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ADU-S100 ammonium salt

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ADU-S100 ammonium salt Basic information

Product Name:
ADU-S100 ammonium salt
Synonyms:
  • ML RR-S2 CDA (ammonium salt)
  • Adenosine, [P(R)]-5'-O-[(R)-hydroxymercaptophosphinyl]-P-thioadenylyl-(2'→5')-, cyclic nucleotide, ammonium salt (1:2)
  • ADU-S100 ammonium salt
  • STING-INDUCER-1 AMMONIUM SALT
  • MIW815 ammonium salt
  • ML RR-S2 CDA ammonium salt(ADU-S100)
  • inhibit,ADU S100 ammonium salt,TMEM173,STING,MIW815,Inhibitor,MIW-815,Stimulator of Interferon Genes,MITA,MPYS,ERIS,ADU-S100,ML RR-S2 CDA,MIW 815,ADUS100 ammonium salt
  • ADU-S100 ammonium salt, 10 mM in DMSO
CAS:
1638750-96-5
MF:
C20H27N11O10P2S2
MW:
707.57
Mol File:
1638750-96-5.mol
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ADU-S100 ammonium salt Chemical Properties

storage temp. 
Store at -20°C
solubility 
DMSO: 15 mg/ml; Water: 12.5 mg/ml
form 
A solid
color 
White to off-white
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ADU-S100 ammonium salt Usage And Synthesis

Description

ML RR-S2 CDA is a synthetic cyclic dinucleotide (CDN) that contains non-canonical 2''5''-phosphodiester bonds and is an activator of stimulator of interferon genes (STING). It contains mixed linkages (ML) with both 2''5'' and 3''5'' linkages, which leads to increased thermal stability of human STING in a differential scanning fluorimetry (DSF) assay. ML RR-S2 CDA increases type I interferon production by THP-1 human monocytes relative to unmodified cyclic di-AMP (CDA; ), indicating the ML enhances its action at human STING. It induces expression of IFN-β and the pro-inflammatory cytokines TNF-α, IL-6, and Mcp-1 in murine bone marrow macrophages (BMM) isolated from wild-type, but not STING-/-, mice. ML RR-S2 CDA also induces IFN-β expression in peripheral blood mononuclear cells (PBMCs) isolated from donors carrying STINGWT/WT, STINGWT/REF, and STINGWT/HAQ alleles. In vivo, ML RR-S2 CDA initiates tumor regression and prevents tumor growth upon tumor cell reimplantation in 4T1 murine mammary and CT26 murine colon cancer models.

Uses

2’3’-c-di-AM(PS)2 (Rp,Rp) ammonium salt (ADU-S100 ammonium salt), an activator of stimulator of interferon genes (STING), leads to potent and systemic tumor regression and immunity[1].

in vivo

2’3’-c-di-AM(PS)2 (Rp,Rp) shows higher anti-tumor control than the endogenous ML cGAMP. A dose response of the 2’3’-c-di-AM(PS)2 (Rp,Rp) compound is performed in B16 tumor-bearing mice, which identifies an optimal antitumor dose level that also elicites maximum tumor antigen-specific CD8+ T cell responses, and improves long-term survival to 50%[1].

References

[1] Corrales L, et al. Direct Activation of STING in the Tumor Microenvironment Leads to Potent and Systemic Tumor Regression and Immunity. Cell Rep. 2015 May 19;11(7):1018-30. DOI:10.1016/j.celrep.2015.04.031

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