ADU-S100_product_DataBase

Bioactivity	ADU-S100 (MIW815), an activator of stimulator of interferon genes (STING), leads to potent and systemic tumor regression and immunity[1].
Target	STING
Invitro	ADU-S100 is unstable in its free base form. ADU-S100 ammonium salt (HY-12885B) improves both stability and lipophilicity, promoting significantly increased STING signaling as compared to endogenous and pathogen-derived cyclic dinucleotides (CDNs)[1].ADU-S100 shows enhanced type I IFN production over CDA in THP-1 human monocytes. In contrast, the dithio, mixed-linkage CDN derivatives (ML RR-CDA, ML RR-S2 CDG, and ML RR-S2 cGAMP) potently activate all five hSTING alleles, including the refractory hSTINGREF and hSTINGQ alleles. ADU-S100 induces the highest expression of IFN-β and the pro-inflammatory cytokines TNF-α, IL-6, and MCP-1 on a molar equivalent basis, as compared to endogenous ML cGAMP and the TLR3 agonist poly I:C. ADU-S100 is also found to induce aggregation of STING and induce phosphorylation of TBK1 and IRF3 in mouse bone marrow macrophage (BMM). ADU-S100 induces significantly higher levels of IFN-α when compared to ML cGAMP[1].
In Vivo	ADU-S100 shows higher anti-tumor control than the endogenous ML cGAMP. A dose response of the ADU-S100 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].
Name	ADU-S100
CAS	1638241-89-0
Formula	C20H24N10O10P2S2
Molar Mass	690.54
Appearance	Solid
Transport	Room temperature in continental US; may vary elsewhere.
Storage	-20°C, protect from light *In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
Reference	[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.

PeptideDB

ADU-S100

CAS: 1638241-89-0 F: C20H24N10O10P2S2 W: 690.54