Recilisib, also known as ON 01210.Na, is a radioprotectant, which modifys cell cycle distribution patterns in cancer cells subjected to radiation therapy, and it has been identified as a potential candidate for radiation protection studies. It appears tha
MitoEbselen-2 is a radiation mitigator which reduces lipid hydroperoxides and prevents apoptotic cell death. When administered 24 hours postirradiation, MitoEbselen-2 was shown to increase the survival of mice exposed to whole body γ-irradiation.
Motexafin gadolinium, also known as PCI 0120, is a synthetic metallotexaphyrin with radiosensitizing and chemosensitizing properties. Motexafin gadolinium accumulates in tumor cells preferentially due to their increased rates of metabolism, generating rea
FSL-1 TFA, a bacterial-derived toll-like receptor 2 6 (TLR2 6) agonist, enhances resistance to experimental HSV-2 infection[1]. FSL-1 TFA induces MMP-9 production through TLR2 and NF-κB AP-1 signaling pathways in monocytic THP-1 cells[2]. FSL-1 significantly reduces HSV-2 replication in human vaginal epithelial cells (EC)[1].FSL-1 induces significant resistance to experimental genital HSV-2 infection through elaboration of a specific cytokine response profile[1].FSL-1 (50 ng mL, 24 hours) induces MMP-9 expression at both mRNA and protein levels in human monocytic THP-1 cells[2].FSL-1 activates the MAP kinase NF-κB signaling pathway[2]. Cell Viability Assay[1] Cell Line: V11I, V12I or V19I immortalized human vaginal EC FSL-1 application significantly protectes against genital HSV-2 challenge in mice[1]. Animal Model: Female Swiss-Webster mice (weighing 20-25 g)[1] [1]. William A Rose 2nd, et al. FSL-1, a bacterial-derived toll-like receptor 2 6 agonist, enhances resistance to experimental HSV-2 infection. Virol J. 2009 Nov 10;6:195. [2]. Cathryn J Kurkjian,et al. The Toll-Like Receptor 2 6 Agonist, FSL-1 Lipopeptide, Therapeutically Mitigates Acute Radiation Syndrome. Sci Rep. 2017 Dec 11;7(1):17355.
CAY10721 is an inhibitor of sirtuin 3 (SIRT3), a class III HDAC (39% SIRT3 inhibition at 200 μM). Upregulation of SIRT3 transcription is associated with oral squamous cell carcinoma (OSCC) and breast cancer with lymph node involvement, while SIRT3 down-regulation inhibits the growth of OSCC cells and sensitizes them to radiation and chemotherapy.
Denibulin (MN-029) is a novel vascular-disrupting agent that reversibly inhibits microtubule assembly, resulting in disruption of the cytoskeleton of tumor vascular endothelial cells. The results of preclinical study demonstrated that MN-029 could cause rapid vascular shutdown in solid tumors, dose-dependent secondary tumor cell killing, and effective enhancement of the antitumor effects of radiation and cisplatin chemotherapy.
SU-11752 is a potent and selective DNA-PK inhibitor. Inhibition kinetics and a direct assay for ATP binding showed that SU11752 inhibited DNA-PK by competing with ATP. SU11752 inhibited DNA double-strand break repair in cells and gave rise to a five-fold sensitization to ionizing radiation. At concentrations of SU11752 that inhibited DNA repair, cell cycle progression was still normal and ATM kinase activity was not inhibited.
NU1085 is a potent poly(ADP-ribose) polymerase (PARP) inhibitors have been developed that potentiate the cytotoxicity of ionizing radiation and anticancer drugs. The biological effects of NU1085 [Ki = 6 nM], in combination with temozolomide (TM) or topotecan (TP) have been studied in 12 human tumor cell lines (lung, colon, ovary, and breast cancer). Cells were treated with increasing concentrations of TM or TP + - NU1085 (10 microM) for 72 h.
PD-128763 is a selective inhibitor of poly(ADP-ribose) polymerase. PD-128763 has an IC50 value against the purified enzyme approximately 50X lower than 3-aminobenzamide (3-AB), a widely used specific inhibitor of the enzyme. Exposure of exponentially growing cells to a noncytotoxic concentration (0.5 mM) of PD 128763 for 2 h immediately following X irradiation increased their radiation sensitivity, modifying both the shoulder and the slope of the survival curve. When recovery from sublethal damage and potentially lethal damage was examined in exponential and plateau-phase cells, respectively, postirradiation incubation with 0.5 mM PD 128763 was found not only to inhibit both these processes fully, but also to enhance further the level of radiation-induced cell killing. This is in contrast to the slight effect seen with the less potent inhibitor, 3-AB. The results presented suggest that the mechanism of radiosensitization by PD 128763 is related to the potent inhibition of pol......