Casuarinin

Casuarinin (0.5-10 μM; 48 h) dose-dependently inhibits the proliferation of human breast adenocarcinoma MCF-7 cells with an IC₅₀ of 6.04 μM^[1].
Casuarinin (5-10 μM; 24 h) induces G0/G1 phase cell cycle arrest in human breast adenocarcinoma MCF-7 cells^[1].
Casuarinin (0.5-10 μM; 48 h) increases the percentage of apoptotic nuclei in human breast adenocarcinoma MCF-7 cells in a dose-independent manner^[1].
Casuarinin (5-10 μM; 6-48 h) time- and dose-dependently induces DNA fragmentation and apoptosis in human breast adenocarcinoma MCF-7 cells, with maximal effects observed at 48 h, while showing no effect on p53 protein expression at concentrations up to 10 μM within 48 h; it also time- and dose-dependently upregulates p21/WAF1, Fas/APO-1 receptor, mFasL and sFasL expression, with maximal induction detected at 24 h^[1].
Casuarinin (10 μM; 48 h) exerts antiproliferative and proapoptotic effects in human breast adenocarcinoma MCF-7 cells, and these effects are significantly attenuated by pre-incubation with 250 ng/mL ZB4 (to block the Fas/FasL system) or 10 μM Z-IETD-FMK (to inhibit caspase-8) for 1 h prior to treatment^[1].
Casuarinin (10 μM; 48 h, preceded by 1 h pre-incubation with 10 μM Z-IETD-FMK) has its antiproliferative and proapoptotic effects significantly reduced by blocking caspase-8 with Z-IETD-FMK in human breast adenocarcinoma MCF-7 cells after 48 h^[1].
Casuarinin (5-10 μM; 12-48 h) time- and dose-dependently activates caspase-8 in human breast adenocarcinoma MCF-7 cells^[1].
Casuarinin (5-20 μg/mL; 1 h pretreatment) dose-dependently inhibits TNF-α-induced ICAM-1 mRNA and protein expression in HaCaT human keratinocyte cells prior to TNF-α stimulation^[2].
Casuarinin (5-20 μg/mL) dose-dependently reduces TNF-α-induced THP-1 monocyte adhesion to HaCaT human keratinocyte cells^[2].
Casuarinin (5-20 μg/mL) blocks TNF-α-induced NF-κB activation in HaCaT human keratinocyte cells by inhibiting IκBα degradation, p65 phosphorylation and nuclear translocation, NF-κB DNA binding, and NF-κB promoter activity^[2].
Casuarinin (5-20 μg/mL) dose-dependently inhibits TNF-α-induced phosphorylation of ERK and p38 MAPK (but not JNK) in HaCaT human keratinocyte cells, and also suppresses TNF-α-induced mRNA and protein expression of IL-6, IL-1β, IL-8, and MCP-1 in a concentration-dependent manner in the same cell line^[2].
Casuarinin (24-48 h) exhibits antifungal activity against Candida albicans ATCC 64548, Candida albicans SC5314, Candida krusei ATCC 6258, Candida parapsilosis ATCC 22019, and Candida tropicalis ATCC 750, with the lowest MIC of 26 μg/mL against Candida krusei ATCC 6258^[4].
Casuarinin (72 h) potently inhibits HSV-2 growth in Vero cells with an IC₅₀ of 3.6 μM, has a CC₅₀ of 89 μM in Vero cells, and exhibits a selectivity index of 25 in the XTT assay^[5].
Casuarinin (1 h adsorption, 2 days total post-overlay) inhibits HSV-2 plaque formation in Vero cells with an IC₅₀ of 1.5 μM and exhibits a selectivity index of 59 in the plaque reduction assay^[5].
Casuarinin (0.5-50 μM; 6 h) exhibits potent virucidal activity against cell-free HSV-2 at 25 μM^[5].
Casuarinin (10 μM; added 0-12 h post-infection, total 24 h infection time) inhibits HSV-2 yield in Vero cells by at least 90% even when added up to 12 h post-infection, indicating activity against late events of HSV-2 infection^[5].
Casuarinin (3 h at 4°C, 48 h total post-overlay) inhibits HSV-2 attachment to Vero cells in a dose-dependent manner^[5].
Casuarinin (10 μM; added after 3 h attachment, evaluated 10-minute intervals post-warming) inhibits HSV-2 penetration into Vero cells by over 85% within 10 minutes of treatment^[5].

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