foreskin

T0901317 是一种口服有效且高度选择性的LXR 激动剂，对 LXRα 的EC50为 20 nM。它激活FXR，EC50为 5 μM。它是RORα和RORγ双重反向激动剂，Ki 值分别为 132 nM 和 51 nM。它诱导细胞凋亡，并抑制低密度脂蛋白受体缺失小鼠动脉粥样硬化的发展。

FIN56 是一种铁死亡特异性诱导剂，能结合并激活角鲨烯合酶，可通过诱导 GPX4 降解来诱导铁死亡。

1,4-DPCA 是一种脯氨酰羟化酶抑制剂，对人源包皮成纤维细胞中胶原羟基化的 IC50 为 2.4 μM，对因子抑制 HIF (FIH) 的 IC50 为 60 μM。

S-Acetyl-L-glutathione is a derivative of glutathione .1 It increases intracellular GSH levels in primary fibroblasts derived from patients with glutathione synthetase deficiency when used at a concentration of 50 μM. S-Acetyl-L-glutathione (5 mM) induces apoptosis in Daudi, Raji, and Jurkat lymphoma cells.2 It inhibits the replication of herpes simplex virus 1 (HSV-1) in human foreskin fibroblasts when used at concentrations of 5 and 10 mM.3 S-Acetyl-L-glutathione (6.25 μg/g per day) increases survival in a mouse model of HSV-1 infection.

Burnettramic acid A is a fungal metabolite originally isolated fromA. burnettiithat has diverse biological activities.1It is active againstB. subtilis,S. aureus,C. albicans, andS. cerevisiae(IC50s = 2.3, 5.9, 0.5, and 0.2 μg/ml, respectively). Burnettramic acid A is cytotoxic to NS-1 murine myeloma cells but not neonatal foreskin fibroblasts (IC50s = 13.8 and >100 μg/ml, respectively). 1.Li, H., Gilchrist, C.L.M., Lacey, H.J., et al.Discovery and heterologous biosynthesis of the burnettramic acids: Rare PKS-NRPS-derived bolaamphiphilic pyrrolizidinediones from an Australian fungus, Aspergillus burnettiiOrg. Lett.21(5)1287-1291(2019)

Burnettramic acid A aglycone is a fungal metabolite and an aglycone form of burnettramic acid A originally isolated fromA. burnettiithat has anticancer activity.1It is cytotoxic to NS-1 murine myeloma cells but not neonatal foreskin fibroblasts (IC50s = 8.4 and >100 μg/ml, respectively). 1.Li, H., Gilchrist, C.L.M., Lacey, H.J., et al.Discovery and heterologous biosynthesis of the burnettramic acids: Rare PKS-NRPS-derived bolaamphiphilic pyrrolizidinediones from an Australian fungus, Aspergillus burnettiiOrg. Lett.21(5)1287-1291(2019)

