title: A randomized phase II study of Xilonix, a targeted therapy against interleukin 1α, for the prevention of superficial femoral artery restenosis after percutaneous revascularization.
abstract: OBJECTIVE
  The purpose of this study was to evaluate an anti-interleukin 1α antibody for its ability to reduce acute postprocedural inflammation, thereby reducing neointimal hyperplasia and restenosis after superficial femoral artery (SFA) angioplasty. Restenosis of the SFA after endovascular intervention is a common problem leading to 1-year primary patency as low as 40%. These failures are primarily due to the development of neointimal hyperplasia, resulting from arterial wall inflammation.
  
  
  METHODS
  This was a randomized, phase II trial examining SFA restenosis in patients after percutaneous revascularization. Randomization occurred after successful revascularization, and patients were assigned to either the standard of care arm or the Xilonix (XBiotech USA, Inc, Austin, Tex) plus standard of care arm (N = 43). Xilonix was administered immediately after revascularization, every 2 weeks intravenously for four doses, and monthly subcutaneously until month 12. The major efficacy end points were target vessel event-free survival and incidence of major adverse cardiovascular events (MACEs).
  
  
  RESULTS
  At 12 months of follow-up, MACE (43% vs 36%; P = .76) and target vessel restenosis (24% vs 27%; log-rank, P = .79) rates were not significantly different between the groups. At 3-month follow-up, which covers the intravenous dosing period, a trend toward lower incidence of restenosis (0 of 22 [0%] vs 2 of 21 [10%]; P = .14) and MACE (2 of 22 [9%] vs 5 of 21 [24%]; P = .22) was observed in the Xilonix cohort. Adverse events were equally distributed in both arms.
  
  
  CONCLUSIONS
  Xilonix was well tolerated. Observed tendency to improved vessel patency with intravenous dosing suggests Xilonix could potentially represent a safe and effective therapeutic approach to preserving vessel patency.
authors.affiliation: Division of Vascular Surgery and Diseases, The Ohio State University, Columbus, Ohio. Electronic address: hosam.elsayed@osumc.edu.
authors.forename: Hosam
authors.initials: H
authors.lastname: El Sayed
authors.affiliation: Department of Cardiology, Archbold Medical Center, Thomasville, Ga.
authors.forename: Richard
authors.initials: R
authors.lastname: Kerensky
authors.affiliation: Clinical Regulatory, XBiotech, Austin, Tex.
authors.forename: Michael
authors.initials: M
authors.lastname: Stecher
authors.affiliation: Clinical Regulatory, XBiotech, Austin, Tex.
authors.forename: Prasant
authors.initials: P
authors.lastname: Mohanty
authors.affiliation: Division of Vascular Surgery, University of Texas, San Antonio, Tex.
authors.forename: Mark
authors.initials: M
authors.lastname: Davies
mesh_terms: D000368:Aged; D017130:Angioplasty / Q000009:adverse effects; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage* / Q000009:adverse effects / Q000493:pharmacokinetics; D000911:Antibodies, Monoclonal / Q000008:administration & dosage* / Q000009:adverse effects / Q000493:pharmacokinetics; D061067:Antibodies, Monoclonal, Humanized; D003251:Constriction, Pathologic; D018572:Disease-Free Survival; D004334:Drug Administration Schedule; D005260:Female; D005263:Femoral Artery / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D006965:Hyperplasia; D007275:Injections, Intravenous; D007279:Injections, Subcutaneous; D008297:Male; D008875:Middle Aged; D058426:Neointima; D058729:Peripheral Arterial Disease / Q000175:diagnosis / Q000503:physiopathology / Q000628:therapy*; D012008:Recurrence; D055502:Secondary Prevention / Q000379:methods*; D013997:Time Factors; D016896:Treatment Outcome; D014481:United States; D014654:Vascular Patency / Q000187:drug effects*
chemical_list: D000893:Anti-Inflammatory Agents; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; C000604877:bermekimab