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].

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].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

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].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

455.63

C₂₅H₂₉NO₃S₂

2460738-32-1

OC1=CC=C(CC=C)C=C1C2=CC(CC=C)=CC=C2OCCS(CCCCN=C=S)=O

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• [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.  [Content Brief]