polycyclic

Chrysene is a high molecular weight (HMW), polycyclic aromatic hydrocarbon (PAH).

Acenaphthylene is environmental polycyclic aromatic hydrocarbon (PAH)pollutants

1-Hydroxypyrene (1-Pyrenol), a biomarker of exposure to polycyclic aromatic hydrocarbons, is analyzed in urine samples.

Baccatin III (Baccatin Ⅲ) is a polycyclic diterpene which can be used for the semi-synthesis of paclitaxel and analogs. It has immunomodulatory and anticancer chemotherapeutic activities.

Rhapontigenin (Protigenin) is a mechanism-based, selective inactivator of cytochrome P450 1A1 (IC50: 400 nM), an aryl hydrocarbon hydroxylase which activates polycyclic aromatic hydrocarbons that act as procarcinogens. Rhapontigenin is a natural analog of resveratrol with antioxidant and anti-cancer activity. At higher concentrations, rhapontigenin inhibits the proliferation of HL-60R and HepG2 cancer cell lines (IC50: 48 μM).

LeDSF3 is a regulator of the biosynthesis of the antifungal polycyclic tetramate macrolactam HSAF in Lysobacter enzymogenes and anti-tumor agent. LeDSF3 down-regulates p-AKT and activates caspase-3.

Beta-Carboline-1-propanoic acid is a reference standard compound, it is also a synthetic precursor compound. It is a derivative of indole and has been used in the synthesis of other indole derivatives such as indole-3-carboxaldehyde and as a starting material for the synthesis of polycyclic aromatic compounds. It has also been used to study the conformational relationships of indole-containing compounds and has been used as a model compound to study indole reactivity.

K 41 is a polycyclic polyether antibiotic from Streptomyces hygroscopicus.

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).

7-epi-Isogarcinol, a polycyclic polyprenylated acylphloroglucinol (PPAP), exhibits moderate antiproliferative activity by blocking the STAT3 signaling pathway, thereby inducing apoptosis and inhibiting cell migration [1].

Concanamycin A (Folimycin), a polycyclic lactone antibiotic, is a selective inhibitor of vacuolar H+-ATPase (V-ATPase) and lysosomal acidification, and can be used to study inflammation.Concanamycin A enhances the immune clearance of infected progenitor cells by cytotoxic T lymphocytes, and inhibits Nef et al. from different branches of HIV and simian immunodeficiency virus. Concanamycin A enhances immune clearance of cytotoxic T lymphocytes from infected progenitor cells, inhibits the Nef allele from different branches of HIV and simian immunodeficiency virus, and can be used to study HIV infection.