CT1-3 是一种有效的抗癌剂。CT1-3 通过调控JNK/BCL-2/Bax/XIAP通路诱导线粒体介导的细胞凋亡 (Apoptosis)。CT1-3 通过调控 E-cadHERin/Snail 轴抑制人癌细胞 (HCCs) 的上皮间充质转化 (EMT) 电位，从而抑制肿瘤发生。CT1-3 在小鼠模型中表现出抗肿瘤作用，且无明显的肝、肾毒性。

CT1-3 is a potent anticancer agent. CT1-3 induces mitochondria-mediated apoptosis by regulating JNK/Bcl-2/Bax/XIAP pathway. CT1-3 suppresses the epithelial mesenchymal transition (EMT) potential of human cancer cells (HCCs) via regulating the E-cadherin/Snail axis, thus inhibits tumorigenesis. CT1-3 has a strong antitumor effect in mice model and exhibits no significant hepatic and renal toxicity [1].

CT1-3 has excellent inhibitory activity against multiple cancer cells with IC 50 range of 5.10~14.06 μM in LOVO, A549, HepG2, MDA-MB-231 and HONE1, et al [1]. CT1-3 (10 μM; 24 h) notably increases ROS production in HCCs, significantly decreases mitochondrial membrane potential, and reduces Bcl-2 and XIAP levels and increases phospho-JNK and Bax levels [1]. CT1-3 (7.5 μM; 24 h) reduces the capacity of migration and invasion of HCCs, significantly promotes the expression level of E-cadherin (E-cad), and markedly decreases the pro-metastatic and pro-invasive protein Snail [1]. Western Blot Analysis [1] Cell Line: A549, H460 and LOVO Concentration: 10 μM Incubation Time: 24 h Result: Notably increased ROS production, significantly decreased mitochondrial membrane potential, and reduced Bcl-2 and XIAP levels and increased phospho-JNK and Bax levels.

CT1-3 (20 mg/kg; IP, for 28 days) significantly suppresses tumor growth and exhibits no hepatic and renal toxicity in MDA-MB-231 xenografts model [1]. Animal Model: Male BALB/c-nu/nu mice (injected with A549, OVCAR3 and MDA-MB-231) [1] Dosage: 20 mg/kg Administration: IP, for 28 days Result: Significantly suppresses tumor growth and exhibited no hepatic and renal toxicity.

2460738-32-1

C25H29NO3S2

455.63

(< 1 mg/ml refers to the product slightly soluble or insoluble )
Powder: -20°C for 3 years
In solvent: -80°C for 2 years