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You are here:Home-Inhibitors & Agonists-Immunology/Inflammation-STING

Request The Product List ofSTING STING

STING (Stimulator of Interferon Genes) is a transmembrane protein localized to the endoplasmic reticulum that undergoes a conformational change in response to direct binding of cyclic dinucleotides (CDNs), resulting in a downstream signaling cascade involving TBK1 activation, IRF-3 phosphorylation, and production of IFN-β and other cytokines.

STING is a pattern recognition receptor of cyclic dinucleotides as well as an innate immune adaptor protein that enables signaling from cytoplasmic receptors to the transcription factor interferon regulatory factor 3. Initiation of these pathways leads to the expression of type I interferons and proteins associated with antiviral and antitumor immunity. Small molecules capable of triggering STING-dependent cellular processes are effective at blocking virus replication, enhancing vaccine efficacy, and facilitating immune response to cancer cells.

Cat. No. Product Name CAS No. Information
H9603

STING agonist C53

 		2259624-71-8

STING agonist C53 is a potent small molecule activator of human STING with functional EC50 of 183 nM in immortalised and primary cells;STING agonist C53 directly activates STING from across the major protein variants found in the human population and from both recombinant and primary cells.STING agonist C53 induces a broad panel of cytokines and markers of dendritic cell maturation consistent with its activation of STING.STING agonist C53 binds to a cryptic pocket in the STING transmembrane domain, between the two subunits of the STING dimer. promotes the oligomerization and activation of human STING through a mechanism orthogonal to that of cGAMP.Compound 53 triggers outward shifts of transmembrane helices in the dimer, and induces inter-dimer interactions between these helices to mediate the formation of the high-order oligomer.
H9354

Ulevostinag

 		2082743-96-0

Ulevostinag is a potent stimulator of interferon genes (STING) inhibitor.
H9221

STING agonist M04

 		875158-73-9

STING agonist M04 is a novel STING agonist.STING agonist M04 activates IFN-I response through stimulation, which has different activities in natural protein variants.
H9090

MSA-2

 		129425-81-6

MSA-2 is a potent ,an orally available non-nucleotide STING agonist, has EC50s of 8.3 and 24 μM for human STING isoforms WT and HAQ, respectively; MSA-2 shows antitumor activity and stimulates interferon-β secretion in tumors, induces tumor regression with durable antitumor immunity, and synergizes with anti-PD-1 in syngeneic mouse tumor models.
H9089

SR-301

 		2375419-35-3

SR-301 is an orally, non-nucleotide STING agonist with EC50 value of 0.6 μM,At the dose of 15 mg / kg / day, the tumor of B16.f10 tumor bearing mice could be well controlled.
H8969

2',3'-cGAMP sodium

2',3'-cGAMP sodium (2'-3'-cyclic GMP-AMP sodium) is a endogenous cGAMP in mammalian cells. 2',3'-cGAMP sodium binds to STING with a high affinity and is a potent inducer of interferon-β (IFNβ). 2',3'-cGAMP sodium is produced in mammalian cells in response to DNA in the cytoplasm.
H8689

STING agonist Compound 32

STING agonist Compound 32 is a novel LNA CDN STING agonist with of IC50 values of 2 nM for STING and 10 nM for STINGWT in the HTRF binding assay.
H8508

STING ligand-1

 		2365039-41-2

STING ligand-1 is a lead STING ligand with an IC50 of 68 nM for HAQ STING.
H4096

STING inhibitor H-151

 		941987-60-6

STING inhibitor H-151 (H-151) is a highly potent, selective, covalent small-molecule antagonist of STING that has noteworthy inhibitory activity both in human cells and in vivo; the irreversible modification introduced by H-151 to hsSTING again is dependent on Cys91; markedly reduces systemic cytokine responses in CMA-treated mice.
H4095

STING inhibitor C-178

 		329198-87-0

STING inhibitor C-178 is a covalent, small-molecule inhibitor of STING, blocks palmitoylation (PMA)-induced clustering of STING; covalently binds to Cys91, directly targets mouse STING (mmSTING) but not human STING (hsSTING).

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