PKC412说明

PKC412 是一种蛋白激酶C (PKC) 的抑制剂，同时可抑制 PKC 亚型 (α，β，γ)，PDFRβ，VEGFR2，Syk，PKCη，Flk-1，Flt3，Cdk1/B，PKA，c-Kit，c-Fgr，c-Src，VEGFR1 和 EGFR。
CNDAC产品描述：CNDAC is a major metabolite of oral drug sapacitabine, and a nucleoside analog. In Vitro: CNDAC-induced SSBs can be repaired by the transcription-coupled nucleotide excision repair pathway, wheras lethal DSBs are mainly repaired through homologous recombination. Deficiency in two Rad51 paralogs, Rad51D and XRCC3, greatly sensitize cells to CNDAC. The Rad51D-null cell line is approximately 50-fold more sensitive to CNDAC (IC₅₀=0.006 μM) compared to 51D1.3, the Rad51D-repleted line (IC₅₀=0.32 μM)^[1]. CNDAC shows inhibitory activity against HL-60 and THP-1 cells with IC₅₀s of 1.58 μM and 0.84 μM. CNDAC (10?μM) results in a significant dro in cell survival compared to the untreated on days 4, 7, and 14. CNDAC is more effective at reducing viability and inducing apoptosis than ara-C at equivalent concentrations in the THP-1 cell line, which is defined as displaying resistance to ara-C^[2]. CNDAC induces DSBs, which are


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Purity:98%
MWt:570.6371
Formula:C35H30N4O4
SMILES:O=C(C1=CC=CC=C1)N(C)[C@H]2[C@@H](OC)[C@@]3(C)N(C4=C5C=CC=C4)C6=C5C7=C(C(NC7)=O)C8=C6N(C9=CC=CC=C98)[C@@](O3)([H])C2
Pathway:Epigenetics; TGF-beta/Smad;
Mechanisms:PKC;
Research Area:Cancer
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