Ignite Creation Date:
2024-10-26 @ 3:38 PM
Last Modification Date:
2024-10-26 @ 3:38 PM
Study NCT ID:
NCT06558305
Status:
NOT_YET_RECRUITING
Last Update Posted:
None
First Post:
2024-08-14
Brief Title:
IL-6 IL-12 IL-15 and IL-23 Expression Levels in Rheumatoid Arthritis Patients
Sponsor:
None
Organization:
None
Study Overview
Official Title:
Effect of cDMARD and Baricitinib Therapy on IL-6 IL-12 IL-15 and IL-23 Expression Levels in Rheumatoid Arthritis Patients
Status:
NOT_YET_RECRUITING
Status Verified Date:
2024-08
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
No
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
Rheumatoid Arthritis RA is a systemic autoimmune disease characterized by chronic inflammation and articular damage
Continuous medical research has dramatically improved the outcomes for patients with RA Traditional therapeutic approaches have relied on glucocorticoids nonsteroidal anti-inflammatory drugs NSAIDs and disease modifying antirheumatic drugs DMARDs such as methotrexate sulfasalazine or leflunomide Glucocorticoids and NSAIDs interfere with the inflammatory cascades while DMARDs impede both the inflammatory and the destructive processes of RA
These drugs although efficient are not specifically directed against inflammatory cells or cytokines and are associated with significant toxicity The development of biologic DMARDs bDMARDs has been an important step forward Their ability to neutralize specific cytokines or target distinct immune cells filled a gap in existing treatment options for RA 3 However some patients still have only partial or no response to bDMARDs More recently a group of drugs has been developed that inhibit the janus kinase JAK family of intracellular tyrosine kinases which transmit cytokine- mediated signals via the JAK-signal transducer and activator of transcription STAT pathway 4 Baricitinib with a selectivity to inhibit JAK1 and 2 has been FDA approved for RA in 2018 5
Many cytokines such IL-6 IL-12 IL-15 IL-23 GM-CSF and IFNs are associated with the pathogenesis of RA These cytokines transduce signals via the JAK-STAT pathway
Continuous medical research has dramatically improved the outcomes for patients with RA Traditional therapeutic approaches have relied on glucocorticoids nonsteroidal anti-inflammatory drugs NSAIDs and disease modifying antirheumatic drugs DMARDs such as methotrexate sulfasalazine or leflunomide Glucocorticoids and NSAIDs interfere with the inflammatory cascades while DMARDs impede both the inflammatory and the destructive processes of RA
These drugs although efficient are not specifically directed against inflammatory cells or cytokines and are associated with significant toxicity The development of biologic DMARDs bDMARDs has been an important step forward Their ability to neutralize specific cytokines or target distinct immune cells filled a gap in existing treatment options for RA 3 However some patients still have only partial or no response to bDMARDs More recently a group of drugs has been developed that inhibit the janus kinase JAK family of intracellular tyrosine kinases which transmit cytokine- mediated signals via the JAK-signal transducer and activator of transcription STAT pathway 4 Baricitinib with a selectivity to inhibit JAK1 and 2 has been FDA approved for RA in 2018 5
Many cytokines such IL-6 IL-12 IL-15 IL-23 GM-CSF and IFNs are associated with the pathogenesis of RA These cytokines transduce signals via the JAK-STAT pathway
Detailed Description:
None
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None