目录号 | 产品详情 | 靶点 | |
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T8800 | DNA/RNA Synthesis | ||
NSAH (2-hydroxy-N'-[(E)-(2-hydroxynaphthalen-1-yl)methylidene]benzohydrazide) 是一种可逆竞争性非核苷类的核苷酸还原酶抑制剂,无细胞 IC50 为 32 μM,基于细胞的 IC50 约为 250 nM。 | |||
T16961 | Apoptosis DNA/RNA Synthesis | ||
Supinoxin (RX-5902) 是磷酸化 p68 RNA 解旋酶的强效口服活性抑制剂,是一种抗肿瘤试剂。它与 Y593 磷酸化的 p68 相互作用并减弱 β-catenin 的核穿梭性。它诱导细胞凋亡并抑制 TNBC 癌细胞系的生长,IC50的范围为 10 nM 至 20 nM。 | |||
T2763 | Others HIF/HIF Prolyl-Hydroxylase | ||
Panaxadiol (20(R)-Panaxadiol) 是从人参根中获得,具有神经保护和抗肿瘤作用,能够抑制程序性细胞死亡配体-1(PD-L1)的表达和肿瘤增殖。 | |||
T1290 | Others Antibiotic Antifection Antifungal | ||
Oxiconazole nitrate (Ro 13-8996) 是广谱抗真菌药物,抑制T. tonsurans 和T.rubrum 的生长,MIC90值分别为 0.25 和 0.5 μg/mL。 | |||
T2617 | Aurora Kinase | ||
SNS-314 Mesylate (SNS-314) 是一种有效且特异性的极光激酶抑制剂,对极光激酶 A、B、C 的 IC50值分别为 9,31 和 3 nM。 | |||
T15396 | HIF | ||
GN44028 (N-(2,3-Dihydro-1,4-benzodioxin-6-yl)-1,4-dihydroindeno[1,2-c]pyrazol-3-amine) 是缺氧诱导因子(HIF)-1的有效抑制剂,其 IC50=14 nM。它可以抑制低氧诱导的 HIF-1α 的转录特性,但不抑制 HIF-1α mRNA 的表达,HIF-1α 蛋白的累积或HIF-1α/HIF-1β 的异缘二聚化。 | |||
T0132 | Apoptosis Mitophagy Topoisomerase Antibacterial Antibiotic Autophagy | ||
Etoposide (VP-16-213) 是一种拓扑异构酶 II 的抑制剂,通过与拓扑异构酶 II 和 DNA 形成复合物来抑制 DNA 合成 (IC50=60.3 μM)。Etoposide 具有抗肿瘤活性,可以诱导细胞凋亡、自噬。 | |||
T6583 | Cysteine Protease Proteasome | ||
MG-101 (Calpain inhibitor I) 是一种有效的半胱氨酸蛋白酶抑制剂,能够抑制钙蛋白酶I (Ki:190 pM),钙蛋白酶II (Ki:220 pM),组织蛋白酶B (Ki:150 pM)和组织蛋白酶L (Ki:500 pM)。 | |||
T9078 | CDK | ||
LY3405105 (1-Piperidinecarboxylic acid, 4-[[5-methyl-3-(1-methylethyl)pyrazolo[1,5-a]pyrimidin-7-yl]amino]-, 1-[(2E)-4-(dimethylamino)-1-oxo-2-buten-1-yl]-3-pyrrolidinyl ester) 是一种新型 CDK7 抑制剂。 | |||
T6442 | HSP | ||
CH5138303 是一种可口服的 Hsp90 抑制剂,Kd 为 0.48 nM。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPY-04023 | BCCIP Protein, Human, Recombinant (His & GST) | Human | Baculovirus-Insect Cells | ||
BCCIP was originally identified as a BRCA2 and CDKN1A interacting protein that has been implicated in maintenance of genomic stability, cell cycle regulation, and microtubule dynamics. The secondary genetic alternations may overcome the progression suppression imposed by BCCIP deficiency through a synthetic viability mechanism. Knockdown of YY1 inhibited the binding of BCCIP itself at BCCIP promoter region proximal to TSS, demonstrating that transcriptional regulation of the YY1 on BCCIP can be modulated by BCCIP itself in a YY1-dependent fashion. BCCIP (BRCA2 and CDKN1A interacting protein) plays a critical role in maintaining the critical functions of p53 in tumor suppression and response to therapy. Celecoxib affects the functions of p53 and inhibits the recovery from the irradiation-induced injury by up-regulating the expression of BCCIP, and subsequently regulates the expressions of genes such as p21 and Cyclin B1 to enhance the radiosensitivity of HCT116 cells in a COX-2 independent manner.
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TMPY-00578 | BCCIP Protein, Human, Recombinant | Human | Baculovirus-Insect Cells | ||
BCCIP was originally identified as a BRCA2 and CDKN1A interacting protein that has been implicated in maintenance of genomic stability, cell cycle regulation, and microtubule dynamics. The secondary genetic alternations may overcome the progression suppression imposed by BCCIP deficiency through a synthetic viability mechanism. Knockdown of YY1 inhibited the binding of BCCIP itself at BCCIP promoter region proximal to TSS, demonstrating that transcriptional regulation of the YY1 on BCCIP can be modulated by BCCIP itself in a YY1-dependent fashion. BCCIP (BRCA2 and CDKN1A interacting protein) plays a critical role in maintaining the critical functions of p53 in tumor suppression and response to therapy. Celecoxib affects the functions of p53 and inhibits the recovery from the irradiation-induced injury by up-regulating the expression of BCCIP, and subsequently regulates the expressions of genes such as p21 and Cyclin B1 to enhance the radiosensitivity of HCT116 cells in a COX-2 independent manner.
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