Live from Open Targets Platform, fetched 2026-11-11 18:19 UTC. Every row links to its source record.

STING1 stimulator of interferon response cGAMP interactor 1

ENSG00000184584 · protein coding · Open Targets profile

Key innate immune signaling adapter that promotes the production of type I interferon (IFN-alpha and IFN-beta) in response to the presence of DNA from bacteria and viruses in the cytosol (PubMed:18724357, PubMed:18818105, PubMed:19433799, PubMed:19776740, PubMed:23027953, PubMed:23747010, PubMed:23910378, PubMed:25704810, PubMed:27801882, PubMed:29973723, PubMed:30842659, PubMed:31992625, PubMed:32926474, PubMed:35045565, PubMed:35388221, PubMed:36808561, PubMed:37086726, PubMed:37832545, PubMed:39255680, PubMed:39947179). Innate immune response is triggered by non-CpG double-stranded DNA from viruses and bacteria delivered to the cytoplasm, which induces production of cyclic dinucleotides that bind and activate STING1: STING1 recognizes and binds cyclic di-GMP (c-di-GMP), a second messenger produced by bacteria, cyclic UMP-AMP (2',3'-cUAMP), and cyclic GMP-AMP (cGAMP), a messenger produced by CGAS in response to DNA in the cytosol (PubMed:21947006, PubMed:23258412, PubMed:23707065, PubMed:23722158, PubMed:23747010, PubMed:23910378, PubMed:26229117, PubMed:26300263, PubMed:30842659, PubMed:35388221, PubMed:37086726, PubMed:37379839). Upon binding to c-di-GMP, cUAMP or cGAMP, STING1 oligomerizes and buds from the endoplasmic reticulum into COPII vesicles, which then form the endoplasmic reticulum-Golgi intermediate compartment (ERGIC) (PubMed:30842662, PubMed:41639452, PubMed:41639454, PubMed:41887218). It is then phosphorylated by TBK1 on the pLxIS motif, leading to recruitment and subsequent activation of the transcription factor IRF3 to induce expression of type I interferon and exert a potent antiviral state (PubMed:22394562, PubMed:25636800, PubMed:29973723, PubMed:30643259, PubMed:30842653, PubMed:32926474, PubMed:35045565, PubMed:35388221, PubMed:38917796). Also involved in intercellular immune signaling: cross-activated by 2',3'-cGAMP previously generated in virus-infected cells, triggering type I interferon signaling in macrophages and uninfected neighboring cells to propagate and amplify the antiviral immune response (PubMed:24077100, PubMed:31992625). In addition to promote the production of type I interferon, cGAS-STING signaling also activates the NF-kappa-B signaling: mechanistically, STING1 recruits TRAF6, leading to degradation of the NF-kappa-B inhibitor and subsequent translocation of NF-kappa-B into the nucleus (PubMed:32268090, PubMed:38917796, PubMed:39262777, PubMed:40973797, PubMed:41747053). Activation of NF- kappa-B signaling takes place in the endolysosome and is independent of type I interferon response via direct activation by RNA viruses (PubMed:40973797, PubMed:41747053). Independently of type I interferon production, plays a direct role in autophagy (PubMed:30568238, PubMed:30842662, PubMed:32926474). The ERGIC serves as the membrane source for WIPI2 recruitment and LC3 lipidation, leading to formation of autophagosomes that target cytosolic DNA or DNA viruses for degradation by the lysosome (PubMed:30842662). Promotes autophagy by acting as a proton channel that directs proton efflux from the Golgi to facilitate MAP1LC3B/LC3B lipidation (PubMed:37535724, PubMed:39947179). The autophagy- and interferon-inducing activities can be uncoupled and autophagy induction is independent of TBK1 phosphorylation (PubMed:30568238, PubMed:30842662). Autophagy is also triggered upon infection by bacteria: following c-di-GMP-binding, which is produced by live Gram-positive bacteria, promotes reticulophagy (By similarity). The proton channel activity also regulates lysosome biogenesis by activating transcription factors TFEB and TFE3, driving the expression of lysosome-related genes: activated STING1 in post-Golgi vesicles induces proton efflux and lipidation of GABARAP, sequestering the FLCN- FNIP complex and blocking mTORC1-dependent inhibition of TFEB and TFE3 (PubMed:39423796, PubMed:39689715). May be involved in transduction of apoptotic signals via its association with the major histocompatibility complex class II (MHC-II) (By similarity). {ECO:0000250|UniProtKB:Q3TBT3, ECO:0000269|PubMed:18724357, ECO:0000269|PubMed:18818105, ECO:0000269|PubMed:19433799, ECO:0000269|PubMed:19776740, ECO:0000269|PubMed:21947006, ECO:0000269|PubMed:22394562, ECO:0000269|PubMed:23027953, ECO:0000269|PubMed:23258412, ECO:0000269|PubMed:23707065, ECO:0000269|PubMed:23722158, ECO:0000269|PubMed:23747010, ECO:0000269|PubMed:23910378, ECO:0000269|PubMed:24077100, ECO:0000269|PubMed:25636800, ECO:0000269|PubMed:25704810, ECO:0000269|PubMed:26229117, ECO:0000269|PubMed:26300263, ECO:0000269|PubMed:27801882, ECO:0000269|PubMed:29973723, ECO:0000269|PubMed:30568238, ECO:0000269|PubMed:30643259, ECO:0000269|PubMed:30842653, ECO:0000269|PubMed:30842659, ECO:0000269|PubMed:30842662, ECO:0000269|PubMed:31992625, ECO:0000269|PubMed:32268090, ECO:0000269|PubMed:32926474, ECO:0000269|PubMed:35045565, ECO:0000269|PubMed:35388221, ECO:0000269|PubMed:36808561, ECO:0000269|PubMed:37086726, ECO:0000269|PubMed:37379839, ECO:0000269|PubMed:37535724, ECO:0000269|PubMed:37832545, ECO:0000269|PubMed:38917796, ECO:0000269|PubMed:39255680, ECO:0000269|PubMed:39262777, ECO:0000269|PubMed:39423796, ECO:0000269|PubMed:39689715, ECO:0000269|PubMed:39947179, ECO:0000269|PubMed:40973797, ECO:0000269|PubMed:41639452, ECO:0000269|PubMed:41639454, ECO:0000269|PubMed:41747053, ECO:0000269|PubMed:41887218}.

