CG500354 plays a tumor suppressive role through the cAMP CREB signaling pathway and is a novel inducer of neural differentiation and growth arrest in primary HUMAN GBM derived cells.
β-Endorphin (β-EP) is an endogenous opioid neuropeptide with diverse biological activities. It is produced via piomelanocortin cleavage in the pituitary gland, hypothalamus, and in lymphocytes, then migrates to its sites of action which include plasma, gut, skin, placenta, cerebrospinal fluid, and cardiac tissues. β-EP induces concentration-dependent decreases in electrically stimulated contraction of the mouse vas deferens that can be reversed by the μ-opioid antagonist CTP and δ-opioid antagonist ICI 174,864. In vivo, β-EP (5 μg, i.c.v.) slows gastrointestinal transit in mice. β-EP (0.5 or 5 μg, i.c.v.) stimulates food intake in rats for 4 to 6 hours, however, this effect is not prolonged with continuous infusion. It antagonizes the appetite-suppressive effects of α-melanocyte-stimulating hormone (α-MSH) for the first three days post administration. β-EP also reduces paralytic demyelination induced by the murine coronavirus MHV-JHM in immunocompetent, but not irradiated or immune-incompetent, mice and rats.
Destruxin B2 is a cyclic hexadepsipeptide mycotoxin that has been found in M. anisopliae and has antiviral, insecticidal, and phytotoxic activities.1,2,3 It inhibits secretion of hepatitis B virus surface antigen (HBsAg) by Hep3B cells expressing hepatitis B virus (HBV) DNA (IC50 = 1.3 μM).1 Destruxin B2 is toxic to Sf9 insect cells in an electric cell-substrate impedance sensing (ECIS) test with a 50% inhibitory concentration (ECIS50) value of 92 μM.4 It is also phytotoxic to B. napus leaves.3 |1. Yeh, S.F., Pan, W., Ong, G.-T., et al. Study of structure-activity correlation in destruxins, a class of cyclodepsipeptides possessing suppressive effect on the generation of hepatitis B virus surface antigen in human hepatoma cells. Biochem. Biophys. Res. Commun. 229(1), 65-72 (1996).|2. Male, K.B., Tzeng, Y.-M., Montes, J., et al. Probing inhibitory effects of destruxins from Metarhizium anisopliae using insect cell based impedance spectroscopy: Inhibition vs chemical structure. Analyst 134(7), 1447-1452 (2009).|3. Buchwaldt, L., and Green, H. Phytotoxicity of destruxin B and its possible role in the pathogenesis of Alternaria brassicae. Plant Pathol. 41(1), 55-63 (1992).
TEI-9648, a Vitamin D3 Lactone analogue, is a potent and specific vitamin D receptor (VDR) antagonist. TEI-9648 inhibits VDR/VDRE-mediated genomic actions of 1α,25(OH)2D3. TEI-9648 also inhibits HL-60 cell differentiation induced by of 1α,25(OH)2D3. TEI-9648 has the potential for bone metabolism research[1][2]. TEI-9648 (10-1000 nM) dose-dependently blocks the reciprocal changes of CD11b and CD71 expression associated with HL-60 cell differentiation induced by 1α,25(OH)2D3[1]. TEI-9648 has consistently weaker suppressive effect than TEI-9647[1]. TEI-9648 can not induce cell differentiation even after treatment at 1 μM in HL-60 cell[1]. TEI-9648 alone can not induce activation of NBT-reducing activity or α-NB esterase activity. In contrast, TEI-9648 markedly suppresses the up-regulation induced by 1α,25(OH)2D3 (0.1 nM) in HL-60 cells[1]. [1]. Miura D, et al. Antagonistic action of novel 1α,25-dihydroxyvitamin D3-26, 23-lactone analogs on differentiation of human leukemia cells (HL-60) induced by 1α,25-dihydroxyvitamin D3. J Biol Chem. 1999 Jun 4;274(23):16392-9. [2]. Kazuya Takenouchi, et al. Synthesis and structure-activity relationships of TEI-9647 derivatives as Vitamin D3 antagonists. J Steroid Biochem Mol Biol. 2004 May;89-90(1-5):31-4.