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항목
AntibodyCurated CoreFDAstaleApproved
bimekizumab (Bimzelx, UCB4940, bimekizumab-bkzx)
UCB·IL-17A / IL-17F
58 trials
AntibodyCurated CoreFDAstaleApproved
secukinumab (Cosentyx, AIN457)
Novartis·IL-17A
229 trials
AntibodyCurated CorestaleApproved
Ixekizumab (Ixekizumab)
Eli Lilly and Company·Psoriatic Arthritis
53 trials
Overview
Program
Bimzelx (bimekizumab)Cosentyx (secukinumab)Ixekizumab
Overview
Company
UCBNovartisEli Lilly and Company
Overview
Modality
ANTIBODYANTIBODYANTIBODY
Overview
Target
IL-17A / IL-17FIL-17APsoriatic Arthritis
Overview
Indication
Plaque psoriasis, psoriatic arthritis, axial spondyloarthritis, hidradenitis suppurativaPsoriasis, PsA, AS, nr-axSpA, HSPsoriasis; Atopic Dermatitis
Overview
Phase
APPROVEDAPPROVEDAPPROVED
Overview
Status
APPROVEDAPPROVEDRECRUITING
Overview
Content status
Curated CoreCurated CoreCurated Core
Overview
Data Confidence
Editorial scope · Curated CoreEditorial scope · Curated CoreEditorial scope · Curated Core
Overview
Development Signal
Development Signal · EstablishedDevelopment Signal · EstablishedDevelopment Signal · Established
Overview
Approval status
FDA approvedFDA approvedApproved (flag incomplete)
Positioning
Key differentiator
IL-17F contributes independently to tissue inflammation, so blocking it as well raises the ceiling on complete skin clearance.Novel approaches, including tolerogenic DC therapy and neuroimmune modulation, hold promise for refining treatment and addresNovel approaches, including tolerogenic DC therapy and neuroimmune modulation, hold promise for refining treatment and addres
Positioning
Known limitation
Anti-drug antibodies and non-IL-17-driven inflammatory phenotypes.bypassed its classic signal adaptor and directly interacted with the calcium-binding protein S100A9—
Positioning
Development positioning
1L–2L biologic——
MoA
Mechanism
Binds IL-17A and IL-17F, preventing engagement of the IL-17RA/RC complex and shutting down downstream keratinocyte and synovial inflammatory signaling more completely than IL-17A blockade alone.Secukinumab binds IL-17A and prevents interaction with IL-17RA/RC receptor complex, inhibiting keratinocyte and synovial inflammation driven by Th17 pathway.targets and signaling pathway
MoA
Biomarker
PASI/IGA response, hs-CRP in axial disease.PASI, ASAS response, radiographic progression in SpA.—
Toxicology
Species
Cynomolgus monkeyMouse—
Toxicology
Major finding
Oral candidiasis is the signature toxicity of IL-17F co-blockade and occurs in roughly 10–20% of patients. Upper respiratory infection is common; inflammatory bowel disease requires monitoring.Nasopharyngitis, candidiasis (mucocutaneous), neutropenia; IBD caution in label.—
Toxicology
CRS
N/AN/A—
Clinical
Safety signal
Oral candidiasis is the signature toxicity of IL-17F co-blockade and occurs in roughly 10–20% of patients. Upper respiratory infection is common; inflammatory bowel disease requires monitoring.Nasopharyngitis, candidiasis (mucocutaneous), neutropenia; IBD caution in label.—
Clinical
Program phase
APPROVEDAPPROVEDAPPROVED
Clinical
Trial activity
No active/completed countsNo active/completed counts—