http://rdf.ncbi.nlm.nih.gov/pubchem/patent/WO-2021013911-A1
Outgoing Links
| Predicate | Object |
|---|---|
| assignee | http://rdf.ncbi.nlm.nih.gov/pubchem/patentassignee/MD5_43a72884e25aaecffebe0942132d704f http://rdf.ncbi.nlm.nih.gov/pubchem/patentassignee/MD5_a0e4c112c42f7a155a467679cf99e67c http://rdf.ncbi.nlm.nih.gov/pubchem/patentassignee/MD5_df02dc2eab1779ebc7dfb5accf94318b |
| classificationCPCInventive | http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K31-341 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K31-4045 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61P31-04 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61P17-10 |
| classificationIPCInventive | http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61P17-10 http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61P31-04 http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K31-341 http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K31-4045 |
| filingDate | 2020-07-23-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| inventor | http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_83bea3e0d90a55d12ce4d6a69548b7d5 http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_a636dca8f7c1da83e2c0b3866ff4700c http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_49212f303e2138f0953153c62e2f747b http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_ead2a6780de4a1a3d5ed1be0edb6b2a6 |
| publicationDate | 2021-01-28-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| publicationNumber | WO-2021013911-A1 |
| titleOfInvention | Inhibitors of the sting pathway for the treatment of hidradenitis suppurativa |
| abstract | Hidradenitis suppurativa (HS) is a chronic, relapsing, inflammatory skin disease in which the primary abnormality appears to affect the pilosebaceous-apocrine unit. Here, inventors' objective was to characterize the molecular mechanisms involved in the pro- inflammatory phenotype of HS-ORS cells. Transcriptomic analyses of HS-ORS cells demonstrated dysregulation of genes involved in cell proliferation and differentiation, as well as upregulation of the DNA damage response (DDR) and IFN signature. The inventors identified abnormalities in the HF-SC compartment from patients with HS, including high counts of proliferating progenitor cells and loss of quiescent bulge stem cells. Fork progression analysis revealed replicative stress responsible for ATR-CHK1 pathway activation. Accumulation of ssDNA and micronuclei in the cytosol of HS-ORS cells was found to contribute to STING activation via the DNA sensor IFI16, inducing IFN synthesis independently of cGAS. STING depletion in ORS cells resulted in modulation of fork progression. These findings support the concept that, in patients with HS, impaired HF-SC homeostasis responsible for increased proliferation induces replicative stress and cytosolic ssDNA accumulation, thereby stimulating IFN synthesis through the STING pathway. Accordingly, inhibiting said pathway would be suitable of the treatment of HS. |
| isCitedBy | http://rdf.ncbi.nlm.nih.gov/pubchem/patent/WO-2022178443-A1 |
| priorityDate | 2019-07-24-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| type | http://data.epo.org/linked-data/def/patent/Publication |
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