Nemorosone is a polycyclic polyprenylated acylphloroglucinol (PPAP) originally isolated from C. rosea that has antiproliferative properties.1 Nemorosone inhibits growth of NB69, Kelly, SK-N-AS, and LAN-1 neuroblastoma cells (IC50s = 3.1-6.3 μM), including several drug-resistant clones, but not MRC-5 human embryonic fibroblasts (IC50 = >40 μM).2 It increases DNA fragmentation in LAN-1 cells in a dose-dependent manner, and decreases N-Myc protein levels and phosphorylation of ERK1/2 by MEK1/2. Nemorosone also inhibits growth of Capan-1, AsPC-1, and MIA-PaCa-2 pancreatic cancer cells (IC50s = 4.5-5.0 μM following a 72-hour treatment) but not human dermal and foreskin fibroblasts (IC50s = >35 μM).1 It induces apoptosis, abolishes the mitochondrial membrane potential, and increases cytosolic calcium concentration in pancreatic cancer cells in a dose-dependent manner. Nemorosone activates the caspase cascade in a dose-dependent manner and inhibits cell cycle progression, increasing the proportion of cells in the G0/G1 phase, in both neuroblastoma and pancreatic cancer cells.1,2 Nemorosone (50 mg/kg, i.p., per day) also reduces tumor growth in an MIA-PaCa-2 mouse xenograft model.3References1. Holtrup, F., Bauer, A., Fellenberg, K., et al. Microarray analysis of nemorosone-induced cytotoxic effects on pancreatic cancer cells reveals activation of the unfolded protein response (UPR). Br. J. Pharmacol. 162(5), 1045-1059 (2011).2. Díaz-Carballo, D., Malak, S., Bardenheuer, W., et al. Cytotoxic activity of nemorosone in neuroblastoma cells. J. Cell. Mol. Med. 12(6B), 2598-2608 (2008).3. Wold, R.J., Hilger, R.A., Hoheisel, J.D., et al. In vivo activity and pharmacokinetics of nemorosone on pancreatic cancer xenografts. PLoS One 8(9), e74555 (2013). Nemorosone is a polycyclic polyprenylated acylphloroglucinol (PPAP) originally isolated from C. rosea that has antiproliferative properties.1 Nemorosone inhibits growth of NB69, Kelly, SK-N-AS, and LAN-1 neuroblastoma cells (IC50s = 3.1-6.3 μM), including several drug-resistant clones, but not MRC-5 human embryonic fibroblasts (IC50 = >40 μM).2 It increases DNA fragmentation in LAN-1 cells in a dose-dependent manner, and decreases N-Myc protein levels and phosphorylation of ERK1/2 by MEK1/2. Nemorosone also inhibits growth of Capan-1, AsPC-1, and MIA-PaCa-2 pancreatic cancer cells (IC50s = 4.5-5.0 μM following a 72-hour treatment) but not human dermal and foreskin fibroblasts (IC50s = >35 μM).1 It induces apoptosis, abolishes the mitochondrial membrane potential, and increases cytosolic calcium concentration in pancreatic cancer cells in a dose-dependent manner. Nemorosone activates the caspase cascade in a dose-dependent manner and inhibits cell cycle progression, increasing the proportion of cells in the G0/G1 phase, in both neuroblastoma and pancreatic cancer cells.1,2 Nemorosone (50 mg/kg, i.p., per day) also reduces tumor growth in an MIA-PaCa-2 mouse xenograft model.3 References1. Holtrup, F., Bauer, A., Fellenberg, K., et al. Microarray analysis of nemorosone-induced cytotoxic effects on pancreatic cancer cells reveals activation of the unfolded protein response (UPR). Br. J. Pharmacol. 162(5), 1045-1059 (2011).2. Díaz-Carballo, D., Malak, S., Bardenheuer, W., et al. Cytotoxic activity of nemorosone in neuroblastoma cells. J. Cell. Mol. Med. 12(6B), 2598-2608 (2008).3. Wold, R.J., Hilger, R.A., Hoheisel, J.D., et al. In vivo activity and pharmacokinetics of nemorosone on pancreatic cancer xenografts. PLoS One 8(9), e74555 (2013).

L-K6L9 是由 L-亮氨酸和 L-赖氨酸的L-异构体组成的溶细胞肽。对LNCaP-CL1 雄激素独立型和22Rv1以及LNCaP雄激素依赖型人类前列腺癌细胞具有细胞毒性（LC50分别为4、4和6 µM），同时也对非癌性NIH3T3小鼠成纤维细胞和OL人类包皮成纤维细胞具有细胞毒性（LC50分别为7和5 µM）。在100 µM的浓度下，引起分离的人类红细胞溶血。

U-51605, a stable analog of the endoperoxide prostaglandin H2 (PGH2), functions as an inhibitor with greater selectivity towards prostacyclin (PGI) synthase over thromboxane (TX) synthase. It also acts as a partial agonist at TP receptors. Studies show that at a concentration of 2.8 µM, U-51605 effectively inhibits PGI synthase in human foreskin fibroblasts, while a concentration of 5.6 µM is required to inhibit human platelet TX synthase. Furthermore, U-51605, at up to 1 µM, decreases the release of prostacyclin in SHR aorta triggered by the calcium ionophore A-23187 without impacting TXA2 production, and notably enhances the release of PGE2 and PGF2α.