AS101 - CAS 106566-58-9
Not Intended for Therapeutic Use. For research use only.
Category:
Inhibitor
Product Name:
AS101
Catalog Number:
B0084-256533
Synonyms:
US brand name: Ossirene; IVX-Q-101. Ammonium trichloro(dioxoethylene-O,O') tellurate.
CAS Number:
106566-58-9
Description:
AS101 is a synthetic non-toxic tellurium derivative, structurally similar to cisplatin, with immuno-modulating, antiviral, and hair growth-promoting activities. This agent is also a potent inducer of IL-1 and IL-6. Accordingly, ammonium trichlorotellurate may protect against chemotherapy-induced alopecia.
COA:
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MSDS:
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Targets:
Cytokine Receptor
Catalog Number Size Price Stock Quantity
B0084-256533 25 mg $168 In stock
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Chemical Structure
CAS 106566-58-9 AS101

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Reference Reading


1.Multifunctional activity of a small tellurium redox immunomodulator compound, AS101, on dextran sodium sulfate-induced murine colitis.
Halpert G1, Eitan T1, Voronov E2, Apte RN2, Rath-Wolfson L3, Albeck M4, Kalechman Y1, Sredni B5. J Biol Chem. 2014 Jun 13;289(24):17215-27. doi: 10.1074/jbc.M113.536664. Epub 2014 Apr 24.
Inflammatory bowel diseases (IBDs) are a group of idiopathic, chronic immune-mediated diseases characterized by an aberrant immune response, including imbalances of inflammatory cytokine production and activated innate and adaptive immunity. Selective blockade of leukocyte migration into the gut is a promising strategy for the treatment of IBD. This study explored the effect of the immunomodulating tellurium compound ammonium trichloro (dioxoethylene-o,o') tellurate (AS101) on dextran sodium sulfate (DSS)-induced murine colitis. Both oral and intraperitoneal administration of AS101 significantly reduced clinical manifestations of IBD. Colonic inflammatory cytokine levels (IL-17 and IL-1β) were significantly down-regulated by AS101 treatment, whereas IFN-γ was not affected. Neutrophil and α4β7(+) macrophage migration into the tissue was inhibited by AS101 treatment. Adhesion of mesenteric lymph node cells to mucosal addressin cell adhesion molecule (MAdCAM-1), the ligand for α4β7 integrin, was blocked by AS101 treatment both in vitro and in vivo.
2.Novel microwave-assisted synthesis of the immunomodulator organotellurium compound ammonium trichloro(dioxoethylene-O,O')tellurate (AS101).
Vázquez-Tato MP1, Mena-Menéndez A2, Feás X3, Seijas JA4. Int J Mol Sci. 2014 Feb 21;15(2):3287-98. doi: 10.3390/ijms15023287.
Ammonium trichloro[1,2-ethanediolato-O,O']-tellurate (AS101) is the most important synthetic Te compound from the standpoint of its biological activity. It is a potent immunomodulator with a variety of potential therapeutic applications and antitumoral action in several preclinical and clinical studies. An experimental design has been used to develop and optimize a novel microwave-assisted synthesis (MAOS) of the AS101. In comparison to the results observed in the literature, refluxing Te(IV) chloride and ethylene glycol in acetonitrile (Method A), or by refluxing Te(IV) chloride and ammonium chloride in ethylene glycol (Method B), it was found that the developed methods in the present work are an effective alternative, because although performance slightly decreases compared to conventional procedures (75% vs. 79% by Method A, and 45% vs. 51% by Method B), reaction times decreased from 4 h to 30 min and from 4 h to 10 min, by Methods A and B respectively.
3.Tellurium compound AS101 ameliorates experimental autoimmune encephalomyelitis by VLA-4 inhibition and suppression of monocyte and T cell infiltration into the CNS.
Lee JH1, Halperin-Sheinfeld M, Baatar D, Mughal MR, Tae HJ, Kim JW, Carter A, Lustig A, Snir O, Lavie G, Okun E, Mattson MP, Sredni B, Taub DD. Neuromolecular Med. 2014 Jun;16(2):292-307. doi: 10.1007/s12017-013-8277-3. Epub 2013 Nov 23.
Multiple sclerosis (MS) is an inflammatory autoimmune disease of the central nervous system (CNS) involving demyelinating and neurodegenerative processes. Several of the major pathological CNS alterations and behavioral deficits of MS are recapitulated in the experimental autoimmune encephalitis (EAE) mouse model in which the disease process is induced by administration of myelin peptides. Development of EAE requires infiltration of inflammatory cytokine-generating monocytes and macrophages, and auto-reactive T cells, into the CNS. Very late antigen-4 (VLA-4, α4β1) is an integrin molecule that plays a role in inflammatory responses by facilitating the migration of leukocytes across the blood-brain barrier during inflammatory disease, and antibodies against VLA-4 exhibit therapeutic efficacy in mouse and monkey MS models. Here, we report that the tellurium compound AS101 (ammonium trichloro (dioxoethylene-o,o') tellurate) ameliorates EAE by inhibiting monocyte and T cell infiltration into the CNS.
4.The effect of the novel tellurium compound AS101 on autoimmune diseases.
Halpert G1, Sredni B2. Autoimmun Rev. 2014 Dec;13(12):1230-5. doi: 10.1016/j.autrev.2014.08.003. Epub 2014 Aug 19.
Tellurium is a rare element, which has been regarded as a non-essential trace element despite its relative abundance in the human body. The chemistry of tellurium supports a plethora of activities, but its biochemistry is not clearly established to date. The small tellurium(IV) compound, ammonium trichloro (dioxoethylene-o,o')tellurate (AS101) developed and initially investigated by us, is currently being evaluated in Phase II clinical trials in psoriasis patients. AS101 is the first tellurium compound to be tested for clinical efficacy. This compound is a potent immunomodulator both in vitro and in vivo with a variety of potential therapeutic applications. The present review will focus on the immunomodulatory properties of AS101, and specifically, its effects in mitigating autoimmune diseases. AS101 has several activities that act on the immune system, including: 1) its ability to reduce IL-17 levels and to inhibit the function of Th17 cells; 2) its specific unique redox-modulating activities enabling the inhibition of specific leukocyte integrins such as α4β1 and α4β7, that are pivotal for diapedesis of macrophages and CD4(+) T inflammatory/auto-reactive cells into the autoimmune tissues; and 3) its ability to enhance the activity of regulatory T cells (Treg).