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Submit ReviewAS 101
Description: Immunomodulator; inhibits IL-10 synthesis and potentiates IL-1α, IL-2 and TNF-α release
Chemical Name: Ammonium trichloro[1,2-ethanediolato-O,O']-tellurate
Biological Activity for AS 101
AS 101 is an immunomodulator; inhibits IL-10 synthesis and potentiates IL-1α, IL-2 and TNF-α release.
Technical Data for AS 101
| M. Wt | 312.05 |
| Formula | C2H4Cl3O2Te.NH4 |
| Storage | Desiccate at RT |
| CAS Number | 106566-58-9 |
| PubChem ID | 24985142 |
| InChI Key | AXWLPMGUUAIGJK-UHFFFAOYSA-O |
| Smiles | [Cl-][Te+4]1([Cl-])([O-]CC[O-]1)[Cl-].[NH4+] |
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Product Datasheets for AS 101
References for AS 101
References are publications that support the biological activity of the product.
Kalechman et al (2004) Inhibition of interleukin-10 by the immunomodulator AS101 reduces mesangial cell proliferation in experimental mesangioproliferative glomerulonephritis. J.Biol.Chem. 279 24724 PMID: 15001575
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Keywords: AS 101, AS 101 supplier, Immunomodulators, inhibits, inhibitors, IL-10, synthesis, potentiates, IL-1alpha, IL-2, TNFalpha, release, TNF-α, TNF-alpha, Interleukins, Tumor, Necrosis, Factor-α, Factor-alpha, Cytokines, Cytokine, NF-κB, NF-kappaB, Signaling, Signalling, AS101, 2446, Tocris Bioscience
1 Citation for AS 101
Citations are publications that use Tocris products. Selected citations for AS 101 include:
Souza-Fonseca-Guimaraes et al (2012) NK cell tolerance to TLR agonists mediated by regulatory T cells after polymicrobial sepsis. J Immunol 188 5850 PMID: 22566566
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Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
Rheumatoid Arthritis Poster
Rheumatoid arthritis (RA) is a chronic destructive inflammatory autoimmune disease that results from a breakdown in immune tolerance, for reasons that are as yet unknown. This poster summarizes the pathology of RA and the inflammatory processes involved, as well as describing some of the epigenetic modifications associated with the disease and the potential for targeting these changes in the discovery of new treatments.