A mixed linkage (ML) cyclic di-adenosine bisthiophosphate with potent STING-activating activity and in vivo anti-tumor efficacy.
ML-RR-S2 CDA is a potent STING-activating cyclic di-adenosine (CDA or c-diAMP) nucleotide ligand with the 2′-5′, 3′-5′ mixed phosphodiester linkage (ML) in the [Rp,Rp] configuration and doubly substituted thiophosphate (S2) for optimal phosphodiesterase-resistance and thereby enhanced cellular potency. ML-RR-S2 CDA effectively induces IRF3, NF-kB, and STAT6 transcription activities in a STING-dependent manner in both murine (DC2.4 & BMMs) and human (THP1 & PBMCs) cultures (5-100 μM) as well as displays profound anti-tumor efficacy in vivo (100% growth inhibition of established B16.F10, 4T-1 or CT26 tumor with 3X 50 μg/mouse/96 hr intratumoral injections) with lasting immune-mediated tumor rejection.
Code de la classe de stockage
11 - Combustible Solids
Classe de danger pour l'eau (WGK)
WGK 3
Point d'éclair (°F)
Not applicable
Point d'éclair (°C)
Not applicable
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Spontaneous tumor-initiated T cell priming is dependent on IFN-β production by tumor-resident dendritic cells. On the basis of recent observations indicating that IFN-β expression was dependent upon activation of the host STING pathway, we hypothesized that direct engagement of STING
Stimulator of interferon genes (STING) is a cytosolic receptor that senses both exogenous and endogenous cytosolic cyclic dinucleotides (CDNs), activating TBK1/IRF3 (interferon regulatory factor 3), NF-κB (nuclear factor κB), and STAT6 (signal transducer and activator of transcription 6) signaling pathways
Type I interferon (IFN), essential for spontaneous T cell priming against solid tumors, is generated through recognition of tumor DNA by STING. Interestingly, we observe that type I IFN is not elicited in animals with disseminated acute myeloid leukemia (AML). Further
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