ar-Turmerone ((+)-ar-Turmerone) is a major bioactive compound of the herb Curcuma longa with anti-tumorigenesis and anti-inflammatory activities[1][2][3]. ar-Turmerone ((+)-ar-Turmerone) exerts positive modulation on murine DCs, induces NSC proliferation.
Bepafant is a platelet activating factor (PAF) antagonist. Bepafant may produce significant anti-inflammatory effects. Bepafant triggered apoptosis in NB4, KG1, and NB4-MR4 cells where PTEN was expressed, but not in THP1 and U937cells where PTEN was abse
Cytochalasin D is an actin inhibitor, the removal of actin stress fibers is crucial for the chondrogenic differentiation. It may be an inhibitor of some fertilization processes such as sperm penetration or sperm head decondensation. Cytochalasin D inhibit
α-Melanocyte-stimulating hormone (α-MSH) is a 13-amino acid peptide hormone produced by post-translational processing of proopiomelanocortin (POMC) in the pituitary gland, as well as in keratinocytes, astrocytes, monocytes, and gastrointestinal cells.1It is an agonist of melanocortin receptor 3 (MC3R) and MC4R that induces cAMP production in Hepa cells expressing the human receptors (EC50s = 0.16 and 56 nM, respectively).2α-MSH (100 pM) reducesS. aureuscolony formation andC. albicansgerm tube formationin vitro.3It inhibits endotoxin-, ceramide-, TNF-α-, or okadaic acid-induced activation of NF-κB in U937cells.1α-MSH reduces IL-6- or TNF-α-induced ear edema in mice.4It also prevents the development of adjuvant-induced arthritis in rats and increases survival in a mouse model of septic shock. Increased plasma levels of α-MSH are positively correlated with delayed disease progression and reduced death in patients with HIV.1 1.Catania, A., Airaghi, L., Colombo, G., et al.α-melanocyte-stimulating hormone in normal human physiology and disease statesTrends Endocrinol. Metab.11(8)304-308(2000) 2.Miwa, H., Gantz, I., Konda, Y., et al.Structural determinants of the melanocortin peptides required for activation of melanocortin-3 and melanocortin-4 receptorsJ. Pharmacol. Exp. Ther.273(1)367-372(1995) 3.Cutuli, M., Cristiani, S., Lipton, J.M., et al.Antimicrobial effects of a-MSH peptidesJ. Leukoc. Biol.67(2)233-239(2000) 4.Lipton, J.M., Ceriani, G., Macaluso, A., et al.Antiiinflammatory effect of the neuropeptide a-MSH in acute, chronic, and systemic inflammationAnn. N.Y. Acad. Sci.25(741)137-148(1994)
Tpl2 kinase inhibitor is an inhibitor of tumor progression locus 2 (Tpl2; IC50= 0.05 μM).1It is selective for Tpl2 over MEK, p38 MAPK, Src, MK2, and PKC (IC50s = >40, 180, >400, 110, and >400 μM, respectively). Tpl2 kinase inhibitor inhibits LPS-induced TNF-α production in isolated human monocytes and whole blood (IC50s = 0.7 and 8.5 μM, respectively). It enhances differentiation induced by calcitriol in HL-60 and U937 leukemia cells when used at a concentration of 5 μM.2Tpl2 kinase inhibitor (5 μM) inhibits the proliferation of KG-1a leukemia cells.3 1.Garvin, L.K., Green, N., Hu, Y., et al.Inhibition of Tpl2 kinase and TNF-α production with 1,7-naphthyridine-3-carbonitriles: Synthesis and structure-activity relationshipsBioor. Med. Chem. Lett.15(23)5288-5292(2005) 2.Wang, X., and Studzinski, G.P.Expression of MAP3 kinase COT1 is up-regulated by 1,25-dihydroxyvitamin D3 in parallel with activated c-jun during differentiation of human myeloid leukemia cellsJ. Steroid. Biochem. Mol. Biol.121(1-2)395-398(2010) 3.Wang, X., Gocek, E., Novik, V., et al.Inhibition of Cot1/Tlp2 oncogene in AML cells reduces ERK5 activation and up-regulates p27Kip1 concomitant with enhancement of differentiation and cell cycle arrest induced by silibinin and 1,25-dihydroxyvitamin D3Cell Cycle9(22)4542-4551(2010)
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)
O-Demethyl apremilast is an active metabolite of the phosphodiesterase 4 (PDE4) inhibitor apremilast .1It inhibits the activity of PDE4 isolated from U937cells and LPS-induced TNF-α production in isolated human peripheral blood mononuclear cells (PBMCs; IC50s = 8.3 and 5.6 μM, respectively). O-Demethyl apremilast is also an oxidative degradation product of apremilast.2,3 1.Hoffmann, M., Kumar, G., Schafer, P., et al.Disposition, metabolism and mass balance of [14C]apremilast following oral administrationXenobiotica41(12)1063-1075(2011) 2.Lu, Y., Shen, X., Hang, T., et al.Identification and characterization of process-related substances and degradation products in apremilast: Process optimization and degradation pathway elucidationJ. Pharm. Biomed. Anal.14170-78(2017) 3.Bhole, R.P., Naksakhare, S.R., and Bonde, C.G.A stability indicating HPTLC method for apremilast and identification of degradation products using MS MSJ. Pharm. Sci. & Res.11(5)1861-1869(2019)
C6 L-erythro Ceramide is a bioactive sphingolipid and cell-permeable analog of naturally occurring ceramides. It is metabolized by ceramide glucosyltransferase to form C6 L-erythro glucosylceramide. C6 L-erythro Ceramide is cytotoxic to U937cells (IC50 = 18 μM).
C6 L-threo Ceramide is a bioactive sphingolipid and cell-permeable analog of naturally occurring ceramides., C6 L-threo Ceramide is cytotoxic to U937cells in vitro (IC50 = 18 μM). It is metabolically inactive and, unlike C6 L-erythro ceramide , C6 L-threo ceramide cannot be converted to C6 glucosylceramide by ceramide glucosyltransferase. C6 L-threo Ceramide enhances IL-4 production induced by phorbol 12-myristate 13-acetate in EL4 T cells when used at a concentration of 10 μM.