CT1-3

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].

Signaling Pathways >> Apoptosis >> Bcl-2 Family

Signaling Pathways >> Apoptosis >> Apoptosis

Research Areas >> Cancer

Signaling Pathways >> MAPK/ERK Pathway >> JNK

CT1-3 has excellent inhibitory activity against multiple cancer cells with IC50 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.

[1]. Tao C, et al. CT1-3, a novel magnolol-sulforaphane hybrid suppresses tumorigenesis through inducing mitochondria-mediated apoptosis and inhibiting epithelial mesenchymal transition. Eur J Med Chem. 2020 Aug 1;199:112441.