proteasomal degradation and allows activation of the transcription factor PPARGC1A. Limits the production of reactive oxygen species (ROS). Regulates cyclin-E during neuronal apoptosis. In collaboration with CHPF isoform 2, may enhance cell viability and protect cells from oxidative stress. Independently of its ubiquitin ligase activity, protects from apoptosis by the transcriptional repression of p53/TP53. May protect neurons against alpha synuclein toxicity, proteasomal dysfunction, GPR37 accumulation, and kainate-induced excitotoxicity. May play a role in controlling neurotransmitter trafficking at the presynaptic terminal and in calcium-dependent exocytosis. May represent a tumor suppressor gene.
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TMPH-01263 | PRKN Protein, Human, Recombinant (His & SUMO) | Human | E. coli | ||
Functions within a multiprotein E3 ubiquitin ligase complex, catalyzing the covalent attachment of ubiquitin moieties onto substrate proteins. Substrates include SYT11 and VDAC1. Other substrates are BCL2, CCNE1, GPR37, RHOT1/MIRO1, MFN1, MFN2, STUB1, SNCAIP, SEPTIN5, TOMM20, USP30, ZNF746, MIRO1 and AIMP2. Mediates monoubiquitination as well as 'Lys-6', 'Lys-11', 'Lys-48'-linked and 'Lys-63'-linked polyubiquitination of substrates depending on the context. Participates in the removal and/or detoxification of abnormally folded or damaged protein by mediating 'Lys-63'-linked polyubiquitination of misfolded proteins such as PARK7: 'Lys-63'-linked polyubiquitinated misfolded proteins are then recognized by HDAC6, leading to their recruitment to aggresomes, followed by degradation. Mediates 'Lys-63'-linked polyubiquitination of a 22 kDa O-linked glycosylated isoform of SNCAIP, possibly playing a role in Lewy-body formation. Mediates monoubiquitination of BCL2, thereby acting as a positive regulator of autophagy. Protects against mitochondrial dysfunction during cellular stress, by acting downstream of PINK1 to coordinate mitochondrial quality control mechanisms that remove and replace dysfunctional mitochondrial components. Depending on the severity of mitochondrial damage and/or dysfunction, activity ranges from preventing apoptosis and stimulating mitochondrial biogenesis to regulating mitochondrial dynamics and eliminating severely damaged mitochondria via mitophagy. Activation and recruitment onto the outer membrane of damaged/dysfunctional mitochondria (OMM) requires PINK1-mediated phosphorylation of both PRKN and ubiquitin. After mitochondrial damage, functions with PINK1 to mediate the decision between mitophagy or preventing apoptosis by inducing either the poly- or monoubiquitination of VDAC1, respectively; polyubiquitination of VDAC1 promotes mitophagy, while monoubiquitination of VDAC1 decreases mitochondrial calcium influx which ultimately inhibits apoptosis. When cellular stress results in irreversible mitochondrial damage, promotes the autophagic degradation of dysfunctional depolarized mitochondria (mitophagy) by promoting the ubiquitination of mitochondrial proteins such as TOMM20, RHOT1/MIRO1, MFN1 and USP30. Preferentially assembles 'Lys-6'-, 'Lys-11'- and 'Lys-63'-linked polyubiquitin chains, leading to mitophagy. The PINK1-PRKN pathway also promotes fission of damaged mitochondria by PINK1-mediated phosphorylation which promotes the PRKN-dependent degradation of mitochondrial proteins involved in fission such as MFN2. This prevents the refusion of unhealthy mitochondria with the mitochondrial network or initiates mitochondrial fragmentation facilitating their later engulfment by autophagosomes. Regulates motility of damaged mitochondria via the ubiquitination and subsequent degradation of MIRO1 and MIRO2; in motor neurons, this likely inhibits mitochondrial intracellular anterograde transport along the axons which probably increases the chance of the mitochondria undergoing mitophagy in the soma. Involved in mitochondrial biogenesis via the 'Lys-48'-linked polyubiquitination of transcriptional repressor ZNF746/PARIS which leads to its subsequent proteasomal degradation and allows activation of the transcription factor PPARGC1A. Limits the production of reactive oxygen species (ROS). Regulates cyclin-E during neuronal apoptosis. In collaboration with CHPF isoform 2, may enhance cell viability and protect cells from oxidative stress. Independently of its ubiquitin ligase activity, protects from apoptosis by the transcriptional repression of p53/TP53. May protect neurons against alpha synuclein toxicity, proteasomal dysfunction, GPR37 accumulation, and kainate-induced excitotoxicity. May play a role in controlling neurotransmitter trafficking at the presynaptic terminal and in calcium-dependent exocytosis. May represent a tumor suppressor gene.
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