For research use only.
CAS No. 300802-28-2
CA3 (CIL56) has potent inhibitory effects on YAP1/Tead transcriptional activity and primarily targets YAP1 high and therapy-resistant esophageal adenocarcinoma cells endowed with CSC properties. CA3(CIL56) induces ferroptosis and iron-dependent reactive oxygen species (ROS).
Selleck's CA3 (CIL56) has been cited by 10 publications
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|Description||CA3 (CIL56) has potent inhibitory effects on YAP1/Tead transcriptional activity and primarily targets YAP1 high and therapy-resistant esophageal adenocarcinoma cells endowed with CSC properties. CA3(CIL56) induces ferroptosis and iron-dependent reactive oxygen species (ROS).|
CA3 strongly inhibits esophageal adenocarcinoma cell growth in vitro. CA3 can effectively suppress tumor cell proliferation, induce apoptosis, reduce tumor sphere formation, and the population of ALDH1+ cells. CA3 specially inhibits Tead/YAP1 transcriptional activity but shows no inhibitory activity on other transcriptional factors-Super-TOP/Wnt, CBF1/Notch, and AP-1 after cotransfection of their respective individual promoter luciferases in 293T cells. CA3 preferentially inhibits CSC properties enriched in radiation-resistant esophageal adenocarcinoma cells.
|In vivo||CA3 exerts strong antitumor activity in xenograft model with no apparent toxicity.|
|In vitro||DMSO||97 mg/mL (198.11 mM)|
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Clinical Trial Information
|NCT Number||Recruitment||interventions||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT04643327||Recruiting||Drug: Levetiracetam|Drug: Placebo||Parkinson Disease|Mild Cognitive Impairment|Memory Impairment||The University of Queensland|Queensland University of Technology|Johns Hopkins University|Cleveland Clinic Lou Ruvo Center for Brain Health|Royal Brisbane and Women''s Hospital||February 9 2021||Phase 2|
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