Mollugin is a JAK2 inhibitor and inhibits LPS-induced inflammatory responses by blocking the activation of the JAK-STAT pathway. Mollugin may be a novel therapeutic candidate for bone loss-associated disorders including osteoporosis, rheumatoid arthritis, and periodontitis. Mollugin has anticancer efficacy, can modulate the HER2, HO-1, Nrf2 , and NF- κB pathways.
Cinobufotalin is a main cardiac toxin in toad, it is a novel anti-HCC agent, it induces growth inhibition and apoptosis in cultured HCC cells through ceramide production. Cinobufotalin is also an effective reversal agent for the multidrug resistance of tumors, it can reverse the adriamycin-resistance in Raji/ADR cells and the expression of P-gp and MRP-1 proteins. Cinobufotalin can promote the dendritic cells(DCs) derived from peripheral blood of patients with chronic hepatitis B to mature and effectively enhance its(the DCs') capabilities, therefore the treatment of cinobufotalin may potentiate the antiviral immunity of the patients with chronic hepatitis B(CHB).
1. Mahanine has a dose- and time-dependent anti-proliferative activity in acute lymphoid (MOLT-3) and chronic myeloid (K562) leukemic cell lines.
2. Mahanine has effects on the activation of the apoptotic pathway in human leukemia U937 cells, causes the mitochondrial membranes to lose their permeability, resulting in caspase-3 activation and apoptosis.
3. Mahanine can reverse an epigenetically silenced gene, RASSF1A in prostate cancer cells by inhibiting DNMT activity that in turn down-regulates a key cell cycle regulator, cyclin D1, is an encouraging therapeutic choice for advanced prostatic cancer.
4. Mahanine inhibited growth of PC3 and LNCaP prostate cancer cells in a dose and time-dependent manner, inhibits growth and induces apoptosis in both androgen-responsive, LNCaP and androgen-independent, PC3 cells by targeting cell survival pathway.
1. (-)-Syringaresinol inhibits the proliferation of human promyelocytic HL-60 cells through G(1) arrest and induction of apoptosis, may be a potential chemotherapeutic agent for the treatment of cancer.
Ingenol-3-angelate shows anticancer activity, and P-gp-mediated absorptive transport, dermal penetration, and vascular damage contribute to the anticancer activity of ingenol-3-angelate in vivo; it activates a broad range of PKC isoforms and induces apoptosis in acute myeloid leukemia cells by activating the PKC isoform PKCdelta. Ingenol-3-angelate suppresses HIV infection of primary CD4+ T cells through down-modulation of cell surface expression of HIV co-receptors. Ingenol-3-angelate emerges as a unique local chemotherapeutic immunostimulatory debulking agent that could be used in conjunction with immunotherapies to promote regression of metastases.