Products with Immunosuppression bioactivity
| Cat.No. | Product Name |
|---|---|
| BCN2416 | Cyclo(Phe-Pro) |
| Cyclo(Phe-Pro) inhibition of cholera toxin and toxin-coregulated pilus production correlated with reduced transcription of the virulence regulator tcpPH and was alleviated by overexpression of tcpPH.Cyclo(Phe-Pro) has been shown to inhibit cancer cell growth and induce apoptosis in HT-29 colon cancer cells. | |
| BCN2623 | Cimicifugoside |
| 1. Cimicifugoside is a novel specific nucleoside transport inhibitor that displays synergistic potentiation of methotrexate cytotoxicity. 2. Cimicifugoside is a phytoestrogen, it can selectively inhibit nicotinic acetylcholine receptor (nAChR) -mediated response in bovine chromaffin cells. 3. Cimicifugoside shows immunosuppressive activity, which is preferentially directed toward B-cell function with larger doses being required for suppression of T-cell function. | |
| BCN2769 | Asarinin |
| Asarinin, a mammalian lignan precursor, has immunosuppression activity and can inhibit acute rejection in vitro. Asarinin may have a role on TLR4 pathway and produce prolongation of allograft heart survival. Asarinin induces dopamine biosynthesis via activation of the PKA-CREB-TH system and protects against 6-OHDA-induced cytotoxicity by inhibiting the sustained activation of the ERK-p38MAPK-JNK1/2-caspase-3 system in PC12 cells. | |
| BCN2858 | Jionoside B1 |
| 1. Jionoside B1 exhibits the obvious inhibition against aldose reductase. 2. Jionoside B1 shows the hepato-protective activity in the H2O2 induced liver injury experiments. 3. Jionoside B1 has immunosuppressive activity. | |
| BCN2985 | Kurarinone |
| Kurarinone exhibits anti-tumor, estrogenic, and anti-inflammatory activities, it also shows strong inhibitory effect on immune responses. Kurarinone may ameliorate chronic inflammatory skin diseases through the suppression of pathogenic CD4(+) T-cell differentiation and the overall immune response. Kurarinone sensitizes TNF-related apoptosis inducing ligand (TRAIL)-induced tumor cell apoptosis via suppression of NF-κB-dependent cFLIP expression; it may be by way of down-regulating Smad3 expression to interfere its induction on intercellular signal transduction and consequently ameliorate renal interstitial fibrosis. | |
