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Bioactive Products
Antileukaemic Compound Library
A unique collection of 35 Antileukaemic natural compound library for Antileukaemic screening
Catalog No: B29 Antileukaemic Compound Library
Screening Details
Size: 1mg/well * 35 Compounds
2mg/well * 35 Compounds
Cat. No. Information
CFN98579 Bakkenolide A

Bakkenolide A has antifeedant and growth inhibitory effects on neonate variegated cutworms, it inhibits leukemia by regulation of HDAC3 and PI3K/Akt-related signaling pathways.
CFN90007 5-Aza-2'-deoxycytidine

1. Decitabine (5-Aza-2'-deoxycytidine) is a DNA methyltransferase inhibitor and an archetypal epigenetic drug for the therapy of myeloid leukemias.
2. Aza-2'-deoxycitidine exerts its anti-tumor effects in hepatocellular carcinoma(HCC) cells by inhibiting the telomerase activity.
CFN90010 Canertinib

Canertinib is a pan-ErbB inhibitor for EGFR and ErbB2 with IC50 of 1.5 nM and 9.0 nM, no activity to PDGFR, FGFR, InsR, PKC, or CDK1/2/4. Canertinib displays anti-proliferative and pro-apoptotic effects in human myeloid leukemia cells devoid of ErbB-receptors, downregulates important signaling pathways and activates caspase-mediated intrinsic apoptosis pathway in human T-cell leukemia cells.
CFN90026 Retinoic acid

Retinoic acid is a metabolite of vitamin A that plays important roles in cell growth, differentiation, and organogenesis. Retinoic acid is a natural agonist of RAR nuclear receptors, with IC50s of 14 nM for RARα/β/γ. Retinoic acid bind to PPARβ/δ with Kd of 17 nM. It also helps repair Smad3/TGF-β1-induced lung damage in hyperoxic mice.
CFN98727 Berbamine

Berbamine is a novel inhibitor of bcr/abl fusion gene with potent anti-leukemia activity and also an inhibitor of NF-κB. Berbamine may be the first ATP-competitive inhibitor of CaMKII γ, could be as a new type of molecular targeted agent through inhibition of the CaMKII γ activity for treatment of leukemia.Berbamine confers cardioprotection against I/R injury by attenuating [Ca(2+)inf(i) overloading and preventing calpain activation through the activation of the PI3K-Akt-GSK3β pathway and, subsequently, opening of the mitoK(ATP) channel.