In 7 of 15 cancers, the evidence for STING1 comes mainly from inherited variants

Each row is a cancer, strongest overall evidence first. The two dots show how strong the inherited (germline) and tumour-mutation (somatic) evidence is; the line between them is the gap.

Inherited (germline) variantsMutations in tumours (somatic)

Scores run from 0 (no evidence) to 1 (strongest). A missing dot at 0 means Open Targets holds no evidence of that kind. Source: Open Targets Platform, fetched live.

Tractability

Small molecule: Structure with Ligand, High-Quality Ligand
Antibody: GO CC high conf, UniProt loc med conf, UniProt SigP or TMHMM
PROTAC: UniProt Ubiquitination, Database Ubiquitination, Small Molecule Binder
Other modalities: Advanced Clinical

gnomAD loss of function constraint: o/e 0.6005899906158447 (upper bound 0.8812599778175354). Low values mean loss of function is poorly tolerated, a safety flag for inhibition.

Who runs trials of these drugs

No named investigators on registry trials of STING1's approved or late-stage drugs in the last three years.

3 trials of drugs against STING1 were stopped early

Terminated, withdrawn and suspended interventional trials of adu-s100, newest update first, live from ClinicalTrials.gov. Each reason is quoted exactly as the registry gives it; we do not sort reasons into safety, efficacy or business. Dates are the last registry update. Showing the 3 most recent of 3.

Ph1NCT03172936 brief why it stopped
terminated · 2022-05-03 · Novartis Pharmaceuticals · matched by the registry's drug synonyms
“Sponsor's decision”
Ph2NCT03937141 brief why it stopped
terminated · 2022-01-03 · Chinook Therapeutics, Inc. (formerly Aduro) · ADU-S100
“No substantial anti-tumor activity was observed.”
Ph1NCT02675439 brief why it stopped
terminated · 2021-12-30 · Chinook Therapeutics, Inc. (formerly Aduro) · ADU-S100
“No substantial anti-tumor activity was observed.”

Paediatric incentives and obligations for STING1's drugs

For adu-s100: what EMA and FDA publish about paediatric plans, orphan status and pediatric approvals, and how many registered studies take children. Each line is a yes, no or not published fact from the record linked under it; none of it is a forecast.

FDA pediatric target list: yes · STING1 is on the list. Membership alone neither requires nor waives a pediatric study.
Rule: Target is on FDA's Pediatric Molecular Target List (relevant targets). Source: FDA Pediatric Molecular Target List (Listed as February 2026 on the FDA Pediatric Oncology page; the file served is 9.7.22_the_relevant_molecular_target_list.xlsx, whose Summary of Changes sheet is headed 'SEPTEMBER 2022 UPDATE' (footnote date 2022-09-01)), 2026-11-11
EU paediatric investigation plan: no · No EMA paediatric investigation plan decision names adu-s100
Rule: An EMA PIP decision (agreement, modification or waiver) lists the drug as its active substance, exact name. Source: EMA data download (dated snapshot), 2026-11-11
EU orphan designation: no · No EU orphan designation names adu-s100
Rule: An EU orphan designation lists the drug as its active substance (exact name) or belongs to a medicine that does; withdrawn and expired designations are listed with their status. Source: EMA data download (dated snapshot), 2026-11-11
Authorised in the EU: no · EMA lists no centrally authorised medicine of adu-s100
Rule: An EMA medicine record lists the drug as its active substance or INN, exact name; national-only authorisations are not in this file. Source: EMA data download (dated snapshot), 2026-11-11
FDA orphan designation: not published · FDA's orphan designation database turns away automated requests, so this app does not read it; search it by hand at the link
Rule: Would be: an FDA orphan designation names the drug. Source: FDA orphan designations search
FDA pediatric oncology approval: no · FDA's table lists no pediatric approval of adu-s100
Rule: FDA's Pediatric Oncology Drug Approvals table names the drug. Source: FDA Pediatric Oncology Drug Approvals (content current as of 2026-03-03), 2026-11-11
Registered studies open to children: no · No interventional study of adu-s100 includes patients under 18
Rule: The registry's age group includes Child (birth to 17 years), which also counts studies that set no minimum age. Source: ClinicalTrials.gov search, 2026-11-11

Rare pediatric disease voucher. FDA, content current as of 29 Apr 2026: “As of February 3, 2026, enactment of the Consolidated Appropriations Act, 2026, the rare pediatric disease PRV program will sunset after September 30, 2029. FDA may not award any PRVs under this program after September 30, 2029.” Voucher sale prices are not shown here; they appear only as company-reported news. FDA: Rare Pediatric Disease Designation and Priority Review Voucher Programs

All 1 drugs and clinical candidates as a table

Each drug, stage and indication links to its Open Targets record, where the trials and approvals behind it are listed. Salt forms (for example a mesylate) are listed as Open Targets records them, as separate entries.

Drug	Type	Highest stage	Indications	Source records
ADU-S100	Unknown	phase 2	head and neck cancer, head and neck squamous cell carcinoma, lymphoma	Open Targets · ChEMBL