目录号 | 产品详情 | 靶点 | |
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T5699 | Apoptosis Microtubule Associated | ||
SSE15206 是一种克服多药耐药性的微管聚合抑制剂,其在 HCT116 细胞中的 GI50值为 197 nM。由于癌细胞中纺锤体形成不完整,导致 G2/M 停滞,有丝分裂异常。 | |||
T6S0735 | Apoptosis Others | ||
Flavokawain B (Flavokavain B) 是从卡瓦醉椒的根提取物中,分离出的查尔酮。它是一种凋亡诱导剂,可抑制各种癌细胞株生长。它以极低的无毒浓度抑制人脑内皮细胞的迁移和血管形成,具有抗血管生成活性。 | |||
T13436 | Nrf2 | ||
(E)-[6]-Dehydroparadol ((6)-Dehydroparadol) 是 [6]-Shogaol 的氧化代谢产物,是有效的 Nrf2 活化剂。 | |||
T9575 | Histone Methyltransferase | ||
MRTX-9768 是一种有效的、选择性的、具有口服活性的 PRMT5-MTA 复合体抑制剂,可选择性靶向 MTAP/CDKN2A 缺失的肿瘤。 | |||
T9557 | Wnt/beta-catenin | ||
TNIK-IN-2 是有效的TNIK 抑制剂,IC50为 1.3337 μM。 | |||
T22632 | APC | ||
TASIN-1 是截短的APC 基因(结肠腺瘤样息肉基因)选择性抑制剂,可以抑制胆固醇生物合成并发挥细胞毒性作用。它是一种预防和干预APC 突变型结直肠癌的潜在治疗策略。 | |||
T71891 | |||
G-573 is an allosteric inhibitor of MEK that is both potent and selective. The IC(50) value for pERK inhibition in HCT116 tumours by G-573 was estimated to be 0.406 µM. The IC(50) values for tumour growth inhibition in HCT116 and H2122 were estimated to be 3.43 and 2.56 µM, respectively. ED(50) estimates in HCT116 and H2122 mouse xenograft models were estimated to be ~4.6 and 1.9 mg/kg/day, respectively. | |||
T83079 | |||
Anticanceragent 172 (8d) 具有显著的抗癌活性,在 HCT116 细胞中表现出 6.96 μM 的 IC50 值。 | |||
T37010 | |||
D-threo Sphinganine (d18:0) is a synthetic bioactive sphingolipid and stereoisomer of sphinganine (d18:0) and L-erythro sphinganine (d18:0) . It induces autophagy in HCT116 cells when used at a concentration of 12 μM. D-threo Sphinganine (d18:0) is metabolized via sphinganine N-acyltransferase and sphinganine kinase in vivo in rat liver. | |||
T74455 | |||
JPS035 是一种基于苯甲酰胺的Von Hippel-Lindau (VHL)E3-连接酶蛋白水解靶向嵌合体 (PROTAC)。JPS035 降解 I 类组蛋白脱乙酰酶 (HDAC)。JPS035 是一种有效的 HDAC1/2 降解剂,与 HCT116 细胞中更大的总差异表达基因和增强的细胞凋亡 (apoptosis) 相关。 |
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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