f 35

Furagin (Furazidine) 是 nitrofurantoin 类似物，有抗菌活性，用于尿路感染。

AF-353 (Ro-4) 是一种选择性、可口服的 P2X3 P2X2 3 受体拮抗剂，抑制人和大鼠 P2X3 的 pIC50值为 8.0，抑制人 P2X2 3 的 pIC50值为 7.3。

GNF351 是芳烃受体 (AhR) 的完全拮抗剂，具有抑制 DRE 依赖性和非依赖性活性的能力。它与结合到 AhR 的光亲和性 AhR 配体竞争，IC50为 62 nM。它在小鼠或人角质形成细胞中的毒性极小。

Hydronidone (F-351) 是一种 pyridine 衍生物。Hydronidone 对肝纤维化具有潜在的治疗作用。

DMTr-4'-CF3-5-Me-U-CED phosphoramidite (DMTr-4'-CF3-5-Methyluridine-CED phosphoramidite) 为一种修饰寡脱氧核苷酸 (ODN)，作为用于寡核苷酸标记的染料试剂，在 RNA 研究领域有其应用价值。

This novel compound is an orally bioavailable antagonist of P2X3 P2X2 3 receptors, exhibiting potent activity with a pIC50 of 8 in both human and rat, and a pIC50 of 7.3 specifically for the human P2X2 3 receptor. It demonstrates high brain penetration, evidenced by a brain to plasma ratio of 6, and effectively blocks agonist-evoked intracellular Ca2+ flux and inward currents within the nanomolar range (10 nM to 1 µM) in cell lines that express human P2X3 and P2X2 3 receptors recombinantly. The compound also shows favorable pharmacokinetic properties, with a half-life (t1 2) of 1.63 hours and a time to reach maximum concentration (Tmax) of 30 minutes.

Bovine Serum Albumin-AF350 (BSA-AF350) 是一种生物材料和有机化合物，适用于生命科学研究。

ATX-IN-1 (compound 35) 是一种 ATX 抑制剂 (IC50=0.7 nM)，展现出抗炎活性。该化合物能够通过抑制 TGF-β Smad 通路和减少胶原蛋白沉积来缓解 Bleomycin 引发的小鼠纤维化模型。ATX-IN-1 在口服时具备良好的生物利用率 (F=69.5%) 和微粒稳定性。

HT-2 toxin-13C22is intended for use as an internal standard for the quantification of HT-2 toxin by GC- or LC-MS. HT-2 toxin is a type A trichothecene mycotoxin and an active, deacetylated metabolite of the trichothecene mycotoxin T-2 toxin .1,2Like T-2 toxin, HT-2 toxin inhibits protein synthesis and cell proliferation in plants.2HT-2 toxin also reduces viability of HepG2, A549, HEp-2, Caco-2, A-204, U937, Jurkat, and RPMI-8226 cancer cells with IC50values ranging from 3.1 to 23 ng ml and human umbilical vein endothelial cells with an IC50value of 56.4 ng ml.1It induces oxidative stress, DNA damage, and autophagy in, as well as halts the development of, cultured mouse embryos when used at a concentration of 10 nM.3HT-2 toxin has been found in cereal grains and food products.4,5 1.Nielsen, C., Casteel, M., Didier, A., et al.Trichothecene-induced cytotoxicity on human cell linesMycotoxin Res.25(2)77-84(2009) 2.Nathanail, A.V., Varga, E., Meng-Reiterer, J., et al.Metabolism of the fusarium mycotoxins T-2 toxin and HT-2 toxin in wheatJ. Agric. Food Chem.63(35)7862-7872(2015) 3.Zhang, L., Li, L., Xu, J., et al.HT-2 toxin exposure induces mitochondria dysfunction and DNA damage during mouse early embryo developmentReprod. Toxicol.85104-109(2019) 4.Langseth, W., and Rundberget, T.The occurrence of HT-2 toxin and other trichothecenes in Norwegian cerealsMycopathologia147(3)157-165(1999) 5.Al-Taher, F., Cappozzo, J., Zweigenbaum, J., et al.Detection and quantitation of mycotoxins in infant cereals in the U.S. market by LC-MS MS using a stable isotope dilution assayFood Control72(Part A)27-35(2017)

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).

Elaidamide is a fatty acid amide that has been found in the cerebrospinal fluid of sleep-deprived cats.1 It inhibits rat microsomal epoxide hydrolase (mEH; Ki = 70 nM).2 Elaidamide also inhibits porcine pancreatic and human synovial phospholipase A2 (PLA2).3 In vivo, elaidamide (10 mg/animal) induces physiological sleep in rats.1References1. Cravatt, B.F., Prospero-Garcia, O., Siuzdak, G., et al. Chemical characterization of a family of brain lipids that induce sleep. Science 268(5216), 1506-1509 (1995).2. Morisseau, C., Newman, J.W., Dowdy, D.L., et al. Inhibition of microsomal epoxide hydrolases by ureas, amides, and amines. Chem. Res. Toxicol. 14(4), 409-415 (2001).3. Jain, M.K., Ghomashchi, F., Yu, B.Z., et al. Fatty acid amides: scooting mode-based discovery of tight-binding competitive inhibitors of secreted phospholipases A2. J. Med. Chem. 35(19), 3584-3586 (1992). Elaidamide is a fatty acid amide that has been found in the cerebrospinal fluid of sleep-deprived cats.1 It inhibits rat microsomal epoxide hydrolase (mEH; Ki = 70 nM).2 Elaidamide also inhibits porcine pancreatic and human synovial phospholipase A2 (PLA2).3 In vivo, elaidamide (10 mg/animal) induces physiological sleep in rats.1 References1. Cravatt, B.F., Prospero-Garcia, O., Siuzdak, G., et al. Chemical characterization of a family of brain lipids that induce sleep. Science 268(5216), 1506-1509 (1995).2. Morisseau, C., Newman, J.W., Dowdy, D.L., et al. Inhibition of microsomal epoxide hydrolases by ureas, amides, and amines. Chem. Res. Toxicol. 14(4), 409-415 (2001).3. Jain, M.K., Ghomashchi, F., Yu, B.Z., et al. Fatty acid amides: scooting mode-based discovery of tight-binding competitive inhibitors of secreted phospholipases A2. J. Med. Chem. 35(19), 3584-3586 (1992).